1 

I 



A 

TEXT-BOOK OF MEDICINE 

FOR STUDENTS AND PRACTITIONERS 



BY 

Dr. ADOLF STRUMPELL 

M 

PROFESSOR AND DIRECTOR OF THE MEDICAL CLINIQUE AT 
THE UNIVERSITY OF ERLANGEN 



TTbtrfc Hmerican BMtion 

TRANSLATED BY PERMISSION FROM THE THIRTEENTH 
GERMAN EDITION, BY 

HERMAN F. VICKERY, A. B., M. D. 

Instructor in Clinical Medicine, Harvard University ; Visiting Physician to the 
Massachusetts General Hospital ; Member of the Association of American 
Physicians ; Fellow of the Massachusetts Medical Society, etc. 

AND 

PHILIP COOMBS KNAPP, A.M., M. D. 

Ex-President of the American Neurological Association ; Clinical Instructor 
in Diseases of the Nervous System, Harvard University ; Physician for 
Diseases of the Nervous System, Boston City Hospital ; Fellow 
of the Massachusetts Medical Society, etc. 



WITH EDITORIAL NOTES BY 

FREDERICK C. SHATTUCK, A.M., M. D. 

Jackson Professor of Clinical Medicine, Harvard University ; Visiting Physician to 
the Massachusetts General Hospital ; Member of the Association of American 
Physicians ; Fellow of the Massachusetts Medical Society, etc. 



WITH ONE HUNDRED AND EIGHTY-FIVE ILLUSTRATIONS 
IN THE TEXT, AND ONE PLATE 



NEW YORK 
D. APPLETON AND COMPANY 
1 90 1 



THE LIBRARY OF 

CONGRESS, 
Two CoHttii Received 

OCT. 12 1901 

Copyright entry 
CLASS XXc. No. 

copy a 



Copyright, 1886, 1893, 1901, 
By D. APPLETON AND COMPANY. 

All rights reserved. 



Electrotyped and Printed 
at the Appleton Press, TJ. S. A. 



LC Control Number 




tmp96 029095 



AUTHOR'S PREFACE TO THE THIRTEENTH EDITION 



The extent to which my text-book has been used, both in Germany and in 
other countries,* justifies me in the assumption that it has exercised some little 
influence upon the professional thought and practice of numerous medical read- 
ers, and imposes upon me the obligation of employing every opportunity for the 
improvement and perfection of my work. Yet I must confess that this task seems 
more difficult to me with every new edition of the book, for scientific workers are 
making deep and extensive investigations into the many subdivisions of internal 
medicine, with such zeal and skill that it becomes difficult for any one man to 
keep step with the unceasing progress of investigation in this wide domain, and 
to maintain that complete and universal command of facts and theories which 
is essential for a presentation of the subject, which shall be at once brief and 
true to the present standpoint of science. The author has often been painfully 
sensible of these limitations of his personal knowledge and ability, but he hopes 
that this will be regarded not merely as subject for criticism, but also as an 
excuse and an incentive to clemency, in case a reader who is expert in any 
specialty finds here and there an omission or an error. Above all, I beg the 
reader to consider that no text -book such as the present one ought to replace, or 
could replace, the vast material of the larger reference books. My purpose was 
not to collect all the facts of pathology which have been discovered up to date, 
nor all the methods of treatment which may have been recommended, wisely or 
unwisely, nor ail the theories or views which have been propounded. My wish was 
to give a complete presentation of the essentials of our present knowledge and 
views with regard to the various diseases, from a scientific and individual stand- 
point ; and I desired particularly to impart to the reader an insight into the origin 
and relation of the various morbid phenomena. To this end I have brought the 
facts of clinical experience into the closest possible relation with the data of path- 
ological anatomy and of general pathology, and have endeavored, also, in discuss- 
ing therapeutics, to deduce from the nature of the symptoms a basis for rational 
medical opinion and treatment, although I have not undervalued the importance 

* So far as I have been informed, translations of my text- book have appeared in the following lan- 
guages : French, English, Italian, Spanish, Russian, modern Greek, Turkish, and Japanese : and some 
of these translations have had several editions. 

iii 



iv 



AUTHOK'S PKEFACE 



of simple experience. A text-book intended for students and a larger circle of 
graduate readers ought not to incline too decidedly toward any one of the pre- 
vailing currents of scientific opinion. It should, however, acquaint the reader 
to such an extent with the questions at present under discussion relating to 
internal medicine, as to give him at least a fair start in his further studies. 

The author has made an honest effort to bring the present thirteenth edition 
of this book up to the level of contemporary medical thought and knowledge. 
Large portions of the book have been almost completely rewritten — in particular, 
the whole doctrine of gastric diseases and several chapters in other sections, in- 
cluding gall-stones, intestinal parasites, etc. Almost all portions of the book 
have received numerous additions and improvements, so that this edition may be 
said with justice to be completely revised. That even now my work is imperfect I 
am well aware. I shall, therefore, be thankful to any one who will inform me of 
the mistakes or omissions he discovers. 

A. Strumpell. 



TRANSLATORS' PREFACE 



The work of Professor Striimpell has been so long familiar that it is hardly 
necessary for the translators to introduce it again to the English-speaking por- 
tion of the medical profession or to express again their admiration of the work. 
Since the second edition of this translation was published in 1893 seven new 
editions have appeared in Germany, so that the book has been almost wholly re- 
written, although it still retains all the merits of the earlier production, with the 
advantage of being fully in line with the most recent medical investigations. 
The translators have kept as close to the original as seemed consistent with clear- 
ness. The doses in the metric system have been changed to the approximate 
equivalents in apothecaries' weight, the original doses being retained in paren- 
theses. As in the former editions, the translators have substituted specimens of 
handwriting in English in the chapter on general paralysis for the original in 
German script. These specimens were kindly furnished them by the late Dr. 
E. P. Elliot, of the Danvers Insane Hospital. The translators have also added a 
chapter upon the plague and various notes which they hope may prove of assist- 
ance to the American practitioner. These additions are inclosed in brackets and 
signed by the initials of the translators, to distinguish them from the (unsigned) 
additions, also in brackets, of Dr. Shattuck. 

Boston, June, 1901. 



c oj^teistt s 



Acute General Infectious Diseases 

CHAPTER PAGE 

I. Typhoid Fever .1 

Phenomena and Complications relating to the Separate Organs . . 9 
Peculiarities in the Course of the Disease ....... 20 

Relapses of Typhoid Fever ......... 21 

IT. Typhus Fever . . 30 

III. Relapsing Fever .33 

IV. Scarlet Fever 38 

V. Measles . . . . : . . . . . . .48 

VI. Rotheln . . ... . .53 

VH. Small-pox 54 

Variola Vera ............ 55 

Varioloid • . . . . . . . . . . . .56 

Course of the Fever, Symptoms presented by Separate Organs, and 

Complications ........... 57 

VIII. Varicella .... . .62 

IX. Erysipelas . 63 

X. Diphtheria . / ■ . . . 67 

XI. Influenza (Grippe) . . . . . . . ... .77 

XH. Dysentery - . . . . . . .81 

XIII. Cholera . . . . . ... . . . .85 

XIV. Malarial Diseases 93 

Intermittent Fever ........... 96 

Pernicious Intermittent Fever . . . . . . . .98 

Remittent and Continuous Forms of Malarial Fever . . . .99 

Chronic Malarial Cachexia . . . . . . . .99 

Masked Intermittent Fever .99 

Typho-malarial Fever . . . . . . . . . .100 

XV. Dengue . . . 102 

XVI. Yellow Fever . . . 104 

XVTI. Plague 107 

XVIII. Epidemic Cerebro-spinal Meningitis . Ill 

XIX. Septic and Pysemic Diseases . . . . . . . . .116 

XX. Hydrophobia (Rabies canina) 122 

XXI. Glanders (Farcy) 125 

XXII. Malignant Pustule (Anthrax. Mycosis intestinalis) 127 

XXIII. Trichinosis 131 

Diseases of the Respiratory Organs 

SECTION I 

DISEASES OF THE NOSE 

I. Coryza . . . 135 

II. Chronic Rhinitis * 137 

III. Nose-bleed . . .139 

yii 



viii 



CONTENTS 



SECTION II 



DISEASES OF THE LARYNX 
CHAPTER PAGE 

I. Acute Laryngeal Catarrh (Acute Laryngitis) ...... 140 

II. Chronic Laryngitis (Chronic Laryngeal Catarrh) ..... 143 

III. Laryngeal Perichondritis ......... 145 

IV. (Edema of the Glottis . . 146 

V. Tuberculosis of the Larynx (Consumption of the Larynx) .... 147 

VI. Paralyses of the Laryngeal Muscles ........ 150 

Paralyses in the Distribution of the Superior Laryngeal Nerve . . . 150 
Paralyses in the Distribution of the Inferior Laryngeal or Recurrent Nerve . 150 

VII. Spasm of the Glottis 153 

VIII. New Growths in the Larynx ......... 155 

Benignant Growths in the Larynx ........ 155 

Malignant Growths. Carcinoma of the Larynx ..... 155 

SECTION III 

DISEASES OF THE TRACHEA AND THE BRONCHI 

I. Acute Catarrh of the Trachea and the Bronchi ...... 156 

The Milder Forms of Acute Bronchitis ....... 159 

The Severer Febrile Forms of Acute Bronchitis 159 

Catarrh of the Finer Bronchi. Capillary Bronchitis ..... 160 

II. Chronic Bronchitis . . . . . . . . . . . 162 

III. Foetid Bronchitis (Putrid Bronchitis) 167 

IV. Croupous Bronchitis (Fibrinous Bronchitis) ...... 170 

V. Whooping Cough (Pertussis) ......... 172 

VI. Bronchiectasis ............ 176 

VII. Stenosis of the Trachea and Bronchi ....... 180 

Tracheal Stenosis 180 

Bronchial Stenosis ........... 181 

VIII. Bronchial Asthma 181 

SECTION IV 

DISEASES OF THE LUNGS 

I. Pulmonary Emphysema . . . . . . . . . .187 

Symptoms and Course of the Disease . . . . . . . 190 

Other Symptoms in the Lungs and in Other Organs ..... 193 

II. Pulmonary Atelectasis (Compression of the Lungs. Aplasia of the Lungs) . 195 

III. Pulmonary CEdema . . .197 

IV. Catarrhal Pneumonia (Broncho-pneumonia. Lobular Pneumonia) . . 199 
V. Croupous Pneumonia . . . . . . . . . 204 

Description of Single Symptoms and Complications ..... 209 

Special Peculiarities and Anomalies in the Course of Pneumonia . . 218 

VI. Tuberculosis of the Lungs (Pulmonary Phthisis. Pulmonary Consumption) 226 

General Pathology and iEtiology of Tuberculosis . i . . . 226 

^Etiology of Tuerbculosis in Man ........ 228 

Pathological Anatomy of Tuberculosis, especially of Pulmonary Tuberculosis 231 
Clinical History of Tuberculosis in General and of Pulmonary Tuberculosis 

in Particular 234 

Special Symptoms and Complications ....... 237 

Symptoms on the Part of the Lungs ........ 237 

Symptoms on Physical Examination ....... 241 

General Symptoms in Pulmonary Tuberculosis . . . . . 246 

Symptoms and Complications on the Part of other Organs . . . 248 

VII. Acute General Miliary Tuberculosis ........ 261 



CONTENTS 



ix 



CHAPTER PAGE 

VIII. Gangrene of the Lungs 266 

IX. Diseases from the Inhalation of Dust (Pneunionoconiosis) . . . 270 
X. Embolic Processes in the Lungs (Hsemorrhagic Infarction of the Lungs) . 273 
XL Brown Induration of the Lungs (Lungs of Heart Disease) . . . . 275 
XII. Tumors of the Lungs. Cancer of the Lungs. Echinococcus of the Lungs. 

Pulmonary Syphilis .......... 276 

SECTION V 

DISEASES OF THE PLEURA 

I. Pleurisy . . .279 

Physical Signs 285 

Various Forms of Pleurisy ......... 288 

II. Peripleuritis . . .295 

III. Pneumothorax . . . . . . . . . . . 295 

TV. Hydrothorax. Hsematothorax ........ 299 

V. New Growths of the Pleura 300 

VI. Mediastinal Tumors 301 

VII. Actinomycosis of the Thoracic Cavity ....... 302 

Diseases of the Circulatory Organs 

SECTION I 

DISEASES OF THE HEART 

I. Acute Endocarditis (Endocarditis verrucosa, Endocarditis ulcerosa) . . 304 

EL Valvular Disease of the Heart 308 

General Pathology of Valvular Disease of the Heart ..... 310 
Insufficiency of the Mitral Valve . . . . . . . .311 

Stenosis of the Mitral Orifice (Mitral Stenosis) 314 

Insufficiency of the Semilunar Valves of the Aorta . . . . .316 

Stenosis of the Aortic Orifice ......... 320 

Insufficiency of the Tricuspid Valve ........ 321 

Stenosis of the Tricuspid Orifice ........ 322 

Insufficiency of the Pulmonary Valve ....... 323 

Stenosis of the Pulmonary Orifice (Pulmonary Stenosis) and the other Con- 
genital Lesions of the Heart . . . . . . . 323 

Combined Valvular Diseases of the Heart ....... 325 

General Sequelae and Complications of Valvular Disease of the Heart . 326 
General Course and Prognosis of Valvular Disease of the Heart . . 333 
Treatment of Valvular Heart Disease . . . . . . . 334 

III. Diseases of the Myocardium ......... 340 

Interstitial Myocarditis (Fibrinous Degeneration of the Myocardium. Scle- 
rosis of the Coronary Arteries) . . . . " . . . . 340 

So-called Idiopathic Hypertrophy of the Heart (Mechanical Strain of the 

Heart) .345 

Hypertrophy of the Heart, Associated with Congenital Smallness of the 

Systemic Arteries . . . ... . . . . . 350 

Primary Weakness of the Myocardium ( Congenital Weakness of the Heart ; 
Weakened Heart; Acute Muscular Strain of the Heart; Toxic Weak- 
ness of the Heart) . . . . . . . . . 351 

The So-called Fatty Heart 353 

IV. Cardiac Neuroses ........... 355 

Angina Pectoris (Stenocardia) ......... 355 

Nervous Palpitation .......... 356 

Tachycardia . . . . . . . . .357 



X 



CONTENTS 



SECTION II 



DISEASES OF THE PERICARDIUM 
CHAPTER PAGE 

I. Pericarditis ............ 359 

Special Forms of Pericarditis 363 

II. Hydro-pericardium, Haemo-pericardium, and Pneumopericardium . . 369 

SECTION III 

DISEASES OF THE VESSELS 

I. Arterio-sclerosis (Endarteritis chronica deformans. Atheroma of the Vessels) 370 

II. Aneurism of the Thoracic Aorta . . . . . . . 374 

III. Aneurisms of the Other Vessels , 379 

IV. Rupture of the Aorta .......... 380 

V. Narrowing of the Aorta .......... 380 

Diseases of the Digestive Organs 

SECTION I 

DISEASES OF THE MOUTH, TONGUE, AND SALIVARY GLANDS 

I. Catarrhal Stomatitis .......... 382 

II. Ulcerative Stomatitis . . . . . . . . . . 383 

III. Aphthous Stomatitis .......... 385 

TV. Thrush .386 

V. Glossitis ' 388 

Acute Parenchymatous Glossitis . . . . . . . 388 

Glossitis Dissecans . . . . . . . . . . 388 

Lingual Psoriasis. Leucoplacia ........ 388 

VI. Noma .389 

VII. Parotitis (Mumps) 390 

Idiopathic, Primary Parotitis ......... 390 

Secondary Suppurative Parotitis . . . . . . . .391 

VIII. Angina Ludovici 392 

IX. Anomalies of Dentition .......... 392 

SECTION II 

DISEASES OF THE SOFT PALATE, TONSILS, PHARYNX, AND NASO -PHARYNX 

I. Sore Throat (Inflammation of the Soft Palate and of the Tonsils) . . 394 

Catarrhal Sore Throat . . . . . . ... . 395 

Follicular Tonsillitis . . .396 

Tonsillar and Peritonsillar Abscess (Parenchymatous Sore Throat) . . 396 

Necrotic Tonsillitis (Necrotic Sore Throat) ...... 397 

II. Chronic Hypertrophy of the Tonsils . . ... . . . . 399 

III. Chronic Pharyngitis . . . . . . . . . . 400 

Chronic Catarrh of the Naso-pharynx, Chronic Posterior Nasal Catarrh . 400 

Pharyngitis Sicca . . . . . . . . . . . 401 

Hypertrophic Catarrh in the Pharynx and Naso-pharynx .... 401 

IV. Retropharyngeal Abscess .......... 403 

SECTION III 

DISEASES OF THE OESOPHAGUS 

I. Inflammation and Ulcer of the (Esophagus ....... 404 

II. Dilatation of the (Esophagus ......... 406 



CONTEXTS 



xi 



CHAPTER PAGE 

Diffuse Dilatation ........... 406 

Diverticula . . . . . . . ■ . . . . 406 

m. Stenosis of the (Esophagus ...... . 409 

TV. Cancer of the CEsophagus ......... 412 

V. Rupture of the CEsophagus . 414 

VI. Neuroses of the CEsophagus . . . . . ... . . 414 

Sp*asni of the CEsophagus .......... 414 

Paralysis of the CEsophagus ...... . 415 

SECTION IV 

DISEASES OF THE STOMACH 

I. Brief Preliminary Eemarks on the Examination of the Gastric Contents . 415 
Constituents of the Gastric Juice, particularly Free Hydrochloric Acid. 

Pep sine, and Lactic Acid . . . . . . . . .417 

Determination of the Motor Activity of the Stomach . . . 419 

Estimation of the Size and Position of the Stomach ..... 420 

Testing the Absorptive Powers of the Stomach . . . . . .421 

Demonstration of Blood in the Gastric Contents ..... 422 

II. Acute Gastric Catarrh (Acute Gastritis) 422 

III. Chronic Gastritis. Chronic Catarrh of the Stomach ..... 425 

IV. Phlegmonous Gastritis .......... 432 

V. Gastric Ulcer 432 

VI. Cancer of the Stomach . . . . . . . .' 444 

VII. Anomalies of the Secretion of Gastric Juice ...... 452 

Anacidity of the Stomach (Achlorhydria) . Achylia Gastrica . . . 452 

Hypersecretion and Hyperacidity of the Gastric Juice (Acid Dyspepsia) . 455 

Dyspepsia with Hypersecretion of the Gastric Juice ..... 457 

Periodical (Intermittent) Hypersecretion (Gastroxynsis) .... 459 

VIII. Abnormalities in the Size and Position of the Stomach. Motor Disturb- 
ances of the Stomach ....... . - . 460 

Abnormalities in the Size of the Stomach. Atony of the Stomach . . 460 

Abnormal Position of the Stomach. Gastroptosis ..... 462 

IX. Nervous Dyspepsia ........... 463 

SECTION V 

DISEASES OF THE IXTESTIXES 

I. Intestinal Catarrh - 468 

Appendix. Membranous Enteritis and Mucous Colic .... 474 

EE. Cholera Morbus (Cholera Infantum) . . . . . . . 475 

in. Intestinal Catarrh of Children .477 

TV. Typhlitis and Perityphlitis (Appendicitis) ... . . 482 

V. Perforating Ulcer of the Duodenum ........ 488 

VI. Tuberculosis of the Intestines . . . . . . . . . 488 

VII. Syphilis of the Eectum . 490 

VIII. Cancer of the Intestines .......... 491 

IK. Haemorrhoids 493 

X. Habitual Constipation .......... 495 

XI. Stricture and Obstructions of the Intestines ...... 499 

Intestinal Constriction . . . . . . . . . . 502 

Intestinal Obstruction .......... 503 

XII. Intestinal Parasites .......... 508 

Tape-worms . . . . . . . . ~ . . . . 508 

Round-worms ............ 515 

Oxyuris vermicularis ... . . . . . . . . 516 

Anchylostoma duodenale .......... 518 

Trichocephalus dispar . . . . . . . . .519 



xii 



CONTENTS 



SECTION VI 

DISEASES OF THE PERITONEUM 
CHAPTER PAGE 

I. Acute Peritonitis . . .• • . . . . . . 520 

II. Chronic and Tubercular Peritonitis ........ 529 

III. Ascites . .533 

IV. Cancer of the Peritoneum .......... 535 

SECTION VII 

DISEASES OF THE LIVER, BILE-DUCTS, AND PORTAL VELN 

I. Catarrhal Jaundice ........... 536 

II. Acute Febrile Jaundice (Infectious Jaundice. Weil's Disease) . . . 542 

in. Biliary Calculi 54a 

IV. Suppurative Hepatitis . . . . . . . . . . 553 

V. Cirrhosis of the Liver .......... 555 

VI. Biliary Cirrhosis and Hypertrophic Cirrhosis of the Liver .... 562 
VII. Acute Yellow Atrophy of the Liver ........ 565 

Appendix. Pernicious Jaundice. Cholsemia and Acholia . . . 569 

VIII. Icterus Neonatorum . . . . . . . . . . 570 

LX. Syphilis of the Liver . . . . . . . . . . 571 

X. Cancer of the Liver and Bile-ducts ........ 572 

XL Echinococcus of the Liver ......... 575 

XII. Circulatory Disturbances in the Liver . . . . . . . 578 

XIII. Atrophy, Hypertrophy, and Degenerations of the Liver .... 579 

XIV. Anomalies in the Shape and Position of the Liver ..... 581 
XV. Suppurative Pylephlebitis . ........ 582 

XVI. Thrombosis of the Portal Vein ' . .583 

Appendix. Diseases of the Pancreas ....... 585 

Hsemorrhages into the Pancreas ........ 585 

Atrophy of the Pancreas .......... 585 

Pancreatitis . . . . . . . . . . . . 585 

Cysts of the Pancreas .......... 586 

Cancer of the Pancreas . . . . . . . . . .586 

Pancreatic Calculi . . . . ... . . . . 587 

Diseases of the Kidneys, the Pelvis of the Kidney, and the Bladder 

SECTION I 

diseases of the kidneys 

I. General Preliminary Remarks upon the Pathology of Renal Disease . . 588 

Albuminuria . . . . . . . . . . . . 589 

Casts and other Abnormal Morphological Constituents of the Urine in Renal 

Disease * • 592 

The Dropsy of Renal Disease . . . . . . . • 594 

Uraemia . . . . • . . '. . . . . 596 

The Changes in the Circulatory Apparatus in Renal Disease . . . 601 

II. Acute Nephritis 603 

III. The Subchronic and Chronic Forms of Nephritis, with the Exception of the 

Genuine Contracted Kidney ........ 618 

IV. Contracted Kidney . . . . . ... . ... 625 

V. Amyloid Kidney ........... 635 

VI. Purulent Nephritis and Perinephritis ....... 640 

Purulent Nephritis • -640 

Perinephritic (Paranephritic) Abscess ....... 641 

VII. Disturbances of Circulation in the Kidneys ...... 643 



CONTEXTS 



xiii 



CHAPTER PAGE 

The Congested Kidney .......... 643 

Embolic Infarction in the Kidneys ........ 643 

VIII. New Growths in the Kidneys . . . . . . . . 644 

IX. Parasites of the Kidneys and of the Urinary Passages. Chyluria . . 646 

Echinococcus of the Kidney ......... 646 

Distoraa Haematobium (Bilharzia Hsematobia) ...... 646 

Strongylus or Eustrongylus Gigas ........ 647 

Filaria Sanguinis. Chyluria ......... 647 

X. Movable Kidney (Floating Kidney. Pen Mobilis) ..... 648 

Appendix. The Diseases of the Suprarenal Capsules and Addison's 

Disease (Bronzed Skin) ......... 650 

SECTIOX II 

DISEASES OF THE PELVIS OF THE KIDNEY AND OF THE BLADDER 

I. Inflammation of the Pelvis of the Kidney. Pyelitis ..... 654 

IT. Nephrolithiasis ........... 657 

TIL Tuberculosis of the Genito -urinary Apparatus ...... 662 

TV. Hydronephrosis ........... 665 

V. Cystitis 667 

VI. New Growths in the Bladder . . . . . . . . .672 

VTI. Enuresis Nocturna . . . . . . . . . . 673 

Diseases of the Organs of Locomotion 

I. Acute Articular Rheumatism . . . . * . . . . . 675 

II. Chronic Articular Rheumatism (Chronic Polyarthritis) and Arthritis 

Deformans . . . . - . . . . . . .688 

Til. Acute and Chronic Muscular Rheumatism ....... 694 

IV. Acute Polymyositis 698 

V. Rachitis . . . . . . . ... . . . 699 

VI. Osteomalacia ............ 704 

Diseases affecting 1 the Blood and Tissue-metamorphosis 

( CONSTITUTIONAL DISEASES) 

I. Anaemia and Chlorosis . . . . . . . . ( . . 708 

General Preliminary Remarks as to the Classification and JEtiology of the 

Various Forms of Anaemia ........ 708 

Symptomatology of Anaemia . . . . . . . . .711 

II. Progressive Pernicious Anaemia . . . . . . . .719 

III. Leukaemia . . . . . . . . . . 726 

IV. Pseudo-leukaemia . . . . . . . ' . . 733 

V. HsemoglobinEemia and Hemoglobinuria . . . . . . .736 

VI. Scurvy 738 

Appendix. Barlow's Disease ........ 743 

VII. Purpura. Morbus Maculosus VCerlhoni. Peliosis ..... 744 
VTLT. Haemophilia 746 

EK. Diabetes Mellitus 748 

X. Diabetes Insipidus ........... 767 

XL Gout 770 

XII. Obesity .779 

m Scrofula . . 787 



xiv 



CONTENTS 



II. 



III. 
IV. 



v. 

VI. 
VII. 



Diseases of the Nervous System 

1. The Diseases of the Peripheral Nerves 
SECTION I 

DISEASES OF THE SENSORY NERVES 

General Remarks upon the Disturbances of Sensibility 
Sensibility to Contact . . 
Sense of Locality (Localization of Sensation) 
Sense of Pressure . . . • 
Sense of Temperature .... 

Sensation of Pain ..... 

Electro-cutaneous Sensibility 
Delay of Sensation, Summation of Irritation and After-sensations 
The Sensibility of the Muscles and Joints ..... 

The Special Sensibility to Touch (Stereognostic Sense, Active Touch) 
The Sensory Conduction Tracts and Anaesthesia of the Skin 
Course of the Sensory Conduction Tracts . 
The General Causes of Cutaneous Anaesthesia 
The Symptoms of Cutaneous Anaesthesia . 
Anaesthesia of the Trigeminus . 
Treatment of Cutaneous Anaesthesia . 
Neuralgia in General .... 

The Individual Forms of Neuralgia . 
Neuralgia of the Trigeminus . 
Occipital Neuralgia .... 

Neuralgia in the Region of the Brachial Plexus 
Intercostal Neuralgia .... 

Neuralgia in the Region of the Lumbar Plexus 
Sciatica ....... 

Neuralgia of the Genitals and the Rectal Region 
Achillodynia. Talalgia. Tarsalgia. Metatarsalgia . 
The So-called Articular Neuralgias (Articular Neuroses) 
Aeroparaesthesia ....... 

Habitual Headache ....... 

Anomalies of the Sense of Smell 

Anomalies of the Sense of Taste .... 



SECTION II 



DISEASES OF THE MOTOR NERVES 



TT. 



829 
829 
835 
837 



General Remarks upon the Disturbances of Motility . 
Paralysis 

Symptoms of Motor Irritation 

Ataxia 

General Remarks upon testing the Reflexes and upon the Condition of them 838 
General Remarks upon the Changes of Electrical Excitability in the Motor 

Nerves and Muscles 
Table of the Different Forms of Voluntary Motion and the Muscles and 

Nerves Concerned therein . 
The Different Forms of Peripheral Paralysis 

Paralysis of the Ocular Muscles 

Paralysis of the Motor Branch of the Trigeminus 

Facial Paralysis . • 

Paralyses in the Region of the Muscles of the Shoulder 
Paralyses of the Muscles of the Back and Abdomen . 
Paralyses in the Region of the Upper Extremity . 



842 

851 
854 
854 
858 
858 
863 
865 
866 



CONTENTS 



xv 



CHAPTER PAGE 

Paralysis of the Diaphragm . . . . . . . . .871 

Paralyses in the Region of the Lower Extremity . .871 
Toxic Paralyses . . . . . . . . . . 873 

Lead Paralysis . . . . . . . . . . . 873 

Arsenical Paralysis ........... 875 

III. The Different Forms of Localized Spasm ....... 875 

Spasm in the Motor Distribution of the Trigeminus . . . 875 

Clonic Facial Spasm .......... 876 

Spasm in the Region of the Hypoglossal Nerve. Lingual Spasm . . 877 
Spasms in the Muscles of the Neck ........ 878 

Spasms in the Muscles of the Shoulder and Arm ..... 880 

Spasms in the Muscles of the Lower Extremity . . . . . 880 

Saltatory Reflex Spasm . . . . . . . . .881 

Arthrogryposis ........... 881 

Spasms in the Respiratory Muscles ........ 881 

TV. Writer's Cramp and Allied Professional Neuroses . . . . . 882 
V. Simple and Multiple Degenerative Neuritis ...... 885 

Simple Neuritis _ 885 

Primary Simple Neuritis .......... 885 

Secondary Simple Neuritis . . . . . . ... . 885 

Multiple Degenerative Neuritis ........ 886 

Primary Acute and Chronic Multiple Neuritis . . . . . 890 

The Ataxic Form of Multiple Neuritis (" Acute Curable Ataxia ") . . 892 
The Acute and Chronic Neuritis of Alcoholic Subjects. Alcoholic Paralysis 

(Pseudo-tabes [Ataxia] of Alcoholic Subjects) ..... 893 

Beri-beri. Endemic Multiple Neuritis ....... 895 

VI. New Growths in the Peripheral Nerves . . . . . . . . 896 

II. Vasomotor and Trophic Neuroses 

I. General Preliminary Remarks ......... 898 

Erythromelalgia . . . . . . . . . . . 900 

Symmetrical Spontaneous Gangrene. Raynaud's Disease .... 900 

Acute Angioneurotic (Edema ......... 900 

Myxoedema . . . . ... . . . . . 901 

Cretinism ............ 901 

Myxcedematous Infantilism ......... 901 

Adiposis Dolorosa ........... 902 

Scleroderma ............ 902 

Acromegaly . . . . . . . . . 902 

Gigantism 903 

Hyperostosis Cranii ........... 904 

Hydrops Articulorum Intermittens ........ 904 

Injuries and Diseases of the Cervical Sympathetic ... . . 905 

II. Migraine . . , . . .905 

LTI. Progressive Facial Hemiatrophy ........ 908 

IV. Exophthalmic Goitre . . . .909 

III. The Diseases of the S final Cord 

I. Diseases of the Spinal Meninges . . . . . . . .915 

Acute Inflammations of the Spinal Meninges ...... 915 

Chronic Spinal Leptomeningitis ........ 917 

Pachymeningitis cervicalis hypertrophica ....... 918 

Haemorrhage into the Spinal Meninges ....... 919 

II. Preliminary Remarks on the Localization and Topical Diagnosis (Segmental 

Diagnosis) of Diseases of the Spinal Cord ...... 920 

LTI. Disturbances of Circulation, Haemorrhages, Traumatic Lesions, and Func- 
tional Disturbances of the Spinal Cord 928 

Disturbances of Circulation 92S 



xvi CONTENTS 

-CHAPTER PAGE 

Haemorrhage into the Substance of the Spinal Cord. Spinal Apoplexy. 

Hsematomyelia . . . , . . . . . . . 929 

Traumatic Lesions of the Spinal Cord ....... 930 

Diseases of the Spinal Cord after a Sudden Reduction of the Atmospheric 

Pressure (Caisson Disease) ......... 932 

Functional Disturbances (Spinal Irritation. Spinal Neurasthenia) . . 933 
IV. The Pressure Paralyses of the Spinal Cord ...... 934 

The Pressure Paralyses in Vertebral Caries ...... 937 

The Pressure Paralyses in Cancer of the Vertebrae ..... 941 

V. Acute and Chronic Myelitis ......... 943 

Symptoms of Motor Paralysis ......... 946 

Symptoms of Motor Irritation . . . . . . . . . 946 

Ataxia ............. 947 

Disturbances of Sensibility ......... 947 

Cutaneous Reflexes ........... 948 

Tendon Reflexes .948 

Disturbances in the Bladder and Rectum ....... 949 

Trophic Disturbances . . . . . . . . .. 949 

Disturbances in the Region of the Cerebral Nerves ..... 950 

VI. Multiple Sclerosis of the Brain and Spinal Cord ..... 954 

Appendix. The So-called Pseudo-sclerosis 959 

VII. Tabes Dorsalis 960 

Disturbances of Motility in the Extremities ...... 966 

Disturbances of the Cutaneous and Muscular Sensibility .... 969 

Disturbances of the Reflexes . . . . . . . . .971 

Disturbances in the Eye and the other Organs of Special Sense . . . 972 
Disturbances in the Bladder, the Rectum, and the Sexual Organs . . 973 
Symptoms in the Internal Organs . . . . . . . . 973 

Trophic Disturbances .......... 974 

Cerebral Symptoms ........... 976 

VIII. Hereditary (Juvenile) Ataxia (Friedreich's Disease) ..... 981 

Appendix. Hereditary Cerebellar Ataxia ...... 984 

IX. The Primary Degenerations of the Motor Tract, including the Muscles . . 985 
Preliminary Remarks .......... 985 

Amyotrophic Lateral Sclerosis ......... 986 

Spinal Progressive Muscular Atrophy . ... . . . . 990 

Neurotic Muscular Atrophy . . . ... . . . 996 

Progressive Muscular Dystrophy . . . . . . . . 998 

Primary Degeneration of the Pyramidal Tracts ..... 1007 

Appendix. Congenital Spastic Paraplegia in Children (Spastic Cerebral 
Paralysis. Infantile Spastic Diplegia. Little's Disease) . . . 1012 
X. Acute and Chronic Poliomyelitis . •-. . . . . . 1014 

Spinal Paralysis of Children 1014 

Acute Poliomyelitis of Adults . . . . . . . . 1019 

Subacute and Chronic Poliomyelitis ....... 1020 

XI. The So-called Acute Ascending Spinal Paralysis (Landry's Paralysis) . 1021 
XII. New Growths of the Spinal Cord and of its Membranes .... 1024 

XIII. The Syphilitic Affections of the Spinal Cord . . ... 1026 
Chronic Gummatous Spinal Meningitis and Meningo-niyelitis . . . 1027 
Syphilitic Myelitis and Syphilitic Spastic Spinal Paralysis . . . 1028 

XIV. Syringomyelia and Hydromyelus . . . . . . . 1029 

XV. Spina Bifida . 1032 

XVI. Secondary Degenerations in the Spinal Cord . • . . . . 1033 
XVII. Unilateral Lesion of the Spinal Cord . 1036 

IV. The Diseases of the Medulla Oblongata 

I. Progressive Bulbar Paralysis . . . . . . . . . 1039 

II. The Rarer Forms of Chronic Bulbar Paralysis, Progressive Ophthalmo- 
plegia, and Asthenic Bulbar Paralysis ...... 1045 



CONTENTS 



xvn 



CHAPTER PAGE 

Progressive Ophthalmoplegia . . .. . . . . . 1045 

Asthenic Bulbar Paralysis. Pseudo-paralytic Myasthenia . . . 1040 

Family Periodic Paralysis . . . . . . . . . 1047 

III. Acute and Apoplectiform Bulbar Paralysis . . . . . . 1048 

Haemorrhage into the Medulla Oblongata and the Pons .... 1048 

Embolism and Thrombosis of the Basilar Artery . . . . . 1050 

Acute Inflammatory Bulbar Paralysis . . . . . . .1051 

IV. Compression of the Medulla ......... 1052 



V. The Diseases oe the Brain 
SECTION I 

DISEASES OF THE CEREBRAL MENINGES 

I. Haematoma of the Dura Mater ........ 1053 

II. Purulent Meningitis . . • . . . . . . . 1055 

III. Tubercular Meningitis . . . . . . . . . 1059 

IV. Thrombosis of the Cerebral Sinuses ........ 1064 

SECTION II 

DISEASES OF THE BRAIN-SUBSTANCE 

I. Disturbances of Circulation in the Brain ....... 1006 

II. General Preliminary Remarks upon the Localization of Cerebral Diseases . 1068 

The Motor Region of the Cortex Cerebri 1069 

The other Parts of the Cortex Cerebri, except the Center for Speech . . 1074 
The Centers of Speech and the Disturbances of Speech (Aphasia and Allied 

Conditions) 1077 

The Centrum Ovale, Internal Capsule, Central Ganglia, and Region of the 

Corpora Quadrigemina ......... 1083 

The Cerebellum .1086 

III. Cerebral Haemorrhage . . . . . . . . • . . 1089 

IV. Cerebral Embolism and Thrombosis (Encephalo-malacia) . . . 1103 

V. Inflammation of the Brain ......... 1106 

Abscess of the Brain (Suppurative Encephalitis) . . . . . 1106 

Acute and Chronic Non-suppurative Encephalitis . . . . .1110 

Idiopathic (Inflammatory) Softening of the Brain ..... 1110 

Curable Form of Encephalitis . . . . . .. . .1110 

Diffuse Cerebral Sclerosis . . . . . . . .1110 

The Acute Encephalitis of Children . . . . . . .1111 

VI. Insolation. Sunstroke. Heat Prostration. Thermic Fever . . .1113 

VII. Tumors of the Brain 1115 

Glioma 1116 

Sarcoma . . . . . . . . 1116 

Gumma and Solitary Tubercle . . . ■ . . . .1116 

Carcinoma . . . ... . . % . . .' 1116 

Psammoma ............ 1116 

Cysts of the Brain ........... 1117 

The General Symptoms of Cerebral Tumors . . . . . .1117 

Tumors in the Different Parts of the Brain and their Focal Symptoms . 1119 

Appendix. Hydatids of the Brain 1124 

VIII. Cerebral Syphilis 1125 

IX. Progressive General Paralysis of the Insane (Paralytic Dementia) . . 1129 
X. Chronic Hydrocephalus . . * . . . . . . .1137 

XI. Meniere's Disease 1139 



xviii 



CONTENTS 



VI Neuroses without Known Anatomical Basis 



CHAPTER PAGE 

I. Epilepsy 1141 

Appendix. Infantile Convulsions (Eclampsia Infantum) . . . 1151 

II. Chorea 1152 

Appendix. Chronic Hereditary Chorea. Electrical Chorea. Para- 
myoclonus (Myoclonia) ......... 1156 

III. Paralysis Agitans ........... 1157 

IV. Athetosis . ' . 1161 

V. Tetany . ... . . . . . . . . 1162 

VI. Tetanus 1165 

VII. Congenital Myotonia (Thomsen's Disease) . . . . . . 1169 

VIII. Catalepsy .1170 

IX. Hysteria 1172 

The Symptoms and Manifestations of Hysteria . . . . .1175 
The Hysterical Stigmata, especially Sensory Anaesthesia and Hypersesthesia 1175 
Hysterical Paralysis .......... 1178 

Hysterical Contractures 1179 

Vaso-motor Disturbances. Secretory Disturbances. Symptoms in the 

Internal Organs 1179 

General Mental and Bodily Constitution of the Hysterical . . . 1181 
Hysterical Attacks, Conditions of Spasm, etc. ...... 1182 

X. Neurasthenia . . . . . . . . . . 1193 

Symptoms of Neurasthenia. The Mental Symptoms .... 1194 

The Physical Symptoms .......... 1195 

XL The So-called Traumatic Neuroses (Accident Neuroses) .... 1201 

Appendix I. Summary of the Symptoms and Treatment in Cases of 

Poisoning . . . . . . . . . . . 1206 

Appendix II. Table of Weights and Measures 1214 

Index .... . . . . . . . ' . . 1217 



LIST OF ILLUSTRATIONS 



FIG. PAGE 

Table I. Distribution of the areas of the sensory roots upon the surface of the 

body facing page 924 

1. Typhoid bacilli 1 

2. Temperatures in typhoid fever ......... 7 

3. Example of the temperature curve in relapsing fever ..... 35 

4. Spirilli of relapsing fever in the blood ........ 36 

5. Example of a normal scarlet-fever curve ....... 40 

6. Example of the temperature curve in measles ....... 50 

7. Example of the temperature curve in true small-pox ..... 57 

8. The cocci of erysipelas ........... 63 

9. Comma bacilli ............ 86 

10. Different forms of the malarial plasmodium ....... 94 

11. Quotidian intermittent fever .......... 97 

12. Tertian intermittent fever .......... 97 

13. Anthrax bacilli 127 

14. Anthrax bacilli; spore formation and spore germination . . . . 128 

15. Trichinae . . . . . . . . . . . 131 

16. Paralysis of left vocal cord . . . . . . . . . .151 

17. Bilateral paralysis of the posticus ......... 152 

18. Paralysis of both internal thyro-arytaenoid muscles ..... 152 

19. Paralysis of the arytaenoideus ......... 153 

20. Paralysis of the thyro-arytaenoids and arytaenoideus . . . . . 153 

21. 22. Pediculated fibromata . . . . . . . . . . 155 

23. Turpentine pipe ............ 166 

24. Crystals of fat acids 168 

25. Asthma crystals and Curschmann's spirals ....... 185 

26. Pneumonia diploeocci ........... 206 

27. Example of the temperature curve in croupous pneumonia . . . .216 

28. Example of the temperature curve in " intermitting " pneumonia . . . 217 

29. Cholesterine crystals 222 

30. Influence of a pulmonary haemorrhage upon the temperature .... 239 

31. Elastic fibers .240 

32. Tubercle bacilli in the sputum . . . . . . . . . 240 

33. Sub-febrile state in chronic pulmonary tuberculosis ..... 246 

34. Hectic fever in chronic pulmonary tuberculosis ...... 246 

35. Expectoration of a worker in graphite ........ 271 

36. Sputum containing " cells of heart disease " . . . . . ^ . . 276 

37. Temperature curve in pleurisy before and after tapping ..... 293 

38. Masses of actinomycosis .......... 302 

39. Pulse curve in marked mitral stenosis . . . . . . . .314 

40. Pulse curve in aortic insufficiency ......... 319 

41. Pulse curve in stenosis of the aortic orifice ....... 321 

42. Pulsus bigeminus ............ 328 

43. Pseudo-hepatic cirrhosis due to pericarditis ....... 366 

44. Plan of the dentition . 393 

45. Method of washing out the stomach ........ 416 

46. Haemine crystals ............ 422 

xix 



XX 



LIST OF ILLUSTRATIONS 



FIG. PAGE 

47. Head of taenia solium ........... 509 

48. Head of cysticercus of the brain . . . . . . . . . 509 

49. Taenia solium ............ 509 

50. Eggs of intestinal parasites . . . . . . . . . . 510 

51. Head of taenia mediocanellata ......... 510 

52. Taenia mediocanellata ........... 510 

53. Head of bothriocephalus latus ......... 511 

54. Bothriocephalus latus ........... 511 

55. Embryo of bothriocephalus latus . . . . . . . . .511 

56. Ascaris lumbricoides . . . . . . . . . . . 515 

57. 58. Oxyuris vermicularis .......... 517 

59, 60. Anchylostoma duodenale . . . . . . . . . 518 

61. Egg of anchylostoma duodenale ......... 519 

62. Trichocephalus dispar ........... 519 

63. Leucine and tyrosine crystals ....... 567 

64. Taenia echinococcus . . . . . . . . . . 575 

65. 66. Echinococcus scolices .......... 576 

67. Echinococcus hooklets ........... 576 

68. Different forms of casts . . . ' . . . . . . . 592 

69. Waxy casts . ; ' . . . . . . 593 

70. Epithelial cast . . . . 593 

71. Distoma haematobium . . . . . . . . . . 647 

72. Embryos of filaria . . . . . . . . . . 648 

73. Pelvic renal epithelium . . . . . . . . . . . 655 

74. Crystals of triple phosphate and ammonic urate . . . . . . 669 

75. Temperature chart in acute articular rheumatism ...... 683 

76. Appearance of the hand in protracted arthritis deformans .... 690 

77. Chronic arthritis deformans with contracture . . . . ... 692 

78. Puerperal osteomalacia . . . . . . . . . . 706 

79. Changes in the red blood-corpuscles in pernicious anaemia .... 724 

80. Leukasmic blood ............ 729 

81. Mixed leukaemia (myelaemia) ......... 730 

82. Acute attack of gout in the fingers . . . . . . . . .773 

83. Changes in the fingers in chronic gout . . . . - . . . 774 

84. Course of the posterior root-fibers in the cord and medulla .... 796 

85. Transverse section of the cord, showing the course of the posterior root-fibers . 797 

86. Course of the sensory conduction tracts . . . . . . . 798 

87. 88. Distribution of the sensory cutaneous nerves in the trunk and upper 

extremities . . . . . . . . . . . . 801 

89. Detailed distribution of the nerves to the dorsal surface of the fingers . . 801 

90, 91. Distribution of the sensory cutaneous nerves to the lower extremities . 802 
92, 93. Distribution of the sensory cutaneous nerves in the head .... 803 

94. Sciatic scoliosis in severe sciatica . . . . . . . . . 818 

95. Horizontal section through the right cerebral hemisphere .... 829 

96. Transverse section through the crura cerebri in secondary degeneration . . 830 

97. Transverse section through the cervical enlargement ..... 830 

98. Transverse section through the lumbar enlargement . . . . 830 

99. Motor points of face 843 

100, 101. Motor points of arm .< • . . . 844, 845 

102. Motor points of thigh . . 846 

103, 104. Motor points of leg . . . 847, 848 

105. Right facial paralysis ........... 859 

106. Trunk of the facial 860 

107. Paralysis of the right serratus . . . . . . . - . 864 

108. Position of the hand in paralysis of the radial nerve ..... 867 

109. Paralysis of the ulnar nerve .......... 868 

110. Spasm of the accessory nerve .......... 878 

111. Spasm of the right splenius capitis ......... 879 

112. Radial nerve in alcoholic polyneuritis ........ S89 



LIST OF ILLUSTBATIONS 



xxi 



FIG. PAGE 

113. Acromegaly in a patient thirty years old ....... 903 

114. Left facial hemiatrophy . . . . . • . . . . 909 

115. Patient with Basedow's disease (exophthalmus, goitre) . . . . .911 

116. Position of the hand in pachymeningitis cervicalis hypertrophica . . . 918 

117. Distribution of the sensory root-areas from the lunibo-sacral plexus . . 924 

118. Lesion at the level of the second lumbar segment ...... 925 

119. Lesion at the level of the third lumbar segment ...... 925 

120. Lesion at the level of the filth lumbar segment ...... 925 

121. Lesion of the first sacral segment ......... 925 

122. Lesion of the second sacral segment ........ 926 

123. Lesion of the third sacral segment ......... 926 

124. Lesion of the fourth sacral segment . . . . . . . . 926 

125. Relations of the vertebrae to the spinal roots ....... 928 

126. Vertebral displacement in spondylitis ........ 935 

127. Angular kyphosis in vertebral caries . . . . . . . . 938 

128. Distribution of the sclerosed nodules on the surface of the pons . . . 954 

129. Example of disease of the cord in multiple sclerosis ..... 955 

130. Degeneration of the posterior columns in advanced tabes .... 962 

131. 132. Transverse section of the cord in beginning tabes dorsalis . . . 963 

133. Paralysis of the left oculo-motor nerve in tabes ...... 972 

134. Tabetic arthropathy of the right knee and left ankle . . . . 974 

135. Genu recurvatum in tabes dorsalis ......... 975 

136. Attitude of a patient with hereditary ataxia ....... 983 

137. Diagram of the motor tract . . . . . . . . . . 986 

138. Section of the cervical cord in amyotrophic ]ateral sclerosis .... 987 
139-141. Atrophy of the hand in spinal progressive muscular atrophy . . . 992 
142: Atrophy of the hand and forearm in spinal progressive muscular atrophy . 993 
143, 144. Spinal progressive muscular atrophy ....... 994 

145. Xeurotic muscular atrophy .......... 997 

146. Peroneal muscular atrophy . . . . . . ... . . 998 

147. Positions of a child with pseudo-hypertrophic paralysis on rising . . . 1000 

148. Pseudo-hypertrophy of the muscles . . . . . . 1001 

149. Juvenile myopathic muscular atrophy . . . . . . . 1002 

150. Two brothers with juvenile muscular atrophy ....... 1003 

151. Juvenile muscular dystrophy . . . . ■ . . . . 1004 

152. Muscular dystrophy ........... 1005 

153. Juvenile muscular dystrophy. Myopathic faeies . . . . . 1005 

154. Progressive myopathic muscular atrophy ....... 1006 

155. Spastic spinal paralysis ........... 1009 

156. Spastic spinal paralysis. Impulsive laughing . . . . . . 1010 

157. Family spastic spinal paralysis . . . . . . . . 1011 

158. Position of the legs in congenital spastic cerebral paralysis .... 1013 

159. Section of the cord in anterior poliomyelitis . . . . . .1014 

160. Old spinal infantile paralysis . . . . . . - . . . 1016 

161. Deformity of the hand in syringomyelia . . . . . . . 1031 

162. Secondary descending degeneration of the pyramidal tracts .... 1034 

163. Secondary ascending and descending degeneration ...... 1035 

164. Course of the main tracts in the cord ........ 1037 

165. Representation of the chief symptoms in unilateral lesion . . . . 1038 

166. Position of the nuclei of the cranial nerves ....... 1042 

167. Progressive ophthalmoplegia .......... 1046 

168. Diagram of focal diseases in the pons ........ 1049 

169. 170. Lateral aspect of the brain 1069, 1070 

171. Aspect of the median surface of the cerebrum ....... 1071 

172. Topographical relations between the surface of the brain and the skull . 1072 

173. Localization in the cerebral cortex ......... 1073 

174. Diagram of the course of the optic fibers in the chiasma ..... 1075 

175. Patient with right hemiplegia ......... 1095 

176. Cerebral infantile paralysis .......... 1111 



xxii 



LIST OF ILLUSTKATIONS 



FIG. PAGE 

177. Examples of handwriting in general paralysis ...... 1132 

178. Characteristic position of the body in paralysis agitans . . . . 1158 

179. Example of the position of the fingers in the movements of athetosis . . 1161 

180. Hysterical contracture ........... 1179 

181. Contracture of the foot in traumatic hysteria ....... 1180 

182. Hysterical arc de cercle 1183 

183. Hysterical attack with catalepsy .... .... 1184 

184. Hysterical abasia . . . . . . . . . . v . . 1189 

185. Accident case with hysterical paresis . . . . . . . . . 1202 



ACUTE GENERAL INFECTIOUS DISEASES 



CHAPTER I 

TYPHOID FEVER 

( Typhus abdominalis. Enteric Fever. Ileotyphus) 

etiology. — The sole cause of every attack of typhoid fever is an infection 
of the body by a definite pathogenic bacillus, the " typhoid bacillus " discovered 
by Eberth and Koch, and later made better known by the researches of Gaffky 
and others. Their length (see 
Tig. 1) is about one third the 
diameter of a red blood-glob- 
ule, and their breadth equals 
one third their length, but 
sometimes they may grow out 
in long fibers. It is not yet 
certain whether spore forma- 
tion takes place in their inte- 
rior or not. The typhoid bacilli 
show a very active sponta- 
neous movement in w^ater, 
caused probably by very fine 
filiform threads which Loffier 
Jias discovered on the ends of 
the rods and which he regards 
as the motor organs of the 
bacilli. 

That these typhoid bacilli 
are specific, is shown, how- 
ever, as in the case of many 
micro-organisms, less by their external form than by their peculiarities, as 
observed in pure cultures of them, and by their other biological peculiarities 
(virulence, chemical reaction, etc.). By the latter the pure typhoid bacillus 
is distinguished from a form of bacillus morphologically similar and perhaps 
allied to it, which often is found in the intestine, and is called bacterium coli 
commune (Escherich). The attempt has even been made to regard the typhoid 
oacillus merely as a virulent form of the bacterium coli, but the weight of 
evidence is at present in favor of regarding the typhoid bacillus as an independ- 
ent form. 

In cultures on gelatine the typhoid bacilli develop along the line of puncture 
. in little whitish or yellowish clusters, while a thin gray pellicle extends slowly 
over the surface, but the nutrient gelatine never liquefies. The manner of their 
growth on the cut surface of boiled potatoes is still more characteristic, and espe- 
cially valuable for their recognition. The w T hole cut surface is covered with a 
1 1 




Fig. 1.— Typhoid bacilli. Section from the spleen. 800 : 1. 
(From Fl€ t gge.) 



2 



ACUTE GENERAL INFECTIOUS DISEASES 



dense pellicle, scarcely discernible with the naked eye, and forming an absolutely 
pure culture of typhoid bacilli. It is an important fact that typhoid bacilli may 
also thrive if deprived of oxygen, because we can thus understand their increase 
within the intestine. 

The typhoid bacilli have thus far been found chiefly in the typhoidal infiltra- 
tions in the intestine, where they lie between the cells, and also in single foci 
in the mesenteric glands, the spleen, the liver, the kidneys, the pleura, the me- 
ninges, in typhoidal foci in the bones, etc. By suitable methods of investigation 
they are often found in the stools of typhoid patients and also in the fluid ob- 
tained by puncture of the fresh splenic tumor, in the gall bladder, sometimes in 
the urine, and also in the blood taken from a spot of roseola. As a rule, they are 
not found in the rest of the blood. 

Numerous attempts have been made to produce typhoid fever artificially by 
introducing pure cultures of the typhoid bacilli into the bodies of animals, but the 
results of these efforts have not yet proved perfectly harmonious. The main cause 
of the discrepancy is probably that animals are in general very slightly susceptible 
to the disease. At any rate, the attempts at artificial infection up to this date 
have proved successful only in cases when the animals subjected to the experiment 
(rabbits, guinea-pigs) have received large amounts of the typhoid bacilli directly 
into a vein or into the abdominal cavity (E. Frankel and Simmonds), or when the 
bacilli have been introduced into the duodenum (A. Frankel). Probably, how- 
ever, we have here to do rather with the intoxication of the animals caused by the 
poisonous matters generated in the cultures of bacilli than with an actual in- 
fection, for the pathological changes of typhoid fever are but little developed in 
the animals, and the injected bacilli themselves appear to be for the most part 
destroyed within the body of the animal experimented upon (Fliigge and 
Sirotinin, and others). Attempts to produce the disease by mixing the dejecta 
of typhoid patients with the animal's food have thus far proved invariably un- 
successful. Probably the bacilli are immediately destroyed by the hydrochloric 
acid in the stomach. 

Investigation of the aetiology of typhoid fever must consequently be directed 
to ascertaining in what manner and through what channels the specific typhoid 
bacilli penetrate into the human body, and what circumstances are then essen- 
tial to their further development and to the display of their pathogenic properties. 
It must be confessed that the ability to answer these questions accurately is a goal 
from which we are quite distant. 

It is almost universally believed that, as a rule, typhoid bacilli do not have any 
permanent, independent existence outside the human body, but sometimes under 
favorable conditions they seem to be able to remain for years in a " latent condi- 
tion" in the external world (in moist earth or stagnant water). Often, however, 
the conditions essential to an abundant development of the bacilli arise in certain 
places, and thus make it possible for a greater or less number of persons to absorb 
the pathogenic poison, and, as a result, to be attacked by typhoid fever. In this 
way occur the numerous greater or smaller epidemics of typhoid fever in contrast 
to the sporadic cases, which are likewise possible, and are not infrequent. If 
an epidemic of typhoid appears in a place till then entirely free from the disease, 
we must always refer it to an importation of the disease-germs, and seek their 
source in some previous case of typhoid. We must, therefore, take for granted 
that the poison of typhoid can in some way escape from the body of the patient 
into the outer world. If we believe this, we shall be sure to think, first of all, of 
the intestinal discharges as the source of infection. These discharges, as already 
stated, are known to contain the typhoid bacilli or perhaps their spores. 

As to the exact manner of infection, views are still widely different. Up to 
the present time there are chiefly two contrasted theories, called, respectively, the 



TYPHOID FEVER 



3 



" ground-soil " and the " drinking-water " * theories. According to the former, 
which is maintained principally by Pettenkofer and his pupils, the ground-soil is 
to be regarded as the chief place of development for the schizomycetic fungus of 
typhoid fever. Whether this will flourish depends chiefly on the condition of the 
soil (varying at different times and in different places), and this alone should ex- 
plain all the peculiarities observable in the spread of the disease — e. g., that single 
houses, streets, or wards of a city should suffer. According to Pettenkofer, a soil 
that air and water easily penetrate — e. g., one made up of alluvial or detrital de- 
posits — is most favorable for the spread of the disease, while a firm, rocky bottom 
makes its further development impossible ; and, where this " tendency of the 
ground-soil " is wanting, the disease can neither be introduced nor, if brought in 
by the sick, spread any further; for, according to Pettenkofer, the typhoid 
poison is seldom if ever transferred directly from one person to another. The 
poison in the stools must first be changed by the soil before it becomes infectious. 
The " ground-air," which is continually rising, carries the poison not only into the 
open atmosphere, but into the air of dwelling-rooms, and, being then inhaled, 
produces infection. We can thus understand why Pettenkofer regards typhoid 
fever as not directly contagious. The chief support of the ground-soil theory, 
beyond the results of comparing the character of the soil with the extent of the 
epidemics, consists in the proof which Buhl and Pettenkofer have given (taking 
Munich as an example, and later Berlin and other places) that a relation exists 
between the variations of the standing water in the soil and the frequency of 
typhoid cases. It appears that, when the water stands high (near the surface), 
fewer cases occur, and when it falls below the mean height cases are more numer- 
ous. Pettenkofer explains this relation by the fact that the level of the ground- 
water is certainly an index of the moisture and other conditions of the soil upon 
which the development of the typhoid bacilli depends. 

To be contrasted, or rather compared, with the " ground-air " theory is the view 
held by most physicians, despite the vigorous protest of Pettenkofer, that drinking- 
water plays an increasingly important role in the origin of many epidemics of 
typhoid. In fact, in the case of numerous epidemics, whose extent bears an un- 
mistakable relation to the water-supply, we are forced to believe that the typhoid 
germs are brought into the body by means of water used in drinking or otherwise. 
Even then we are by no means wholly to disregard the character of the soil, for 
the disease-producing poison — not to speak of direct pollution — is probably often 
communicated to the well-water from the soil. The possibility of this will be 
especially great if the wells are near drains or cess-pools containing typhoid dis- 
charges. In epidemics spread by drinking-water, the typhoid bacilli have lately 
been repeatedly found in the suspected water. 

We believe the idea is continually gaining ground that no single " theory " 
can fully explain all the facts, and that the possibility of infection occurring in 
several different ways must be considered. The final source of infection is always 
to be sought for in a previous case of typhoid fever. From this patient the 
typhoid bacilli reach the external world through the dejections, and may some- 
times directly reach another human body and infect it. Hence the experience 
that nurses, laundresses who wash the soiled linen, etc., often have typhoid fever; 
but typhoid fever is not contagious by conduction through the air. In most hos- 
pitals typhoid .patients are not isolated from the rest of the sick, and yet out- 
breaks of typhoid hardly ever occur among them, provided they are not in close 
intercourse with the typhoid cases or do not carelessly use the same dishes, rec- 
tal thermometer, etc. In the further extension of the disease — that is, when 



* Compare with what follows the statements concerning the aetiology of cholera, where the same 
disputed points are considered. 



4 



ACUTE GENERAL INFECTIOUS DISEASES 



there is an epidemic — water contaminated with typhoid bacilli certainly plays a 
frequent and most important part. All persons who indulge directly or indirectly 
(rinsing cooking utensils, etc.) in water from an infected spring or infected aque- 
duct are in danger of becoming ill. For example, it has been remarked in Eng- 
land, and lately in Cologne, that the fever in certain epidemics was limited to 
individuals who had their milk from one common source. In such cases, however, 
the probable cause is not a disease in the cows, but a pollution of the milk or the 
milk-cans by water. It is as yet doubtful if animals can have typhoid fever. This 
fact makes it uncertain whether the illnesses which have been observed to follow 
the ingestion of the flesh of diseased calves (e. g., the epidemic of Kloten) are 
actually to be considered typhoid fever, although the pathological changes are 
said by Huguenin to be very similar to those found in typhoid. 

[It is not probable that sewer-gas in itself is an exciting cause of typhoid fever. 
Especially in large cities typhoid dejections are constantly finding their way into 
the sewers, which afford all the conditions favorable, to the further growth and 
development of the poison. If, then, the drainage of any house is defective, the 
seeds of the disease- can readily gain access to the interior of the house and infect 
susceptible individuals. 

One of the most instructive epidemics on record is that in Plymouth, Pennsyl- 
vania, a town of eight thousand inhabitants. In the spring of 1885 a disease, at 
first supposed to be of a strange character, broke out in the place, and, before it 
ceased, affected twelve hundred persons, causing one hundred and thirty deaths. 
It was soon found that the malady was typhoid fever, which arose from one case, 
briefly in this wise : In January, February, and March there was a case of typhoid 
in a house on a hill sloping toward a water-supply of the town. The dejec- 
tions were thrown out on the snow, under which the ground was deeply frozen. 
On March 25th a sudden and great thaw occurred, the water did not sink into 
the ground, but ran immediately into the natural surface channels, and on April 
10th the epidemic began. There were reasons, which it is not necessary here to 
detail, why the above source of water-supply was drawn upon to an unusual de- 
gree just at that time, but it has been shown that those who derived their water 
from other sources were spared by the disease. The original case came from Phil- 
adelphia.] 

In almost all cases the intestine seems to be the actual gate of entrance for the 
typhoid poison into the human system. This is shown by the fact that in all 
cases which come to autopsy in early stages of the disease, the typhoid bacilli are 
mainly confined to the lymphatic tissues of the intestine. The typhoid poison 
(bacilli or spores) is probably swallowed, either directly with water or polluted 
food, or after being inhaled or in some other way introduced into the mouth. 
[Raw oysters grown in impure waters may convey the infection.' — V.] If 
not destroyed in the stomach, it passes on in viable condition into the alkaline 
contents of the intestine, and here finds the conditions essential to its further 
development. It penetrates at first into the lymphatic follicles and Peyer's 
patches, and thence goes on into the mesenteric glands, the blood-current, the 
spleen, and other organs. 

As in the case of most other infectious diseases, the occurrence of infection in 
typhoid is dependent not only on outward conditions, but also on an individual 
predisposition. Details of the circumstances attending this latter are as yet not 
at all accurately understood. Even in the worst typhoid centers, where the pos- 
sibility of infection must be universal, many escape the disease. 

Age has an indubitable influence upon the liability to the disease. Typhoid is 
especially a disease of youthful, vigorous individuals, of fifteen to thirty years. 
Above that age it is noticeably less frequent, although cases do occur at sixty and 
even seventy years. Formerly it was often said that young children were never 



TYPHOID FEVER 



5 



attacked ; but this was because the disease was not recognized, for in reality it is 
only children under one year old who seem to be seldom infected. At a later age, 
cases are by no means rare. 

Sex can not be shown with certainty to have an especial predisposing influence 
upon the frequency of typhoid fever. 

Mental excitement and gross errors in diet seem to predispose to the disease. 
On the other hand, a certain immunity has been alleged to be given by many cir- 
cumstances, especially pregnancy, the puerperal state, and other diseases already 
existing (tuberculosis, heart disease). Most of these statements are shown, how- 
ever, by more extended experience, to be very doubtful. It is certain, however, 
that the occurrence of typhoid fever gives very probable though not absolute 
immunity against any later new attack. Recent bacteriological investigations 
have suggested a reason for this immunity. Certain chemical albuminoid sub- 
stances (protective substance or " alexine " of Buchner) probably remain in the 
blood-serum and fluids of the tissues and prevent a new infection. 

Finally, it must be mentioned that the necessary conditions for an abundant 
development and conveyance of the typhoid germs are beyond doubt dependent 
on the season. According to statistics, most of the typhoid epidemics come in the 
months from August to November, while generally the number of cases greatly 
diminishes from December to spring. 

General Course of the Disease. — Extended experience shows that, after infec- 
tion with the typhoid poison has taken place, a certain time must elapse before the 
symptoms of the disease appear. The length of this time, the " stage of incuba- 
tion," is, unlike that of many other infectious diseases, not perfectly definite. On 
the average, it lasts two to three weeks, sometimes less time, sometimes longer. 
During this period the patient either feels perfectly well, or has certain slight 
symptoms, to which he pays more or less attention, according to his individual 
susceptibility. These prodromata consist of languor, disinclination to exertion, 
anorexia, slight headache, pain in the limbs, etc. Often they last only a few 
days. 'Not infrequently the patients state afterward that they had felt the dis- 
ease coming on for weeks. 

The transition of the prodromata into the regular disease takes place some- 
times so gradually that it is utterly impossible to take any one day as the first of 
the illness, in order to reckon from it its duration. It is usually, however, the first 
symptoms of a high temperature, chilliness, feverishness, and the accompanying 
increase in general discomfort, which allow one to fix, with at least some accuracy, 
the beginning of the disease. A decided initial rigor is certainly exceptional.* 
After the fever begins, most patients soon take to their beds, although it happens 
often enough that the sick feel either unable or unwilling to give up, and keep on 
at work for days ! 

There have been manifold attempts to divide the whole course of the disease 
into separate periods. The most natural division seems to be into the three stages 
of development, height or fastigium, and decline (stadium incrementi, s. acmes, s. 
deer emeriti). Usually, however, physicians reckon according to the week of the 
disease. The first week corresponds to the developmental stage, the second, and 
in all severer cases the third as well, to the fastigium, the fourth (in light cases 
the third) to the decline. The course of the disease is very variable, however, and 
naturally there is the greatest diversity in the departures from this general plan. 

In the first week, the initial period, the general symptoms augment rapidly. 
The patients become, in severe cases, very languid and feeble, have generally an 



* According to the representations of many authors, a marked initial rigor seems to occur rather 
often in some places. In Leipsic, and also in Erlangen, a pronounced rigor at the beginning of typhoid 
is scarcely ever seen. 



6 



ACUTE GENERAL INFECTIOUS DISEASES 



intense headache, and complete anorexia, with great thirst. The fever, which is 
all the time gradually rising, is recognizable subjectively by alternating sensa- 
tions of heat and cold, and objectively by the hot, dry skin, the parched lips, and 
the dry and coated tongue. The sleep is disturbed. For the most part there are 
no prominent thoracic or abdominal symptoms, except that at times there is a 
sense of oppression in the chest, or some cough. The pulse is quickened, some- 
times even now dicrotic. There is often a temporary epistaxis. The belly is not 
much swollen as a rule, and but little if at all tender. There is generally consti- 
pation. Usually the spleen, even at this time, exhibits a swelling that can be 
easily demonstrated. 

Generally the fastigium has begun before the end of the first week. The 
severe general symptoms persist or even increase. The fever maintains constant- 
ly a considerable elevation. The patients become more stupid. Often delirium 
appears, especially at night. In the lungs there is developed a more or less in- 
tense and extensive bronchitis. The abdomen becomes more swollen. On the 
skin of the trunk appear, generally at the beginning of the second week, a number 
of small, pale-red spots, roseola?. Instead of constipation, there is a moderate 
diarrhoea. There are daily about two to four soft, thin, bright-yellow dejec- 
tions. 

The third week, during which in the severe cases the symptoms already men- 
tioned persist, is the chief time of the numerous complications and of especial 
clinical events, about which we shall speak below at length. If the disease 
takes a favorable course, there comes at the end of the third week a decline of the 
fever; and then the general symptoms also improve as a rule. The mind becomes 
clearer, the patient sleeps better, and gains some appetite. The pulmonary and 
digestive symptoms abate, and convalescence gradually begins. 

This short sketch of the course of the disease corresponds to most of the cases 
of medium severity. There are, however, besides these, so many forms and so 
many variations from the usual picture, that it seems almost impossible to enu- 
merate completely all the events of typhoid fever. And besides, the separate epi- 
demics vary in their general character according to the time and place of their 
occurrence. In many epidemics the cases run a peculiar course and have certain 
special complications not seen in others. 

We will begin the presentation of the chief peculiarities by speaking of the 
course of the fever. 

Course of the Fever. — Observation of the temperature in typhoid is so abso- 
lutely essential for the estimation of each individual case that no scientific physi- 
cian ought to treat a case without regular measurement of the temperature. 
The measurements should be taken, if possible, in the rectum. Their frequency 
must of course be modified by circumstances, but it will probably be possible 
to have three or four measurements daily. At night, especially if the patients are 
asleep, it is generally not requisite to take the temperature. A general idea of the 
course of the fever can be gained only by representing the separate measurements 
graphically in a continuous " temperature curve." 

The typical curve of typhoid fever (see Fig. 2) falls naturally into three or 
four divisions. The first division is the initial period, or the pyrogenetic stage, and 
is seldom observed, since at this time the patients are generally not yet under the 
doctor's care. The initial period of the fever lasts, as a rule, some three or four 
days, seldom longer; and during this time the temperature rises, generally by 
gradual steps, so that the morning as well as the evening temperature is each day 
2° or 3° (1°-1.5° C.) higher than on the day before. A sudden and considerable 
rise of temperature, such as occurs in many other diseases, is very rarely seen in 
the beginning of typhoid fever. 

The second division of the curve represents the so-called fastigium, and cor- 



TYPHOID FEVER 



7 



responds to the height of the disease. During this time the fever presents, in most 
of the severer cases, the general character of " febris continua " — i. e., the spon- 
taneous remissions of the fever seldom exceed 2° (1° C). Almost always the 
lower temperatures come in the morn- 
ing hours and the higher in the even- 
ing. In cases of average severity the 
morning remissions touch 102° -103° 
(39°-39.5° C), and the evening ex- 
acerbations 104°-105° (40°-40.5° C). 
Temperatures which reach or ex- 
ceed 106° (41° C.) are seen only in 
very severe cases. Considerable morn- 
ing remissions are always a favorable 
symptom, while morning temperatures 
of 104° (40° C.) or higher generally 
show the case to be severe. The dura- 
tion of the fastigium varies with the 
severity and obstinacy of the case. It 
may last only a few days or one and a 
half to two weeks; in violent cases 
still longer. 

In many cases of slight or average 
severity the period of decline follows 
directly on the fastigium; but in 
severe cases there frequently inter- 
venes another stage, which Wunder- 
lich has graphically named the " am- 
biguous " period. The temperature- 
curve becomes irregular and more 
variable. The morning remissions 
may be great, even reaching the nor- 
mal, while the evening temperatures 
are often still very high. This stage 
has accordingly been termed the 
"period of the steep curves." It 
may be said that in general the 
longer a case of typhoid lasts the 
more irregular will be the course of 
the fever. 

The last stage — i. e., in cases of 
slight or average severity the third 
stage, and in severe cases commonly 
the fourth — is the period of defer- 
vescence or recovery. The peculiar- 
ity of this period in typhoid fever is 
that the fall of the fever is never by 
crisis, but always gradually, by lysis. 
Commonly the temperature descends 
by degrees, so that on each new day 
the morning remissions as well as 
the evening exacerbations are 1° to 
2° (0.5°-l° C.) lower. The zigzag 

form of curve, in which there are of course very frequently slight irregularities, 
must be taken as the rule. The duration of the defervescence generally exceeds 




8 



ACUTE GENERAL INFECTIOUS DISEASES 



that of the initial period. It lasts five to eight days, often longer. It is not very 
seldom that in defervescence the morning remissions become from the first very- 
marked, even reaching the normal temperature, while the evening exacerbations 
become daily less and less, until they too are not above the normal. A third form 
of decline is much less frequent, in which the morning remissions become every 
day greater, while the evening temperature persists for some days at about the 
same height. Several times we have seen the fever take on a tertian type during 
recovery. 

To this outline must be added a number of observations of practical importance. 

The initial period does not exhibit especial variations from the course we have 
stated. Its entire duration is bounded by certain relatively narrow limits. 

The fastigium presents, as already mentioned, the greatest varieties in its dura- 
tion. In light cases it is wholly wanting, so that these consist only of a period of 
gradually rising fever, and of a gradual defervescence almost immediately con- 
secutive to the rise. The entire duration of such light cases is only one and a half 
to two weeks. In other and tolerably frequent cases, which are often tedious, but 
still for the most part are light, the fever is not continuous, but remittent. The 
difference between the morning and evening temperatures amounts to 3° or 4° 
F. (1.5°-2.0° C), but the absolute height of the temperature is often not very con- 
siderable, so that the temperature curve at first leads to error and excites suspi- 
cion, for example, of tuberculosis. We have seen in Leipsic a number of cases 
in which the fever was perfectly intermittent during almost the entire illness, 
and for two to three weeks afternoon elevations reaching 104° (40° C.) or more 
daily succeeded normal morning temperatures. These cases had the general course 
of light attacks. 

Various influences, not to speak of therapeutic interference, may produce a 
considerable temporary remission of temperature in the course of the fastigium. 
Such a remission sometimes occurs spontaneously from the seventh to tenth day 
of the disease. If a marked intestinal haemorrhage happens (vide infra), the tem- 
perature generally falls several degrees centigrade, and the less frequent instances 
of severe epistaxis have the same effect. If, in female patients, abortion or prema- 
ture delivery occurs, we often observe a similar considerable fall of temperature, 
even without severe attendant haemorrhage. Perforation of the intestine often 
causes the temperature to fall rapidly. At times the occurrence of mental dis- 
turbances effects a moderate though noticeable lowering of temperature. Those 
great and sudden depressions of temperature remain to be mentioned which are 
accompanied by a very small but exceedingly rapid pulse and general prostration. 
Every such collapse, if severe, is a most dangerous event, and demands prompt 
and energetic medical treatment (vide infra). 

The development of local complications, such as pneumonia or inflammation of 
the parotid gland, is generally accompanied by a considerable rise of tempera- 
ture. The fever in such cases often becomes more irregular. This indicates the 
great practical value of thermometry. Almost every new rise of temperature or 
any considerable change in the ordinary course of the temperature has its special 
cause, and is therefore a warning to the attending physician to be vigilant. The 
cause of the change in the temperature is often not apparent until two or three 
days later. 

The period of defervescence departs most frequently from its typical behavior 
by being lengthened out into a " stage of retardation." The morning tempera- 
ture is then generally normal, while in the evening slight or moderate elevations 
continue. The reason for this long continuance of the fever may frequently be 
found in some not yet completely healed local complication, but often no such 
lesion can be demonstrated. Then we are commonly inclined to surmise sluggish 
intestinal ulcers which will not heal, or trouble in the mesenteric glands, etc. 



TYPHOID FEVER 



9 



This slow fever may continue for weeks. It is prone to follow severe cases, 
but lighter attacks, especially in elderly or feeble patients, may also take on this 
sluggish character at a relatively early period. To these last-mentioned cases 
must finally be added a few others in which during the whole course of typhoid 
fever no febrile temperature at all or only a very slight rise can be detected. 

Entrance into complete convalescence is shown with far greater certainty by 
the absence of elevations of temperature than by any other single symptom. 
There sometimes come, however, temporary elevations of temperature during con- 
valescence, following some error in diet, long-continued constipation, or mental 
excitement. In other cases the new fever depends on some local sequela, e. g., a 
boil or a glandular abscess. Often, however, the most accurate investigation fails 
to demonstrate a cause. Especially in the beginning of convalescence there some- 
times comes a high fever, or even a rigor, which may recur several times, but 
which soon gives place to a normal temperature. Generally no definite cause for 
these brief but decided elevations of temperature can be pointed out. Perhaps we 
might consider the possibility of some affection of the mesenteric lymph-glands. 
These sudden and great elevations have seldom any grave significance. 

This new fever which we have just described is best termed febrile recrudes- 
cence, or febrile sequela, in contrast with the proper typhoid relapse. That 
is, after typhoid fever has ended, the whole process may be repeated; and this 
occurrence is called a relapse. Particulars as to the behavior of the fever in such 
cases will be considered below, in connection with all the other peculiarities of 
typhoid relapses. 

Phenomena and Complications relating to the Separate Organs * 

Before we undertake a detailed discussion of the individual symptoms of 
typhoid fever, we must first make a brief general statement which is of very great 
significance for the correct understanding of almost every infectious disease. 
We include among the direct typhoidal symptoms all those morbid phenomena 
which are produced immediately by the typhoid bacillus itself or by its toxic 
chemical action; but, on the other hand, every patient sick with typhoid fever 
is exposed to many secondary infections (from the intestinal ulcers, from the 
mouth, in the lungs, etc.) whose invasion is rendered possible, or at least rendered 
easier, by the pre-existing typhoid infection. All the morbid symptoms arising in 
this way, which unite with the pure typhoidal symptoms in making up the whole 
picture of the disease, must, strictly speaking, be termed complications of typhoid. 
In the individual case it is often hard to decide whether a particular symptom 
is of a typhoidal nature or a complication. We must, however, hold fast to the 
essential difference between these two kinds of morbid phenomena, if we would 
obtain a deep insight into the nature and origin of the whole course of the 
disease. 

1. Digestive Organs. — We think it best to begin our consideration of the more 
special symptoms with the phenomena referable to the intestinal canal, for the 
reason that the anatomical changes in the intestine are pathognomonic. Indeed, 
these alterations may sometimes become of surpassing import in a clinical point 
of view, although in the majority of cases the intestinal symptoms are clinically 
not nearly so prominent as the general symptoms that result from the infection 
of the system as a whole. 

The characteristic typhoid lesion of the intestine consists of an affection of 
Peyer's patches, most marked in the lower part of the ileum. In the first week 
the patches swell gradually (stage of medullary infiltration). The rest of the 



* To avoid repetition, we have in what follows united a description of the anatomical changes with, 
the presentation of the clinical symptoms. 



10 



ACUTE GENERAL INFECTIOUS DISEASES 



mucous membrane exhibits at the same time more or less marked symptoms of 
simple catarrhal inflammation. In the second week, necrotic crusts form on the 
surface of the patches, which are cast off in the third week, leaving behind the 
typhoid ulcers. Toward the end of the third week the ulcers clean up, and then 
in the fourth week, if the case takes a favorable course, the ulcers heal. Smooth 
scars are formed, often diffusely pigmented. Experience shows that these scarcely 
ever lead to stricture of the intestine. The same process also goes on in a greater 
or less number of the solitary follicles as well as in the Peyer's patches themselves. 
We may add that probably in lighter cases of typhoid (vide infra) there is often 
no actual ulceration. The swelling of the lymphatic tissue subsides in this case 
before sloughing occurs. We have already mentioned the occurrence of typhoid 
bacilli in Peyer's patches and the intestinal follicles. 

The number and size of the ulcers formed have no direct relation whatever 
to the severity of the case. Although very extensive lesions in the intestine are 
often found in cases that end fatally, yet, on the other hand, we observe fatal 
cases in which only a few ulcers are found in the intestine. In cases with exten- 
sive intestinal lesions we often see follicular ulcers in the colon as well as in the 
small intestine (colo-typhoid). 

The clinical symptoms referable to the intestinal canal are, as we have said, 
prominent only in exceptional cases. In the beginning of typhoid fever there is 
usually constipation. This may last throughout the illness, so that the patients 
have but one dejection in every two or three days, or often none at all unless an 
enema be given. As a rule, a moderate diarrhoea begins during the second week. 
There are two to four stools, or sometimes more, each day. These usually have 
a characteristic bright-yellow color. On standing, they divide into an upper, 
cloudy, and quite liquid layer, and a lower layer composed of yellow, crumbly 
masses. They have generally an alkaline reaction, and upon microscopic exami- 
nation they are found to contain, besides remnants of the ingesta and granular 
detritus, a few epithelial cells, round cells, many crystals of triple phosphate, and 
numberless bacteria. Pfeiffer and other investigators have been able frequently, 
although not invariably, to demonstrate the true typhoid bacilli in the dejecta 
by means of special methods of cultivation. 

Severe diarrhoea (ten or more stools daily) is relatively infrequent. In some 
bad cases we have seen the stools take on a dysenteric character. The autopsy 
showed in these cases unusually severe lesions of the colon and a diphtheritic 
inflammation of its mucous membrane. They were probably secondary compli- 
cations. 

Gaseous distention affecting the intestine, and especially the colon, is very 
frequent ; a slight but evident gaseous distention, with a fluctuating, " air-cush- 
ion " feeling, is a very valuable symptom in the diagnosis of typhoid fever, but, 
as a rule, the meteorism is moderate. Indeed, severe cases of typhoid are ob- 
served in which the abdomen always remains concave. Marked tympanites is 
always an unpleasant complication. We saw one case, which ended fatally, with 
very great tympanites, in which the lesions were almost exclusively in the colon, 
and it was the enormous distention of its entire length which had so swollen 
the abdomen. The noise that can often be produced by pressure in the ileo-csecal 
region (gurgling) used to be regarded, but probably erroneously, as especially 
characteristic of typhoid fever. Abdominal pain is often entirely absent. Some 
patients, however, complain of abdominal pain during almost the entire illness. 
On pressure, the belly is generally somewhat sensitive, but the tenderness is sel- 
dom extreme. It is more apt to be marked when there is constipation. Often 
such tenderness is due to a participation of the peritoneum in the disease, even 
when there is no perforation (vide infra). 

There still remain two symptoms of the greatest practical importance, both of 



TYPHOID FEVER 



11 



which have a direct connection with the intestinal lesions : they are intestinal 
haemorrhage and perforation. 

Intestinal haemorrhages in the course of typhoid are almost always due to the 
erosion of the walls of blood-vessels in connection with the formation and throw- 
ing off of the crusts of the ulcers. The haemorrhages occur, therefore, most fre- 
quently toward the end of the second and during the third week. The blood pours 
out into the intestine, and is passed with the stools. Its amount may be small, or 
it may reach to one or two pints, or even more. Its color is generally rather dark. 
The later discharges are generally tarry. Liebermeister states that he has ob- 
served intestinal haemorrhages in 7.3 per cent, of typhoid patients, and Griesinger 
in 5.3 per cent. We have ourselves seen, in the medical wards in Leipsic, 45 
intestinal haemorrhages in 472 cases, i. e., in 9.5 per cent. In individual epidemics 
the frequency varies greatly. It rose in 1880 to eighteen per cent. 

Intestinal haemorrhage is always a grave symptom. Even slight haemorrhages 
deserve consideration, for they may be the precursors of severer ones. Yet 
intestinal haemorrhage, even if profuse, is not necessarily fatal. Of the above 
forty-five cases of typhoid with haemorrhage, twenty-six ended in complete recov- 
ery. In eight cases, death occurred as the immediate result of the loss of blood. 
Eleven ended fatally after a time. 

After every considerable intestinal haemorrhage, the symptoms of general 
anaemia, often even of collapse, appear. The fall of the bodily temperature has 
been already mentioned. The haemorrhage has sometimes a favorable influence 
on severe cerebral symptoms, for consciousness succeeds to the previous stupor 
or delirium. Often the haemorrhage is directly followed by recovery from the 
disease. 

Much more ominous than the intestinal haemorrhage is the occurrence of per- 
foration, as a result of the breaking through of a typhoid ulcer into the abdominal 
cavity, because, almost without exception, this is followed by a purulent or even 
ichorous peritonitis. Peritonitis is never caused by the typhoid bacillus itself, 
but by pyogenic organisms (cocci, perhaps bacterium coli?) which enter the ab- 
dominal cavity with the contents of the intestine. The amount of fluid peri- 
tonize exudation is, as a rule, not very great. The serous membrane is often 
found covered merely with a fibrino-purulent or purulent-haemorrhagic deposit. 
The occurrence of perforation is sometimes marked by a violent pain suddenly 
felt by the patient; but it may also, even in severe cases, take place insidiously. 
The abdomen is generally (not always) greatly distended and very tender on 
pressure, so that even in stupor patients groan while being examined. If gas has 
entered through the opening into the peritoneal cavity, we often observe absence 
of the ordinary dullness over the liver ; but this symptom is to be employed cau- 
tiously as a factor in diagnosis, for absence of hepatic dullness may also result 
from distended intestines lying in front of the liver. When perforation has oc- 
curred, the patient soon looks collapsed, with cheeks fallen in and sharp, cool nose. 
Frequent eructations and vomiting often follow. The pulse becomes small and 
very frequent. The temperature generally falls as the peritonitis begins, and 
later it usually undergoes great variations. 

Perforation of the intestine occurs most frequently in the third or fourth week 
of the disease, and much oftener in men than in women. In sluggish cases, how- 
ever, we can not be without apprehensions of it till a late period. The perforation 
generally takes place in a coil of the lower part of the small intestine, and with 
marked relative frequency in the right side of the pelvis, though seldom in the ver- 
miform appendix or in the colon. With few exceptions, death comes quickly, 
after a few days at latest. Only when the perforation is small and the intestines 
have become agglutinated at the onset is the course of the peritonitis slower, so 
that the symptoms are less violent and cause death in a week or ten days. Out 



12 



ACUTE GENERAL INFECTIOUS DISEASES 



of fifty-six fatal typhoid cases in the Leipsic medical clinique we lost five, or nine 
per cent., from peritonitis following perforation. Here and there a case of re- 
covery has been reported, probably resulting from a limitation of the peritonitis 
through speedy adhesion of the intestines. 

It should be mentioned here that sometimes in typhoid fever a local or general 
peritonitis may occur through direct extension of the process to the serous mem- 
brane without actual perforation. We have seen in one case, as the result of the 
peritonitic bands and false membranes, complete occlusion of the intestine (ileus), 
and death. 

Swelling of the mesenteric lymph-glands (less often of the retro-peritoneal 
glands as well) is found in typhoid almost as constantly as the anatomical changes 
in the intestine. Sometimes they break down, i. e., suppurate. In cases that have 
passed through the disease we often find considerable deposits of lime in the 
glands. These changes have a certain clinical importance ; for, as already men- 
tioned, we may often venture to refer a more or less tedious recurrent febrile state 
which has no other demonstrable cause to this lesion of the mesenteric glands. 
In some rare cases a general peritonitis has been observed as a result of the burst- 
ing of a suppurating gland. 

The swelling of the spleen (acute splenic tumor) is, in typhoid fever as well as 
in many other acute infectious diseases, one of the most constant symptoms. The 
enlargement of the spleen can often be demonstrated as early as the end of the 
first week, and is therefore of considerable diagnostic importance ; but percussion 
of the spleen is sometimes decidedly difficult and deceptive in this disease because 
of the existence of tympanites. The surest demonstration of splenic enlargement 
is therefore always by means of palpation, which, after a little practice, gives a 
positive result in the majority of cases. Absence of splenic tumor is most fre- 
quently observed in elderly typhoid patients. The spleen may also diminish con- 
siderably in size after severe intestinal haemorrhage. Pain in the splenic region, 
resulting from tearing of the distended capsule, is comparatively rare. The 
splenic infarctions which sometimes occur may, in exceptional cases, prove the 
starting-point of a peritonitis. 

Hepatic symptoms are seldom seen in typhoid fever, except that there may be a 
moderate swelling of the organ. The anatomical changes of "parenchymatous 
degeneration," and the frequent formation in the liver of the small lymphomata 
which Wagner discovered, have no clinical significance. The bile secreted is gen- 
erally pale and scanty. This is a partial explanation of the light color of the 
stools. A very rare complication, which we ourselves observed in one case, is 
acute yellow atrophy of the liver. 

The stomach presents no especial anatomical changes in typhoid. Anorexia 
is an almost invariable symptom in the beginning and during the course of 
all severer cases. There is seldom any desire for food till recovery begins; but 
then, if convalescence is undisturbed, the appetite soon attains an enviable keen- 
ness. Vomiting in the beginning or course of the disease is an exception, unless 
after some error in diet. We have already mentioned it as a symptom of perito- 
nitis. 

The changes in the mouth and throat of typhoid patients deserve the careful 
attention of the physician. The lips and tongue are in severe cases dry and fis- 
sured. The lips are often covered with dry, black crusts, sometimes described as 
a " fuliginous coating." The tongue is apt to be thickly coated at first, but later 
cleans off from the edges and tip. In severe cases, especially if the mouth is not 
properly cleansed, a rather severe stomatitis may occur and produce superficial 
ulceration of the buccal mucous membrane and of the edges of the tongue. The 
gums sometimes become spongy, and are apt to bleed, as if scorbutic. 

Actual sore throat, at least according to our experience in Leipsic, occurs but 



TYPHOID FEVER 



13 



seldom at the beginning of typhoid fever. The difficulty in swallowing, often 
complained of by patients, is generally due to dryness of the pharynx. In certain 
epidemics, however, the occurrence of sore throat at the beginning- of the illness 
has been frequently observed. It may even happen that this early sore throat is 
accompanied by an. erythema diffused over the body, so that at first suspicions of 
scarlet fever arise. The cases are very interesting and quite rare (although we have 
repeatedly seen them) in which disturbances of swallowing exist with the general 
typhoid symptoms from the beginning. On examining the fauces we see on the 
tonsils peculiar white, slightly elevated spots, which later form superficial ulcers. 
After a time these places heal, and in other respects the disease pursues a normal 
course. The suspicion is justified that in these cases there is a specific typhoidal 
disease of the tonsils (due to the typhoid bacillus itself), and such cases are called 
tonsillar or pharyngeal typhoid (analogous to the laryngeal typhoid, pneumo- 
typhoid, and nephro-typhoid. to be mentioned later). In such cases the typhoid 
bacilli have probably attacked the tonsils at their first invasion. It should also 
be mentioned that in severe cases there is often an extensive growth of thrush in 
the mouth and throat, and this may spread quite a distance down the oesophagus. 

The changes in the mouth and throat are of especial interest, for the reason 
that they may be directly propagated to important neighboring organs. Starting 
from the pharyngeal cavity, the pathogenic agent, probably in most cases the 
staphylococcus, may penetrate through the Eustachian tube into the middle ear. 
Thus arise those inflammations of the middle ear which are not very rare in severe 
cases of typhoid, and which lead to perforation of the membrana tympani and 
to purulent discharges from the ear. The not infrequent inflammation of the 
parotid gland is also, as we believe, occasioned in a similar way, the inflammatory 
agent reaching the parotid gland from the mouth by way of Steno's duct. We do 
not regard the otitis and parotitis as especial localizations of the typhoid poison, 
hut as secondary diseases, for the occurrence of which typhoid fever merely fur- 
nishes the occasion, as when the- mouth is imperfectly cleansed. Purulent otitis 
in typhoid fever can easily be overlooked at first, since stuporous patients only 
Tarely complain, of themselves, of pain in the ear or deafness. The parotitis 
appears most frequently in the third week, and g'enerally on one side, though 
sometimes on both. It almost always becomes purulent, and discharges either 
externally or into the external auditory meatus, unless there is a timely incision. 

2. Organs of Respiration. — Affections of the lungs are among the most fre- 
quent and important complications of typhoid fever, but are for the most part not 
a direct result of the typhoid infection, but pure complications. The bronchitis 
very often found in severe cases, and especially in patients who do not come till 
late under proper care, certainly is dependent on the imperfect expectoration of 
the bronchial secretions and on the inhalation of inflammatory agents coming 
from the mouth and throat. 

Xumerous cases of typhoid of slight or average severity, under proper care, 
Tim their course without any considerable bronchitis. In many other cases, and 
even severe ones, the bronchitis remains within moderate bounds, especially if 
the patient is brought promptly under proper care and treatment : but in severe 
cases, when marked disturbances of the nervous system arise, and the patient in 
his stupor expectorates little, swallows things the wrong way. and lies all the 
time on his back, passive and collapsed, the occurrence of a severe, diffuse bron- 
chitis, especially in the lower lobes of the lungs, can hardly be avoided. Xor in 
such cases is there generally a mere bronchitis, but a more or less extensive 
catarrhal, lobular pneiimonia, to be classed therefore under the so-called inhala- 
tion pneumonias (cf. chapter on lobular pneumonia). TThat was formerly 
termed " hypostatic pneumonia " is also almost invariably to be put in this group. 

From the way in which these pulmonary disorders arise, we can understand 



14 



ACUTE GENERAL INFECTIOUS DISEASES 



why the bronchitis sometimes takes on a putrid character, and why the lobular 
infiltrations are, in severe cases, transformed into genuine gangrene. If such spots 
touch the pleura, they occasion the development of a pleurisy which is almost 
always purulent. In rare cases, pneumothorax may arise as a sequel to the perfo- 
ration of a gangrenous infiltration into the pleural cavity. Various circumstances 
promote the occurrence of pulmonary symptoms. Thus we find it especially easy 
for a severe bronchitis and its sequelse to be developed, in the case of elderly per- 
sons, or the kyphoskoliotic, or the corpulent, or patients who have previously suf- 
fered from emphysema or cardiac disease. 

The subjective thoracic symptoms, in typhoid patients who have pulmonary 
complications, are generally not very prominent. It is only occasionally that 
patients complain in the early stages of typhoid fever of pain, and of a sense of 
oppression in the chest, or of cough, or of a stitch in the side; and even when 
such symptoms exist, the physical examination may give comparatively insignifi- 
cant results. The severer pulmonary complications are seen mainly in those 
whose intelligence is more or less blunted, and who, therefore, make little com- 
plaint, are not much disturbed by the dyspnoea, and cough and expectorate little. 
A careful physical examination alone can enlighten us as to their condition. On 
auscultation, sibilant rhonchi are the chief signs observed in the milder cases. In 
the severer ones there are moist, fine, and coarse rales, especially numerous toward 
the base of the chest. If there are abundant moist rales, we may infer that there 
is a lobular pneumonia, although this can not be demonstrated with certainty till 
the separate islets of infiltration unite into a more extensive solidification, so as to 
afford dullness on percussion. 

In addition to the pulmonary lesions already mentioned, genuine croupous or 
lobar pneumonia does occur in typhoid fever. This is often an actual complica- 
tion, dependent upon a secondary infection with the genuine pneumonia diplo- 
coccus. Such a pneumonia may come on early or sometimes during convalescence, 
and affect both the upper and lower lobes. There is probably also a true typhoid 
pneumonia caused by the entrance of typhoid bacilli into the lungs. Such a 
pneumonia can not at present be recognized anatomically, but only by bacterio- 
logical investigation. Especial interest attaches to those cases of typhoid fever 
which begin with a lobar pneumonia. Often there is at first not the slightest 
suspicion of a typhoid fever, for the disease is regarded as an ordinary croupous 
pneumonia; but it is usually to be noticed that the illness does not begin sud- 
denly with a rigor, but more gradually, and that from its incipiency the constitu- 
tional symptoms, the headache and splenic tumor, are more prominent than is- 
usually the case in pneumonia. At the end of the first week's illness there is no 
crisis, but persistent fever. Now the pulmonary symptoms often retreat more 
and more to the background, while, on the contrary, diarrhoea and rose-spots 
appear. The spleen is enlarged. In short, the clinical picture of typhoid is 
developed. It is not unnatural to suppose, although there is yet no absolute 
proof of the fact, that in these cases, which are fittingly termed " pneumo- 
typhoid," the infection with the typhoid bacilli has taken place exceptionally in 
the pulmonary tissue, and that, therefore, the first pathological changes are devel- 
oped in the lungs. 

Laryngeal Lesions. — The same causes which produce the bronchitis result also 
in a simple catarrhal laryngitis, with hoarseness. This is in severe cases accom- 
panied by superficial ulcers on the vocal cords or the posterior wall of the larynx. 
Sometimes, again, the lesion is due to mechanical causes, constituting the so-called 
" decubitus laryngisP The disorders which attack the less superficial structures 
of the larynx are fortunately rare. Chief among them is a laryngeal perichon- 
dritis of the arytenoid cartilages. This complication is justly regarded as of bad 
omen, and may lead to the rapid development of oedema of the glottis, with great 



TYPHOID FEVER 



15 



laryngeal obstruction and threatening suffocation. These severe laryngeal affec- 
tions in typhoid are regarded by some authorities, especially by Klebs, as always 
the direct effect of the infecting poison ; but in most cases they are probably due 
to an invasion of staphylococci or some similar microbes. We have several times 
seen croup in typhoid fever, and it is a very dangerous symptom. In regard 
to their origin most of these mild and severe laryngeal affections in the course 
of typhoid fever are to be regarded as secondary inflammations; but specific 
typhoid disease of the larynx also seems to exist. The cases are of interest where 
the whole morbid process begins with a severe laryngitis (" laryngeal typhoid ") 
and is followed later by the ordinary symptoms of typhoid (vide supra, pharyngeal 
typhoid). 

Among symptoms referable to the mucous membrane of the nose, epistaxis is 
important. It occurs in the beginning of typhoid with tolerable frequency, and 
is in one way not unfavorable, for it often mitigates the patient's headache. At a 
later period nose-bleed may become a most unpleasant complication, as it is some- 
times very difficult to check. We have even seen one fatal case due to persistent 
nose-bleed. Other nasal symptoms are exceptional. There is an old saying that 
typhoid never begins with a coryza. 

3. Nervous System. — The old term " nervous fever," which is still used by the 
laity, shows how frequent and severe are the nervous derangements which occur 
in typhoid. In cases of any severity there is almost always a certain dullness of 
intellect, often amounting to apathy and somnolence. The patients give mono- 
syllabic and incomplete answers to all questions, and their statements about 
their previous history are often disordered and contradictory. There may even 
be sopor or a deep coma in the worst cases. All cases of this sort in which 
there was a condition of intellectual enfeeblement were termed by the old 
physicians " febris nervosa stupida" in contrast to the " febris nervosa ver- 
satilis" that form in which abnormal mental activity or delirium predominates. 
In severe cases delirium is very frequent. It is generally worse at night, and at 
times when the patient happens to be left alone. Very often he tries to leave his 
bed, because of his delusions, and talks of persons and things with which he was 
formerly familiar; or he is very noisy and restless, sometimes shrieking from 
groundless fears. We may add that these diverse nervous symptoms frequently 
succeed one another, or appear in combination. Sometimes a soporose patient 
may be heard softly whispering to himself in " muttering delirium." 

Certain motor disturbances are often combined with considerable impairment 
of consciousness. There is a slight twitching of the muscles of the face and ex- 
tremities. The old authorities gave the name subsultus tendinum to the sudden 
leaping into prominence of the sinews thus caused. It is best seen on the back 
of the hands. In severe cases the patient is sometimes observed to grind the teeth 
together; this is due to a cramp-like condition of the muscles of mastication, and 
is justly regarded as ominous. We often see persistent tremor of the extremities 
and lower jaw; and it is especially in these cases, as we have demonstrated upon 
numerous patients, that the tendon reflexes and the mechanical excitability of the 
muscles are much increased. If deep coma comes on, the muscles become lax, 
the motions of the eye are not co-ordinated, and reflex excitability diminishes, or 
is wholly extinguished. 

Headache is one of the most constant symptoms in the beginning of the dis- 
ease. It is usually referred to the forehead or temples. The pain may be very 
violent, and sometimes takes on almost a neuralgic character. It almost always 
subsides in the second week. 

If we seek the cause of these nervous symptoms, which are often so severe, we 
find that the anatomical changes in the nervous system, including the brain, bear 
no relation whatever to the severity of the symptoms observed during life. We 



16 



ACUTE GENERAL INFECTIOUS DISEASES 



sometimes meet with minute haemorrhages in the cerebral meninges, or meningeal 
opacity or oedema, or a moist condition of the cerebral parenchyma ; but the con- 
nection of these and similar changes with the symptoms of the disease is often 
more than doubtful. Nor can the microscopic alterations in the brain, which 
have been reported, be regarded as important and authoritative. It is only in 
very rare cases that large cerebral haemorrhages or purulent meningitis have 
been found. As to this last, we should always be very cautious in making a diag- 
nosis, as symptoms which would seem to be most conclusively meningeal — such 
as stiffness of the neck, rigidity of the whole spinal column, and occipital head- 
ache — may appear in typhoid patients, and yet the autopsy may show no trace of 
meningitis. 

One theory, which has Liebermeister for its chief supporter, and which has 
won a tolerably widespread acceptance among physicians, is that the nervous 
symptoms are chiefly a direct result of the febrile temperature. It is impossible, 
however, for us to regard this view as universally true. The unprejudiced con- 
sideration of a large number of personal observations prevents it. Although it is 
undeniable that elevated temperature has a harmful influence on the nervous sys- 
tem, yet in numerous cases there is no relation between the height of the fever 
and the severity of the nervous derangements. There are cases in which the fever 
remains continuously high for days, while the patient feels perfectly comfortable 
and presents no symptoms of any important cerebral disturbance. The opposite 
class of cases is still more numerous, in which from the very start there is always 
a low temperature, and, notwithstanding, the most severe nervous symptoms 
arise. Frantzel and others have published very striking cases of this sort. 

Hence we must seek for some other special cause of the severe nervous symp- 
toms, and according to our present views this cause must be the intoxication re- 
sulting from the specific infection. We know that all bacteria produce, by their 
own tissue-metamorphosis and the chemical processes which they excite in their 
neighborhood, certain chemical matters which, especially in the case of the 
so-called " pathogenic bacteria," seem to be similar to the alkaloids (" ptomaines " 
and " toxines "), and exercise a decidedly poisonous influence upon the body, and 
especially upon the nervous system. These products are formed by the typhoid 
bacilli, enter the blood, and are the chief cause of the nervous phenomena. The 
difference in the violence of the latter in different cases probably depends mainly 
on a difference in the amount, and perhaps also in the quality, of the toxines 
produced by the typhoid bacilli, and probably also in the different susceptibility of 
individuals to the poison. The reason that the influence of these poisons is not 
much greater than it is, is that they are in part destroyed within the body and in 
part excreted with great rapidity, the channel of exit being mainly the kidneys. 
Thus is explained the interesting fact observed by Lepine, Bouchard, and others, 
that the urine of typhoid patients possesses poisonous properties not present in 
normal urine. 

That the appearance of the nervous symptoms is dependent not only on the 
material causes, but also on the susceptibility of the individual, is shown by the 
fact that certain patients are especially prone to exhibit marked nervous phe- 
nomena ; for example, hard drinkers, " nervous " individuals, and also those who 
have suffered violent emotional disturbances shortly before the onset of the 
disease. 

Actual insanity is not very infrequent during the course of typhoid, or in con- 
valescence. It generally takes the form of melancholia. We have repeatedly 
seen patients in such a state that they would lie almost motionless in bed, with 
eyes open, and perhaps assert that they were dead! In other cases there is 
mental excitement, sometimes combined with hallucinations, or there is confu- 
sion of ideas. In one case, in a girl who was evidently predisposed to nervous dis- 



TYPHOID FEVER 



17 



orders, we saw typical hysterical insanity break out during the fever. Sometimes 
the mental excitement at the beginning of a relapse terminates in actual insanity. 
Few of the psychoses which arise during or at the end of typhoid outlast con- 
valescence. 

We have still to mention a number of nervous diseases that develop in the 
course of typhoid or after its decline. Neuralgia is sometimes seen, as well at the 
beginning as at the end of the disease. It is most frequent in the regions supplied 
hy the trigeminus and the occipital nerves. Great hyperesthesia of the skin 
and muscles is not rare during convalescence. It attacks the lower extremities 
by preference. Paralysis of single muscles (e.g., of the serratus magnus), or 
paralysis of a single extremity, has been repeatedly observed as a sequela. The 
paralysis is generally of the atrophic variety, and is probably, as a rule, due 
to neuritis. Ataxia and spastic paralysis of the lower extremities are rare se- 
quelae. Finally, there are sometimes developed, either in the course or at the 
conclusion of typhoid fever, the symptoms of a localized cerebral disorder (e. g., 
hemiplegia and aphasia), the anatomical cause of which varies. There may be 
a haemorrhage or an embolism, and probably in still other cases a localized en- 
cephalitis. 

4. Circulatory System. — Disturbances of the heart such as to produce striking 
anatomical changes are rare. The pericardium macroscopically almost always 
appears normal; the slight mitral or aortic endocarditis sometimes found has 
no clinical significance. The disturbances in the cardiac muscle seem more im- 
portant. It is often more flabby than normal. The cavities, especially on the 
right side, are often dilated. With the naked eye we frequently see in the muscle 
itself cloudiness or fatty changes. Microscopic lesions are usually present and 
are much more pronounced. They consists usually of a granular (" albumi- 
noid ") or more rarely of a fatty or hyaline degeneration of the fibers, and of 
genuine inflammatory foci of interstitial myocarditis (Hayem, Romberg). No 
marked disease of the cardiac ganglia has as yet been found. 

The clinical significance of these changes should not, we believe, be overesti- 
mated. In all probability they are often without serious consequences and dis- 
appear completely with recovery from the disease. Sudden death (heart-fail- 
nre?) occurs in typhoid, but it is very rare (see the chapter on diphtheria). Per- 
manent disturbances of the heart after typhoid are also rare. When they occur 
they are perhaps due to the passage from an acute myocarditis to a chronic inter- 
stitial degeneration. [This slowness of the pulse as compared with the fever is 
common enough to have some diagnostic value, provided brain trouble is ex- 
cluded. The pulse is almost always rapid, although often not so much so as the 
height of the temperature might lead one to expect. — V.] 

It averages from 90 to 110, and often more. When it keeps at 140 or 
higher, in adults, it is always an unfavorable symptom. The abnormal frequency 
is often due in part to the high temperature; but there are other factors. Tem- 
perature and pulse do not correspond in all cases. Sometimes the pulse will 
have a normal or even subnormal frequency throughout the entire attack, de- 
spite the fever. Temporary accelerations are easily produced by mental excite- 
ment or bodily exertion, as by sitting up in bed. In convalescence the rate is fre- 
quently subnormal. 

Slight irregularities of the pulse are not rare, either in the acme or the decline 
of typhoid. Marked irregularity is always a grave symptom, although in many 
cases it passes off and the patient recovers. 

Dicrotism, due to loss of tension in the wall of the artery, is so common that 
it is still regarded by elderly physicians as characteristic of typhoid, although 
it often occurs in the same way in other acute diseases. In many severe cases the 
height and strength of the pulse may cause no alarm, but often the pulse is 



18 



ACUTE GENERAL INFECTIOUS DISEASES 



notably weak and small. This is due not only to the influence of the disease, 
but also to the previous condition of the individual. 

The diminished cardiac activity may result in venous thrombosis, especially 
in the lower extremities and in a crural vein. This sometimes causes swelling 
of one of the lower extremities during the later stages or convalescence. The 
swollen member generally regains its normal size after some weeks. In other cases 
the thrombosis occurs earlier, and in patients who are still too vigorous to suffer 
from cardiac weakness, so that we are forced to the conclusion that there is some 
local specific cause, a local thrombo-phlebitis due to the typhoid bacillus itself, 
or, more probably, to the invasion of the walls of the vein by some secondary 
infection. A possible, but fortunately infrequent, result of these thrombi in the 
lower limbs is pulmonary embolism and sudden death. 

In severe cases, which end in death, cardiac thrombi are sometimes found, with 
emboli in the lungs, spleen, kidneys, or other organs. 

(Edema of the ankles and legs is very often seen in convalescents, especially 
when they first get out of bed. It is due to the weakness of the heart and changes 
in the vascular walls. Once we saw a general dropsy develop at the end of a 
severe attack in a girl of fourteen. The autopsy disclosed no other possible cause 
for it than the extreme atrophy and flabbiness of the heart. 

5. Blood. — As in most febrile diseases associated with great emaciation, so 
in typhoid in severe cases the number of red blood-corpuscles (and correspond- 
ingly the amount of haemoglobin in the blood) is much diminished. We found, 
for example, 2,800,000 to 3,200,000 in a cubic millimetre. In milder cases the 
figures do not differ materially from normal. It is a fact of greater interest and 
also of distinct diagnostic importance that many observers have found that leu- 
cocytosis is absent in typhoid fever, contrary to what is found in many other 
acute febrile diseases, pneumonia, erysipelas, sepsis, etc. We have often confirmed 
this fact in our clinique. We sometimes find with the general emaciation a de- 
crease in leucocytes ; for example, only 3,000 or 5,000 in a cubic millimetre instead 
of the normal number of about 8,000. 

6. Skin. — The eruption seen in typhoid fever is characteristic and extremely 
important in diagnosis. The roseolas or rose-spots (light red, slightly elevated 
spots) appear at the beginning of the second week, usually on the trunk, and 
chiefly on the abdomen and back. The number varies greatly. Rarely they are 
entirely absent, most often in elderly persons. Sometimes they are very abun- 
dant, and extend to the thighs, the arms, and even to the neck and face. Often 
they vanish after a few days, but they may persist much longer. In the latter 
case they may become to a very slight degree petechial, so that they will not 
entirely disappear on pressure. They often occur in successive crops. We have 
even seen several cases where new rose-spots kept coming for some days after the 
fever had disappeared. 

As to other cutaneous eruptions, we may mention first of all that herpes la- 
bialis is so rare in typhoid that in cases of doubtful diagnosis it is a factor in 
excluding that disease. Miliaria, urticaria, and superficial pustules are some- 
times observed. Occasionally little bluish spots appear, especially on the trunk. 
These used to be called " taches hleudtres " (pelioma typhosum) ; but later obser- 
vations show that they are not connected with typhoid fever particularly. They 
are due to pediculi. We might use the term pelioma typhosum to designate the 
kind of vesicles which we have repeatedly seen on the abdomen in severe cases. 
They are about the size of peas, and have sero-haemorrhagic contents. Boils and 
superficial abscesses are frequent, especially as disagreeable sequelae in convales- 
cence from severe attacks. There are often abscesses of the sweat-glands in the 
skin of the axilla during convalescence. All these and similar cases of suppura- 
tion in typhoid fever do not depend, as a rule, upon the original cause of the dis- 



TYPHOID FEVER 



19 



ease, but upon secondary pathogenic germs, especially the staphylococcus, for 
whose entrance the typhoid process has merely prepared the way. Extensive 
ecchymoses are very rare, and are symptomatic of a general hemorrhagic diath- 
esis. Petechia? are frequent during recovery. They are generally seen in the 
follicles of the skin below the knee. There have been a few cases of gangrene 
in the lower extremities, especially in the toes. We saw in one patient an ex- 
tensive gangrene of the skin of the abdomen. Its cause could not be determined 
(ice-bag ?)• 

Finally, we must mention that bed-sores are prone to develop in severe or 
neglected cases. The localities most often attacked are the nates, the furrow be- 
tween them, and the heels. A bed-sore may be so extensive, and accompanied by 
such undermining of the skin, as to be a dangerous or even fatal complication. 

The epidermis often scales off to a considerable extent during convalescence 
after a severe attack of typhoid. Everybody knows how the hair falls out after 
the fever, but it is sure to grow again. The nails also are not infrequently 
affected, becoming rough and brittle, or even falling off. 

7. Muscles, Bones, Joints. — Zenker has discovered a degeneration of the vol- 
untary muscles which occurs in typhoid as well as in other severe diseases. It is 
called the " granular " or " waxy " degeneration. Whether it has clinical symp- 
toms can not be determined. Perhaps it may explain the great muscular hyper- 
esthesia which is often observed, and the muscular pains, which may be very 
trying. Severe cases sometimes have haemorrhages into the muscles, particularly 
the rectus abdominis. 

Lesions of the bones and joints occur but seldom, although other observers and 
we ourselves have repeatedly seen periostitis and ostitis in the ribs, tibia, etc., fol- 
lowing typhoid. It is an interesting fact that lately typhoid bacilli have often 
been found in such foci of disease, so that it is a true typhoid localization. Swell- 
ing of the joints is rare. When of a purulent nature it is usually due to secondary 
" septic " infection. 

8. Genito-urinary Apparatus. — Genuine, acute, hemorrhagic nephritis is a 
very rare complication. It does occur, however, and has even given rise to the 
establishment of a special " renal form of typhoid fever " (nephro-typhoid). This 
name applies especially to those cases in which a severe acute nephritis is the pre- 
dominant symptom at the start, while at a later period the course of the fever, 
the intestinal symptoms, the rose-spots, etc., show the disease to be typhoid fever. 
Xephro-typhoid is analogous to pneumo-typhoid and tonsillo-typhoid. A simple 
so-called febrile albuminuria occurs very frequently at the acme of typhoid, and 
is not to be interpreted unfavorably. It is probably the result of that slight par- 
enchymatous degeneration of the kidneys which occurs in typhoid with the same 
frequency as in most of the other severe infectious diseases. There does not seem 
to be a direct relation between the albuminuria and the fever, although some 
authors assume it to exist. It is more likely that the renal epithelium is injured 
by the noxious products which have been formed in the body and excreted by the 
kidneys. In other respects the urine in typhoid presents the same peculiarities 
as in most other severe febrile diseases : its amount is diminished; its color dark; 
its specific gravity increased; the excretion of urea greater than normal. It 
should be added that the urine at the height of the disease presents Ehrlich's 
" diazo-reaction " in almost all cases.* Cystitis is not a rare development toward 
the end of the illness. It is probably always secondary. 

* Ehrlich's test is carried out as follows : Solution 1 consists of strong hydrochloric acid, one part 
mixed with twenty parts of a one-half-per-cent. solution of siilphanilic acid. Solution 2 is a one-half- 
per-cent. solution of sodic nitrite in water. 

To 250 c. c. of solution 1 is added 6 c. c. of solution 2 ; an equal volume of urine is then added, and, 
lastly, about 60 c. c. of ammonia. On shaking, the urine becomes crimson. 



20 



ACUTE GENERAL INFECTIOUS DISEASES 



In men, orchitis is sometimes observed. Women often have their catamenia 
at the beginning of typhoid. Later in the course of the disease, and in convales- 
cence from severe attacks, the menses are often absent for several periods. In 
pregnant women there is considerable danger of abortion or miscarriage. 

Peculiarities in the Course of the Disease 

The above statements show an almost inexhaustible variety in the possible 
symptoms and complications of typhoid. The course of the disease as a whole 
may likewise present many diverse forms and peculiarities. We shall attempt 
merely to cite the most essential. 

The numerous light and rudimentary attacks (typhus levissimus) are first to 
be mentioned. It was not recognized till lately that they belonged to typhoid 
fever at all (Griesinger). They used to have all sorts of names applied to them, 
the favorite term being " gastric fever." This light form lasts eight to fourteen 
days. The fever is moderate and often decidedly remittent. There is almost no 
proper fastigium. The typhoid symptoms are but slightly developed. There 
is no severe pulmonary or cerebral disturbance. There is generally a moderate 
diarrhoea, the spleen is plainly enlarged, and often rose-spots can be found. The 
diagnosis of these cases is of course difficult in proportion to the scanty develop- 
ment of typhoid symptoms. It is best established by demonstrating an setiolog- 
ical relation between these cases and others which are plainly typhoid fever. 

Abortive typhoid is justly distinguished by Liebermeister from typhus levis. 
The name belongs to cases which begin with severe symptoms and high fever, as 
if they were going to be grave, but in which these violent symptoms disappear 
after a few days and give place to a rapid convalescence. 

On the other hand, there are cases which for a long time cause so little subjec- 
tive discomfort that the patient does not even go to bed (walking typhoid). It is 
not till quite late that there occurs a sudden change for the worse, or some severe 
complication. Thus it has happened that persons who were apparently healthy 
have suddenly had all the symptoms of a severe peritonitis due to perforation and 
have died, the autopsy disclosing the lesions of the third week of typhoid fever; 
or a mild typhoid assumes the walking type and is not detected, but later a severe 
or dangerous relapse may occur. 

The individual circumstances are very important in weighing each case, for 
they may modify the disease in many ways. 

In children it is a remarkable fact that typhoid ulcers are much less frequent 
than in adults. This explains why intestinal haemorrhages and peritonitis are 
much rarer in children. Marked cerebral symptoms are, on the other hand, very 
frequent. In severe cases children sometimes exhibit the peculiar symptom of 
a continuous penetrating screaming. In other, mild, cases the children are sop- 
orose. 

In the aged the diagnosis of typhoid is often very difficult, since the course of 
the disease is frequently irregular. Generally the fever is not very high, and it 
very seldom exhibits distinctly the type described above. The pulmonary or cere- 
bral symptoms predominate as a rule. , 

In the corpulent, typhoid fever is often very severe, so that our prognosis must 
always be rather grave, especially if pulmonary symptoms arise. 

Hard drinkers are also in especial peril in this as in all other acute diseases. 
Dangerous cardiac weakness is prone to appear. Severe cerebral symptoms are 
frequent. It is, however, surprising that true delirium tremens is relatively in- 
frequent, although so common in pneumonia. 

The influence of previous strong mental excitement and of certain already ex- 
isting diseases (cardiac disease, emphysema, kyphoskoliosis, etc.) has been already 
mentioned. Finally, we repeat that often the different epidemics present certain 



TYPHOID FEVER 



21 



peculiarities. For instance, in one the type of the disease will be severe, in 
another mild. In one epidemic relapses are comparatively frequent, in another 
exceptional. The same is true with regard to the frequency of the appearance of 
certain symptoms, such as intestinal haemorrhage, perforation, pneumonia, or 
nephritis. Indeed, it has even been observed that those cases which occur during 
a given epidemic in the same family or house or block sometimes present striking 
resemblances to one another (" group typhoid " of E. Wagner and others). 

Relapses of Typhoid Fever 

Typhoid fever exhibits in many cases the peculiarity of repeating itself com- 
pletely after having run its entire course and disappeared. This process is called 
a relapse. It is in all probability the result, not of a fresh infection of the system 
from without, but of a renewed development of the germs already present, or pos- 
sibly of a fresh auto-infection. A typical relapse is like a first attack in all 
clinical and anatomical particulars, with this difference that everything is 
more condensed, and lasts a shorter time than in the first attack. The interval 
between the two, during which there is no fever, lasts seven to ten days. It may 
be longer, and is often shorter. Sometimes the relapse follows immediately upon 
recovery. Indeed, it may even happen that, before the patient has completely 
recovered, his temperature begins to rise again in the characteristic step-like way. 
To such cases as this last the term recrudescence is applied. Except in the time 
of its beginning, it may be just the same as a genuine relapse. In the interval be- 
tween the two attacks many persons are perfectly comfortable, and appear to be 
fully convalescent. There is often, however, a slight evening rise of temperature. 
It is noticeable that the splenic tumor does not completely disappear after the 
first attack in many cases which are followed by a relapse. 

The relapse is generally briefer, as we have said, than the first attack, seldom 
lasting more than fifteen to eighteen days. The temperature rises more rapidly, 
perhaps in two or three days. The fastigium is shorter, the decline more abrupt. 
The absolute height of the temperature may be very considerable, even exceed- 
ing that in the first attack. Rose-spots appear as soon as the third or fourth day. 
The stools become liquid, the spleen enlarges again, and all sorts of complications 
may arise. The danger occasioned by a relapse may, however, be overestimated. 
On the whole, a relapse is not so very dangerous, and it is especially noticeable 
that the subjective symptoms, such as headache, are often slight. A severe re- 
lapse may follow a mild case. In other instances the relapse may prove merely 
rudimentary. 

The frequency of relapses varies considerably in different epidemics. In 
Leipsic, we had relapses in about nine per cent, of all cases, but in separate years 
the percentage varied between four and sixteen. Out of about five hundred cases 
we have seen three in which there were two successive and typical relapses. 

Diagnosis. — The diagnosis of typhoid fever may be perfectly easy, but, if the 
case be anomalous, or come under observation at a late period, it may be ex- 
tremely obscure. Inasmuch as a search for the specific bacilli is too difficult 
and troublesome for the practicing physician, the diagnosis of the disease must 
be made from its course and symptoms. Important factors are the gradual onset, 
then the height and course of the fever, with no demonstrable localized disease, 
and the rose-spots. Less characteristic, but still of value, are the stools, the tym- 
panites, and the swelling of the spleen. ^Etiological factors, such as the occur- 
rence of undoubted cases of typhoid in the neighborhood, are of great diagnostic 
value in obscure cases. Sometimes the diagnosis can not be established till the 
appearance of certain symptoms, like intestinal haemorrhage, a characteristic 
mode of convalescence — viz., by lysis — or a relapse. It is an important rule not 
to make a diagnosis of typhoid after a single examination. It is generally neces- 



22 



ACUTE GENERAL INFECTIOUS DISEASES 



sary to observe the case accurately for several days before the diagnosis can be 
established. The differential diagnosis from other acute diseases, such as miliary 
tuberculosis, acute endocarditis, meningitis, etc., will be considered in discussing 
these diseases. 

The diagnosis is usually most difficult in the cases with an imperfect history 
which are first seen in a severe " typhoidal " state, with high fever, disturbances 
of consciousness, etc. These are the cases in which we must also consider, beside 
typhoid fever, miliary tuberculosis, acute septic or pysemic infection (including 
acute malignant endocarditis), meningitis, . severe "typhoid pneumonia," etc. 
The accurate differential diagnosis between typhoid and these conditions will be 
spoken of later. We may state here that in such cases a careful examination of 
the blood, especially the absence of leucocytosis in typhoid, may afford very valu- 
able diagnostic criteria. The ordinary diagnostic features. are also to be consid- 
ered, such as the way the disease began, so far as can be learned, the seti- 
ological conditions (i.e., the connection with other cases of typhoid), rose-spots, 
thin pea-colored stools, meteorism, intestinal haemorrhage, etc. 

Widal has lately reported a method for diagnosticating typhoid (Widal's 
serum reaction), which is very interesting theoretically, but which, of course, 
can be used only in cliniques and hospitals. It is based on previous researches 
by Gruber and others. If we mix ten or fifteen drops of a fresh culture of typhoid 
bacilli with a drop of blood-serum from a typhoid patient, the bacilli lose their 
mobility in a few minutes, or at most in a quarter to half an hour, and come 
together in little clumps ("agglutinating" action of the serum). If we add 
blood-serum from a typhoid patient to a uniformly cloudy mixture of typhoid 
bacilli in bouillon, the bacilli again clump together and sink to the bottom, while 
the fluid becomes perfectly clear. Since the blood-serum of healthy persons, or 
those not suffering from typhoid, does not give this reaction at all, or only in a 
slight degree, a very positive result from this test is quite a sure diagnostic sign. 
The reaction often occurs in typhoid even in the first weeks of the disease, but 
it may be delayed. It persists long after the disease has subsided. Widal's 
reaction can also be obtained with serum from a blister or from serous inflamma- 
tory exudation in a typhoid patient. In otherwise doubtful cases a positive 
result is of definite diagnostic significance. 

Prognosis. — A perfectly favorable prognosis should never be made. Cases 
which seem the mildest may become dangerous (from intestinal perforation, etc.). 
Yet, if there are good nursing and good treatment, typhoid fever is not a particu- 
larly dangerous disease, and we may hope for recovery even in very severe attacks. 
The danger lies, first, in the severity of the infection, as shown chiefly (though 
not wholly) by the height of the fever and the intensity of the general symptoms. 
A further danger is the appearance of the complications already enumerated and 
discussed. Thirdly, the constitution and condition of the individual are impor- 
tant. The circumstances coming under this head have likewise been repeatedly 
mentioned above. All these factors must be carefully estimated before we decide 
as to the danger in each case and make our prognosis. 

The mortality in typhoid varies greatly in the separate epidemics. The severe 
cases are undoubtedly more frequent at some times than at others. This renders 
it difficult to give statistics which are universally applicable. We may in general 
reckon on an average mortality of about ten per cent., and measure the severity 
of separate epidemics by this standard. Numerous observers agree that the treat- 
ment now in vogue has decidedly diminished the mortality. It was formerly not 
rare for it to reach twenty or twenty-five per cent. 

Treatment. — A specific cure for typhoid — i. e., some remedy to destroy the 
specific cause of the disease within the system, or to render it harmless — is as yet 
unknown. The different remedies recommended for this purpose (carbolic acid, 



TYPHOID FEVER 



iodine, thalline, ergotine, naphthaline, etc.) have none of them proved their value, 
and we can not advise further trial of them. The interesting experiments lately 
reported of injecting sterilized pure cultures of typhoid bacilli or the bacillus 
pyocyaneus into the patient (Rumpf and Frankel) has as yet led to no definite 
practical result. At present there is only one remedy, whose efficiency, of course, 
should in no way be overrated, which we would be unwilling wholly to give up in 
treating typhoid fever, and that is calomel. Wunderlich noticed that if a few 
rather large doses of calomel be given at the beginning of the disease, it will 
on the average run a lighter and more favorable course than otherwise would 
have been the case. Wunderlich believed that typhoid fever may sometimes be 
aborted by this method. Although we can hardly expect this, it is really an 
efficient means of procedure, which we have almost always employed, to give 
two or three powders of calomel, of five grains (0.30 gramme) each, as the first 
prescription, to patients who come under treatment in the first week or the be- 
ginning of the second. As there is generally constipation, the laxative effect is 
also beneficial. Moreover, it often lowers the temperature somewhat. A moder- 
ate diarrhoea is not a contra-indication, but, if the bowels be very loose, the calo- 
mel should be omitted. 

In other respects the treatment of typhoid must still be chiefly dietetic and 
symptomatic, and in one sense prophylactic. We must fight the symptoms al- 
ready present, and further seek, as far as possible, to defend the patient from 
the attack of certain dangerous secondary disorders. Starting out with this 
view, the proper treatment of typhoid fever is a task of the highest importance, 
and by no means a thankless one. 

We will begin by considering the general treatment. The sick-room must not 
be too warm, and must be frequently and thoroughly aired. The sick-bed must 
he well cared for. If effort be made to prevent bed-sores, we shall obviate one 
source of pain and danger (vide supra), and save ourselves and the nurse much 
trouble. Those who are very ill should therefore be laid on an air-cushion, or, 
if possible, a water-bed. The patient should be told not to lie always upon his 
hack, but to change now and then upon his side. The back, the region of the sa- 
crum, and the heels are to be often bathed with spirits of camphor or brandy. The 
minutest bed-sore is to be treated carefully. It should be cleansed twice a day 
(rinsed off with a weak solution of salicylic or carbolic acid), and dressed with an 
ointment containing Peruvian balsam, 1-30.* If the bed-sore be extensive, dust- 
ing with iodoform is very efficient treatment. We should be particularly careful 
uot to let the skin be undermined. If this has already occurred, we must be 
prompt in the use of the knife or drainage-tube. 

We can not recommend too strongly that the mouth should be kept clean. In 
a light case the patient can see to this himself, but otherwise the mouth and 
tongue must be frequently cleansed with a linen cloth wet in cold water or a solu- 
tion of borax (1 to 30). Perhaps we need hardly repeat the reason for this excess- 
ive cleanliness. It lies in the causative relation between stomatitis and inflam- 
mation of the parotid gland, and of the middle ear. If the tongue and lips be 
dry, they may be touched with glycerine. 

The diet must be at once liquid and nourishing. Milk is excellent, and it should 
always be ordered, but it can, unfortunately, be taken by very few patients continu- 
ously. It is often better borne if coffee or a little brandy be added to it. Cocoa 
made with milk may also be given for a change. In severe cases Nestle's food 
(Kindermehl) has been often employed by us with benefit. Broths and soups, thick- 
ened with sago or rice, are also good. They may be made more nourishing by 



* The unguentum balsami peruviani is made by mixing one part of balsam very thoroughly with 
thirty parts of the glycerite of starch (B. P.). It is not officinal in Germany —Trans. 



24 



ACUTE GENERAL INFECTIOUS DISEASES 



adding an egg to them. If the patient is very anxious to have more solid food, 
as often happens, we need not hesitate to give him a roll or rusk (Zwieback) 
that has been softened by soaking. If a patient becomes exceedingly enfeebled 
we should give him fine shavings of raw beef, regardless of the fever. A little 
dilute hydrochloric acid might be given with the meat. Beef -tea would be still 
better than the raw meat, and is to be strongly recommended. The various prep- 
arations of meat which are now made (meat- juice, meat-peptones, etc.) may be 
useful. When the fever takes a sluggish course, we must often begin to give 
stronger nourishment before the fever has ended. The best drink is cold water, 
which must be offered to the patient even when he does not ask for it. Lem- 
onade and similar preparations generally become distasteful in time. Drinks 
containing carbonic dioxide are to be avoided, because they increase the me- 
teorism. Cold tea with milk is good. In severer cases we should give some 
good strong wine, such as port, Malaga, or Hungarian wine, but it is not necessary 
to force the patient to take wine if he does not care for it. If the patient desires 
beer, we need not hesitate to give it in moderate amount. During convalescence 
we should be very careful about diet, since errors often have disagreeable conse- 
quences. We must wait till there has been no fever at all for seven to ten days 
before we allow a solid, animal diet, and return by degrees to common sorts of 
food. 

The general and dietetic treatment which we have thus far discussed is very 
important. Outside of this, it is our opinion that there is only one method of 
treatment to be chiefly considered — at least under the present limitations of our 
therapeutic ability. This method consists in the persistent use of cool baths, as 
first practiced by Brand in Stettin. We do not indeed believe that the indica- 
tions for this method of treatment are exactly what its original promoter held 
them to be, and we think some of the minutiae of the treatment should be changed. 
Yet there is at present no other single method of treating typhoid fever which has 
so numerous and evident advantages for the patient when properly and moder- 
ately used. To carry it out in private practice may often be more difficult than 
in a well-appointed hospital. However, even in private houses it will generally be 
possible to manage it, and we regard it as the duty of every physician who under- 
takes to treat a severe case of typhoid to try his best to have the baths employed. 

The great advantages of the treatment by baths are : 1. The baths diminish 
the fever, if their temperature be only sufficiently low, by direct absorption of 
heat. The baths thus obviate, as far as possible, all the bad effects which might 
result from a rise of temperature. 2. The direct influence of the baths upon the 
nervous system is still more important. The intellect becomes clearer, the apathy 
and dullness diminish. In fact, if baths be used, we do not see nearly so often as 
formerly the grave " typhoid condition." It is thus evident that bathing not only 
causes an improvement in the subjective sensations of the patient, but brings in 
its train many other beneficial effects. The patient takes his nourishment better, 
does not so often swallow the wrong way, coughs more effectively, is easier to 
move, and his body and his mouth can be better cleansed. 3. The influence of 
the baths upon the respiratory organs is of the greatest importance. We refer 
especially to the stimulation to deeper inspiration, and the promotion of expec- 
toration. The best proof of the benefit of this influence is the circumstance 
that if patients are subjected to baths from the start, it is comparatively a rare 
thing for severe bronchitis, atelectasis, and catarrhal pneumonia to develop. 4. 
The good care of the skin, which the bathing makes possible, is not to be despised. 
Since this treatment has been introduced, bed-sores are much rarer in typhoid 
than before. 5. Lastly, the baths are sometimes observed to have a diuretic 
effect. 

What has been said shows that the height of the fever is by no means the sole 



TYPHOID FEVER 



25 



indication for the employment of baths, at least in our opinion. The condition 
of the nervous system and of the respiratory organs is also to be considered. It i& 
true that numerous mild cases run a favorable course without a single bath; but 
we should always remember that this treatment is not only directed against the 
symptoms already existing, but has also a prophylactic importance, since it tends 
to prevent any severe cerebral or pulmonary manifestations. 

We will pass on to the special method of carrying out balneo-therapeutics in 
typhoid. Eull baths are generally employed, immersing the patient to his neck. 
The tub must stand, if possible, by the bedside. In hospitals, where there are beds 
on rollers, it is a better way to wheel the patients into the bathroom. All who 
are severely ill should be lifted into the bath and there held and supported, to 
avoid any bodily fatigue. During the bath the skin should be gently rubbed. 
This averts unpleasant sensations of chilliness. The temperature of the water- 
should not be set too low, especially for the first baths. We begin at 85° to 90° 
(24° to 26° R.), or, if the individual be elderly or sensitive and timid, at even 
warmer temperatures. When the patient has become accustomed to the tempera- 
ture of the water, we can cool off the bath still -further. Baths below 73° (18° to 
20° R.) have scarcely ever been used by us, and we believe that they are seldom 
needed. A very satisfactory average temperature is 80° to 85° (20° to 24° R.). 
A bath lasts on the average ten minutes. If the patient feels very cold or very 
uneasy in the bath, it must be cut short. After the bath the patient is at once 
lifted into bed, wrapped up in a sheet previously made ready, and wiped dry, with 
rather vigorous rubbing of the extremities and back. The moist sheet is then 
removed. The patient is covered up rather warmly, and is given some hot brotn 
or a sip of good strong wine. The effect of the bath upon the temperature is 
measured about half an hour later by the rectum. If the temperature be 2° to 3° 
(1° to 2° C.) lower than before, the result is deemed satisfactory. Often the dif- 
ference is greater, but in severe cases the fever may be so obstinate that the tem- 
perature remits only a small fraction of a degree. In such cases it is sometimes 
permissible to lower the temperature of the bath still more, or continue it a little 
longer. If cool baths are ill-borne, protracted baths of lukewarm water are some- 
times very efficient (Riess, and others) . 

In so far as the height of the fever furnishes an indication for baths, we may 
accept 103.6° (39.8° C.) in the rectum, as the temperature calling for a bath, 
but spontaneous variations of the temperature of the body are always to be re- 
garded. In cases which show a low morning temperature without special inter- 
ference, the height of the evening temperature is seldom an indication for a cold 
bath. We regard it as very important that the baths be not given too frequent- 
ly, since their advantages may thus be overbalanced by their incontestable evil 
consequences. At present we rarely prescribe more than two to four baths a day. 
At night we have given baths only very seldom, when forced to by extremely 
high temperatures or other bad symptoms. It must be a mistake to wake a pa- 
tient who is quietly sleeping, and put him into cold water, even if his tempera- 
ture is above 104° (40° C). On the other hand, even if the temperature be not 
excessive, or even if it be normal, there is, as we have said, no better remedy than 
the baths for severe pulmonary or cerebral symptoms. In such cases we often 
raise the temperature of the baths a little, and during them we have colder water 
poured upon the head and back. If we do this, the ears must be stopped with 
cotton-wool, lest the cold water find its way into them. 

Advantageous as the bath treatment of typhoid generally is, it must, how- 
ever, like every other therapeutic method, be used with wise moderation and with 
constant regard to individual conditions. If the patients are very weak, show a 
strong aversion to the baths, or feel dull and exhausted instead of refreshed after 
them, it is well to consider whether we really do good by continuing their employ- 



26 



ACUTE GENERAL INFECTIOUS DISEASES 



ment. In such cases we have of late years often advised cold wet packs of the 
whole body in bed, instead of the baths, and we consider such a use of cold 
as very advisable in these cases. The antithermic action of the pack is, of 
course, much less than that of the bath, but it can easily be aided by the exhibi- 
tion of antipyretics internally. The respiration and the nervous system, how- 
ever, are almost always most favorably affected. Most patients readily consent 
to the packs and lie quiet for an hour or two in the wet envelope. We would 
urgently recommend the more frequent use of packs, especially in private prac- 
tice, where the bath treatment often meets with greater difficulties than in 
hospitals. We should here always begin with higher temperatures, and only 
gradually go on to cold packs. There are a number of contra-indications to 
the use of baths which can not be disregarded. First, the occurrence of intes- 
tinal haemorrhage, however slight, and likewise the suspicion that peritonitis 
is developing, prohibit bathing. In these cases quiet is the very first re- 
quirement of the patient, and the baths must be at once discontinued. The 
onset of otitis, severe laryngeal affections, and acute nephritis are also complica- 
tions in which we should properly omit the baths entirely or employ them very 
cautiously, giving them warmer and less frequently. Sometimes rheumatic 
pains in the limbs or an attack of boils render the continued use of baths difficult. 
In short, we see that nothing could be more foolish than to try to establish a 
general rule for the bath treatment of typhoid. 

Passing to the consideration of the further symptomatic treatment of typhoid, 
the first important question is about giving drugs to reduce the fever. The one- 
sided point of view which considered that the chief task of the physician in the 
treatment of acute febrile disease was to lower the temperature has been grad- 
ually abandoned. In describing the bath treatment of typhoid we have em- 
phasized the fact that the action of the bath in reducing the temperature was 
only one factor, and perhaps neither the most efficient nor the most impor- 
tant factor, in the curative action aimed at. In giving antipyretics inter- 
nally their antifebrile action is of chief importance, but some of them also have 
a certain sedative action on the nervous system. The important influence of 
the bath on the respiration and skin they do not possess. If we had to decide 
whether to treat typhoid exclusively by baths or exclusively by antipyrine and 
similar drugs we should decidedly prefer the former. We would not wholly 
exclude the use of antipyretics internally in the treatment of typhoid, but we 
would limit their use more than is often the case. In our opinion they are indi- 
cated only when with existing high fever baths are for any reason impossible or 
contra-indicated (vide supra), or when, in spite of the baths, the fever remains 
constantly high. In such cases the baths can often be judiciously combined with 
the use of antipyretics internally if the patient bears the drug well and feels 
better subjectively after the reduction of temperature than before. We often 
treat typhoid patients by baths in the day, and, if the fever be high, by a dose of 
antipyrine (fifteen to thirty grains, grammes 1-2) at night. With severe head- 
ache, nervous restlessness, etc., this remedy is especially indicated; but we 
regard it as at least useless and often improper to give a patient with moderate 
fever large doses of an antipyretic without any sufficient reason, as unfortu- 
nately is often the case in practice; the only permanent result is to make the 
patient feel worse and upset his stomach. 

In regard to the different antipyretics so frequently brought forward and 
recommended of late, we are of the opinion that antipyrine is most to be rec- 
ommended. It was introduced by L. Knorr and first recommended by Filehne. 
In doses of fifteen to thirty grains (grammes 1-2), best given in wafers, 
it usually reduces the temperature considerably, although we may find that 
the height and the obstinacy of the fever are not identical terms. We do not 



TYPHOID FEVER 



27 



often see unpleasant effects from antipyrine (such as vomiting, profuse sweat- 
ing with defervescence, a chill when the temperature rises again, and some- 
times a measles-like eruption). The patient often feels better than before while 
under the influence of antipyrine, since the drug, as we have said, also acts favor- 
ably on the nervous symptoms (headache, restlessness). The dose of fifteen to 
thirty grains (grammes 1-2) can in severe cases be repeated several times a day, 
but, as a rule, we should not exceed eighty or ninety grains (grammes 5-6) in the 
twenty-four hours. One or two doses a day are usually all-sufficient. Lactophe- 
nine is also much recommended and even held as a specific in typhoid. In doses 
of seven to fifteen grains (gramme 0.5-1) it reduces the temperature considerably 
and usually causes a marked improvement in the general condition. A total of 
eighty or ninety grains (grammes 5-6) can be used in a day. Of the many other 
antipyretics which, of course, have often been tried in typhoid, we may first men- 
tion antifebrine (acetanilide), which in doses of four to seven grains (gramme 
0.25-0.5) has a similar action to antipyrine (Cahn and Hepp), and it should be 
used in practice among the poor because it is much cheaper. If we avoid too 
large doses we seldom see unpleasant results. .The appearance of a pale-cyanotic 
hue of the skin is the only disturbing feature; this, as in aniline poisoning, is 
probably due to a change in the coloring matter of the blood, and therefore warns 
us to be cautious. Other new antipyretics are phenacetine (fifteen grains, 
gramme 1, at a dose), salipyrine, etc., which have no special advantages. Qui- 
nine in doses of fifteen to thirty grains (grammes 1-2) and salicylate of soda in 
doses of seventy-five grains (grammes 5) are now little used as antipyretics, and 
properly, since their unpleasant action (vomiting, tinnitus, sweating, etc.) is 
much greater than that of the other drugs mentioned above. 

[Water or an acid drink should be given frequently by the nurse without wait- 
ing for the patient to ask for it, unless the mind is unusually clear. Phenacetine 
seems to have proved itself less depressing to the heart than its predecessors. The 
antipyretic dose usual in this country is five grains. A strong protest should be 
entered against the routine or frequent use of any of these internal antipyretics. 
If the temperature seems, in itself, to cause restlessness and discomfort, an occa- 
sional dose may be given. When used early in the course of the disease, anti- 
pyretics may seriously embarrass the diagnosis in doubtful cases. The method of 
Brand has been slowly working its way in America of late years, and perhaps 
would have spread more widely and rapidly were it not that we have long been in 
the habit of frequently sponging our typhoid patients with alcohol and water.] 

Another important symptom which needs special treatment is intestinal 
haemorrhage. It has been already mentioned that if this occurs, the baths should 
cease at once. Further than this, the chief remedies are ice and opium. Flat 
ice-bags are laid upon the abdomen. They should not be too heavy, and should, 
if possible, be suspended from a hoop. Internally, the patient is given every two 
hours fifteen or twenty drops of laudanum or a powder of one-half grain or one 
grain (gramme 0.03 to 0.05) of opium, either pure or combined with acetate of 
lead (opii, gr. ss., grm. 0.03; plumbi acetatis, gr. j, grm. 0.05; sacchari albi, gr. 
j, grm. 0.05). The object of the opium is to check peristalsis, and thus promote 
the formation of a clot in the bleeding vessel. In severe cases we may try injec- 
tions of ergotine or fluid extract of hydrastis, twenty drops three or four times. 
Liquor ferri chloridi (five to ten drops in water every hour) is often employed, 
hut is of extremely doubtful value. The baths can not be resumed till there has 
been no bleeding for at least three or four days — and then only cautiously. 

If peritonitis occurs, the treatment is much the same. Above all, opium must 
be used in still larger doses, but, unfortunately, as a rule, in vain. The surgical 
treatment of peritonitis has rather more of a future and more success, but experi- 
ence of this is still scanty. 



28 



ACUTE GENERAL INFECTIOUS DISEASES 



If there is considerable diarrhoea, we can give mistura gummosa [P. G., gum 
arabic and sugar, each 15 parts; water, 170 parts], or small doses of opium, the 
latter sometimes combined with tannin, tannigen, etc. In general it is certainly 
proper not to check the ordinary moderate diarrhoea of typhoid. Persistent con- 
stipation is always to be avoided. Constipation at the beginning of the disease 
is overcome by calomel (vide supra). In later stages we always try enemata first, 
to produce an operation. If this does not succeed, then we must employ rhubarb 
or castor-oil. Great tympanites may be diminished by laying cold wet cloths or 
ice-bags upon the belly. Considerable amounts of gas may often be removed by 
introducing a long rectal tube. As to puncturing the greatly inflated intestines, 
a method practiced by some physicians, we have no personal experience. 

If there are severe pulmonary symptoms, baths or wet packs are, as we have 
said, the best remedies. Internally we may try liquor ammonii anisatus [P. G., 
olei anisi, 1 part ; aquae destillatae, 24 parts ; aquae ammoniae, 5 parts] and benzoic 
acid (grains ij to iij, gramme 0.1 to 0.2, in powder). If the pulse be very rapid, 
we may put an ice-bag over the heart. If at the same time the pulse is small 
and weak, we give stimulants. Of late we have most frequently given tincture of 
strophanthus (ten to fifteen drops several times) with the best results. We only 
rarely use digitalis in typhoid. If symptoms of severe cardiac weakness — so-called 
collapse — suddenly occur a rapid and energetic interference is urgently demanded, 
Subcutaneous stimulation, injections of ether or camphorated oil,* should be 
given, with wine, stropanthus, etc., internally. If the respiration stops it can 
sometimes be started up again by douches of cold water on the back of the neck, 
or we may often restore it by artificial respiration. Digitalis (one-half grain of 
the leaves, gramme 0.03, two or three times daily) may also be employed if the 
pulse be rapid; but it should be used with great caution. 

For nervous symptoms the baths and douching are the most effective reme- 
dies. The head is meanwhile covered by an ice-bag. Antipyrine sometimes acts 
favorably on the nervous symptoms. If there be great excitement, as shown by 
excessive restlessness or delirium, small doses of morphine internally, or, better, 
subcutaneously, are often very useful. 

The numerous other complications and sequelae which may occur, but which 
can not all be mentioned here, should be treated on general principles. 

The prophylactic measures to avoid the spreading of the disease can be only 
briefly referred to. Of chief importance is careful disinfection of the excreta. 
The best means for this purpose is a two-per-cent. solution of corrosive sublimate 
or a five-per-cent. solution of carbolic acid. We may also pour on milk of lime- 
until the reaction becomes alkaline, or use concentrated mineral acids. We 
should take care that bed-pans, bed-clothes, linen, the rectal thermometer, etc., 
should be handled by other persons as little as possible, and should be care- 
fully disinfected. If there seems reason to suspect that the disease was due to 
bad water, of course the source of such suspected water must be cut off. 

[Recent experiments tend to show that the above solution of carbolic acid does 
not kill spores except after prolonged contact. 

The following are the measures of disinfection recommended by the American 
Public Health Association. It will be observed that they apply to all infectious 
diseases, and it seems well to give them here nearly in extenso, as the directions 
for disinfection in most text -books are far too vague. 

Disinfection of Excreta, etc. — The infectious character of the dejections of 
patients suffering from cholera and from typhoid fever is well established; and 
this is true of mild cases and of the earlier stages of these diseases as well as of 



* One part of camphor to four of olive-oil in doses of seven to fifteen minims (gramme 0.5 to 1> 
every hour or two. 



TYPHOID FEVER 



29 



severe and fatal cases. It is probable that epidemic dysentery, tuberculosis, and 
perhaps diphtheria, yellow fever, scarlet fever, and typhus fever, may be trans- 
mitted by means of the alvine discharges of the sick. In cholera, diphtheria, 
yellow fever, and scarlet fever, all vomited material should be looked upon as 
infectious; and in tuberculosis, diphtheria, scarlet fever, and infectious pneu- 
monia, the sputa of the sick should be disinfected or destroyed by fire. It seems 
advisable also to treat the urine of patients sick with an infectious disease with 
one of the disinfecting solutions below recommended. 

Chloride of lime, or bleaching powder, is, perhaps, entitled to the first place 
for disinfecting excreta, on account of the rapidity of its action. The following 
standard solution is recommended : 

Standard Solution No. 1 

Dissolve chloride of lime, of the best quality,* in pure water, in the proportion 
of four ounces to the gallon. Use one quart of this solution for the disinfection 
of each discharge in cholera, typhoid fever, etc. Mix well and leave in vessel for 
at least one hour before throwing into privy-vault or water-closet. The same 
directions apply for the disinfection of vomited matters. 

Standard Solution No. 2 

Dissolve corrosive sublimate and permanganate of potash in pure water, in the 
proportion of two drachms of each salt to the gallon. This is to be used for the 
same purposes and in the same manner as Standard Solution No. 1. It is equally 
effective, but it must be left a longer time in contact with the material to be dis- 
infected — at least four hours. The only advantage this solution has over No. 1 
consists in the fact that it is odorless. It costs about two cents a gallon. It is 
very poisonous, and will injure lead pipes if passed through them in considerable 
quantities. Solutions of corrosive sublimate should not be placed in metal re- 
ceptacles. 

Disinfection of the Person. — The surface of the body of a sick person, or of 
his attendants, when soiled with infectious discharges, should be at once cleansed 
with a suitable disinfecting agent. For this purpose solution of chlorinated soda, 
diluted with three parts of water, or Standard Solution No. 1, diluted with three 
parts of water, may be used. A two-per-cent. solution of carbolic acid is also 
suitable for this purpose, and, under proper supervision, the use of a solution of 
•corrosive sublimate (1-1,000) is to be recommended. 

In diseases like small-pox and scarlet fever, in which the infectious agent is 
given off from the entire surface of the body, occasional ablutions with solution 
of chlorinated soda, diluted with twenty parts of water, will be more suitable than 
the stronger solution above recommended. 

In all infectious diseases the body of the dead should be enveloped in a sheet 
saturated with Standard Solution No. 1, or with a five-per-cent. solution of car- 
bolic acid, or a 1-500 solution of corrosive sublimate. 

Disinfection of Clothing. — Boiling for half an hour will destroy the vitality 
of all known disease-germs, and there is no better way of disinfecting clothing or 
hedding which can be washed than to put it through the ordinary operations of 
the laundry. No delay should occur, however, between the time of removing 
soiled clothing from the person or bed of the sick and its immersion in boiling 
water, or in one of the following solutions; and no article should be permitted 
to leave the infected room until so treated. 



* Good chloride of lime should contain at least twenty-five per cent, of available chlorine. The cost 
of the solution is less than ©ne cent a gallon. The sediment does no harm. 



30 



ACUTE GENERAL INFECTIOUS DISEASES 



Standard Solution No. 3 

Dissolve four ounces of corrosive sublimate and one pound of sulphate of 
copper in a gallon of water. Two fluid ounces of this standard solution to the 
gallon of water will make a suitable solution for the disinfection of clothing. 
The articles to be disinfected must be thoroughly soaked with the disinfecting 
solution, and left in it for at least two hours, after which they may be wrung out 
and sent to the wash. 

Clothing may also be disinfected by immersing it for four hours in a two-per- 
cent, solution of carbolic acid. Soiled mattresses, pillows, feather beds, and 
articles of this nature can not be effectually disinfected by sulphur fumigation, 
owing to the fact that the gas does not penetrate to their interior in sufficient 
amount. For articles of this kind, and in general for articles of little value, 
which have been soiled by the discharges of the sick, destruction by fire will be 
advisable. 

Disinfection of the Sick-Room. — No disinfectant can take the place of free 
ventilation and cleanliness, and it is impracticable to disinfect an occupied apart- 
ment. Neutralizing bad odors is not disinfection. 

All surfaces should be thoroughly washed with Standard Solution No. 1, diluted 
with three parts of water, or with a 1-1,000 solution of corrosive sublimate. 
Standard Solution No. 3, diluted in the proportion of four ounces to the gallon of 
water, may be used. 

The walls and ceiling, if plastered, should be brushed over with one of these 
solutions, and subsequently washed over with a lime-wash. 

Especial care must be taken to wash away all dust from window ledges and 
other places where it may have settled, and thoroughly to cleanse crevices and 
out-of-the-way places. After this application of the disinfecting solution, and an 
interval of twenty-four hours or longer for free ventilation, the floors and wood- 
work should be well scrubbed with soap and hot water, and this should be followed 
by a second more prolonged exposure to fresh air, admitted through open doors 
and windows. 

As an additional precaution, fumigation with sulphur-dioxide gas is to be 
recommended, especially for rooms which have been occupied by patients with 
small-pox, scarlet fever, diphtheria, typhus fever, and yellow fever. All apertures 
into the room should be carefully closed, and not less than three pounds of sul- 
phur for each thousand feet of air-space should be burned. To secure complete 
combustion, the sulphur, in powder or small fragments, and moistened with 
alcohol, should be placed in a shallow iron pan, and this should be placed on 
bricks in a tub partly filled with water to guard against fire. — Editor.] 

[Formaldehyde gas is superior to sulphur dioxide, because of its greater 
efficiency and rapidity of action, and because it does less harm to household goods. 
Both gases have merely a superficial action. — V.] 



CHAPTER II 

TYPHUS FEVER 

(Spotted Fever. Ship Fever) 

Typhus fever is an acute infectious disease, perfectly distinct from typhoid 
fever, but formerly often confounded with it. The similarity of the two diseases, 
which led to their similar names, consists only in the grave general condition with 



TYPHUS FEVEE 



31 



fever, and in a number of complications which may appear in both. There is, 
however, an essential difference in the whole course of the two diseases, and espe- 
cially in the circumstance that the intestinal lesion which is characteristic of 
typhoid is never seen in typhus. The chief distinction between the two affections, 
which must undoubtedly lie in the difference in their causes, can not yet be dem- 
onstrated. We do not yet know the organized pathogenic agents of typhus fever, 
although it must be presupposed that they exist. 

etiology. — As to the way in which infection occurs, we have much less infor- 
mation even than in relation to typhoid. We know nothing as yet as to the 
supposed specific agents which produce typhus, although micro-organisms have 
been repeatedly found in the blood. It is an incontestable fact that the appear- 
ance of typhus in a place previously free from the disease is always to be referred 
to an importation of the pathogenic poison from without. It is likewise deter- 
mined, through numerous observations, that typhus is one of the contagious dis- 
eases — that is, that the specific poison can be directly transferred from the patient 
to others around him. How it is transferred we have no certain knowledge. Per- 
haps the poison is contained in the expired air ; - or, as is still more probable, in 
the scales of epidermis; or, perhaps, in the other excretions and secretions of the 
patient. We are equally ignorant through what channel the infectious agent 
enters the system — whether it is inspired or swallowed. It is certain that the 
poison may be transferred in the clothes, etc., of the patient (fomites). 

Favorable hygienic surroundings decidedly diminish the contagiousness of 
typhus fever. For example, in the well-ventilated pavilions of the Leipsic hos- 
pital there have rarely been cases of transfer of the disease to physicians, nurses, 
or other patients. On the other hand, if the hygienic influences be unfavorable, 
typhus fever may appear in very widespread epidemics. Those terrible epidemics 
which have been described under the names of " famine fever," " camp fever " 
(Hungertyphus, Kriegstyphus), etc., were for the most part typhus fever. In the 
smaller epidemics it is often possible to trace the disease to some wretched, over- 
filled tenement-house. 

At present typhus fever appears constantly in Great Britain. Ireland has been 
notorious for many years as a breeding-place of the disease. It is also frequent in 
the eastern part of Germany (Posen, East Prussia and West Prussia, Silesia), in 
Poland, Galicia, Russia, and in parts of southern Europe. The isolated cases 
which occur every year here and there in central Germany, though more or less 
numerous, are, almost without exception, to be referred to an importation of the 
disease. 

Typhus fever attacks by preference young adults of twenty to forty years ; but 
it occurs in children, and is comparatively frequent in elderly persons. There is 
no marked dependence of the epidemics upon any particular season of the year. 
As in the case of typhoid fever, a person who has once had the disease seems to 
enjoy immunity from any fresh attack. 

[The practical acquaintance of American physicians with typhus fever is, for- 
tunately, limited. Many of the outbreaks which have occurred were traceable to 
immigrants, especially from Ireland. 

During our civil war the disease broke out neither among the armies in the 
field nor among the prisoners of war. A number of cases were reported at the 
time, but great doubt has since been thrown upon the correctness of the diagnosis.] 

Course and Symptoms of the Disease.— If we try to sketch the characteristic 
behavior of typhus fever, especially as contrasted with typhoid, we may say that 
the disease begins much more abruptly and rapidly, and that the fever quickly 
becomes very high and the general disturbance very severe, but the illness lasts 
a shorter time, seldom more than two weeks, and generally passes by crisis into 
recovery. 



ACUTE GENERAL INFECTIOUS DISEASES 



The length of incubation seems to vary. Murchison thinks it is usually 
more than nine days. Sometimes, though not invariably, slight prodromata 
precede by some days the actual outbreak of the disease. These are languor, 
anorexia, headache, and pain in the limbs. Then the regular illness begins, as a 
rule, rather suddenly, and often with a pronounced rigor. With this the tem- 
perature rises quickly, and may on the very first evening reach 104° or 105° 
(40°— ±0.5° G.)« Vomiting is not rare, and may be repeated. A grave general 
condition, with fever, is developed in a few days. The patient feels exhausted. 
There is often violent pain in the loins and extremities. Nervous symptoms 
soon appear: persistent and intense headache, vertigo, spots before the eyes, 
ringing in the ears, and in many cases quickly increasing stupor and delirium. 
In severe cases the fever often reaches 106 c (41° C). and may be even higher, and 
it is almost constant, with but slight morning remissions. The skin is hot and 
dry. the tongue dry and thickly coated, the respiration moderate, the pulse very 
rapid. We very frequently find in the chest the signs of an extensive bronchitis. 
Nasal catarrh and conjunctivitis also occur. Serious intestinal symptoms are 
generally absent, although there may be slight tympanites or diarrhoea. The 
spleen is almost always greatly enlarged. Only in a few epidemics is the splenic 
tumor said to have been wanting (?). The urine is concentrated and scanty, and 
sometimes has a trace of albumen. 

On the third to the seventh day of the disease the characteristic eruption ap- 
pears. To this the disease owes its name of " spotted fever." The eruption con- 
sists of rose-spots, generally very numerous and widespread, upon the trunk and 
extremities, often also on the face. Sometimes the spots are larger, and may then 
bear great resemblance to a fresh eruption of measles. The skin between the sep- 
arate rose-spots is not infrequently diffusely reddened. After two or three days 
the roseola? become hemorrhagic, and change into lighter or darker petechia?. 
It is commonly only in the lighter cases that the rose-spots fade away without 
nrsfbecoming petechial. In rare though well-substantiated cases the eruption has 
been scanty, or even wholly wanting. Herpes does occur, but only seldom. 

The fever begins to abate in light cases as early as the second week, coin- 
eidently with an improvement in the general symptoms. Often this change is 
indicated about the seventh day by a considerable remission in the temperature. 
On the other hand, in severe cases, all the symptoms grow worse. The weakness 
increases. The nervous derangement reaches the extreme of a severe " typhoidal 
state." expressed either by marked stupor, which sometimes passes into complete 
coma, or by violent delirium. Lobular pneumonia attacks the lunges, and the 
fever continues with unabated violence. These symptoms may end with death, 
hut in favorable cases they decline rapidly. Sometimes this decline is preceded 
by a great rise in temperature (perturbatio critical, especially about the seven- 
teenth day. rarely a few days earlier or later. In such cases the temperature is 
apt to fall by crisis, sinking in a day or two. with but slight interruption, down to 
the normal level. Even in those cases in which the descent is by gradations it is 
always decidedly more abrupt than in typhoid. The eruption quickly fades, the 
patients gradually improve, and. as a rule, become completely and permanently 
convalescent. It is true that some observers have seen relapses, but they are. at 
least in our present epidemics, extremely rare. 

Complications and Varieties in the Course of the Disease. — From what we 
have said of its course, it is evident that the symptoms are essentially those of an 
intense general infection of the system. The sole demonstrable local lesion which 
is almost invariably present is the characteristic eruption, and this has evidently 
no causal relation to the severe symptoms of the disease. It is likewise extremely 
probable that most of the complications, which not infrequently arise in severe 
cases, are secondary, and occur in the way already described with considerable 



EELAPSING FEVER 



detail in the preceding chapter. They are just such complications as are possible 
in every severe general disease, and embrace otitis, parotitis, extensive lobular 
pneumonia, more rarely gangrene of the lungs, and pleurisy; also furunculosis, 
purulent cellulitis, bed-sores, dysentery, icterus, etc. Whether some of the local 
lesions which are observed may not be direct results of the pathogenic poison, 
we can not at present decide. Among these would come, first of all, the rare 
cases of lobar pneumonia and nephritis. Sequelae are, on the whole, rare, though 
sometimes there is a tedious anaemic condition, or neuralgia, paralysis, etc. 

The separate epidemics of typhus present considerable variety, not only as 
regards the occurrence of individual complications, but more especially in the 
general course and character of the cases. For instance, some epidemics are dis- 
tinguished by the greater frequency of light attacks (typhus exanthematicus 
levissimus, unsuitably termed by some " febricula ")• Here the entire attack runs 
its course in five to eight days. The fever is generally comparatively moderate; 
there are no severe general symptoms, and complications are exceptional. 

Diagnosis. — It may be very difficult for a time to distinguish typhus from 
typhoid. The following factors are of chief importance: 1. The onset is much 
more abrupt in typhus than in typhoid, and is often accompanied by a pronounced 
rigor. 2. In typhus, the nervous disturbances usually appear earlier and are more 
severe than in typhoid. 3. The rash is seldom so extensive in typhoid as in ty- 
phus, and in typhoid it hardly ever becomes petechial. 4. In typhus the pains in 
the loins and limbs are generally much more pronounced. 5. If we still find it 
hard to decide, the manner of recovery will almost always settle the question. 
Recovery in severe cases of typhoid is, on the average, much more tardy and 
gradual, by lysis. In typhus it occurs generally by the seventeenth day, and by 
crisis. 

The prognosis is chiefly determined by the severity of the fever and of the 
nervous symptoms. Extensive lobular pneumonia is the most frequent dangerous 
complication. The mortality varies greatly in the separate epidemics. It is some- 
times only six or seven per cent., but may rise to twenty per cent. 

Treatment is based on the same principles as in typhoid fever. There is no 
specific remedy. Besides good nursing, a judicious employment of baths is cer- 
tainly our chief reliance for lessening the severity of many of the symptoms, such 
as febrile, nervous, and pulmonary disturbances, as well as for averting many 
dangerous complications. For all details of treatment we may refer to the pre- 
ceding chapter. 



CHAPTER III 

RELAPSING FEVER 

{Relapsing Typhus — Febris recurrens) 

-ZEtiology. — This disease was first named by English pathologists relapsing 
fever, and by Griesinger febris recurrens. It has a peculiar course, made up of 
separate attacks, and is further of great interest because it is one of the first infec- 
tious diseases in which the specific pathogenic organisms became known, and, 
being easily demonstrable in each separate case, were utilized for the speedy 
and certain diagnosis of the disease. Obermeier discovered in Berlin, in the year 
1873, that in relapsing fever the blood, at certain times, invariably contains 
peculiar thread-like micro-organisms. This discovery has since been universally 
confirmed; and it may be maintained that if once the presence of these " spirilli " 



34 



ACUTE GENEEAL INFECTIOUS DISEASES 



be demonstrated in the blood, we are justified in making an absolute diagnosis of 
relapsing fever. 

In Germany the disease did not become epidemic till the year 1868. In 1S72 
and 1873 there were considerable epidemics in Breslau and Berlin. Its last exten- 
sive appearance was in 1879 and 1880, when it spread over most of northern and 
central Germany, and was accurately studied by numerous observers. People of 
the poorer classes were almost exclusively attacked, and especially the " tramps." 
The uncleanly dens where these people lodge were found everywhere to be the 
chief centers of infection. 

The precise manner of infection is as yet almost wholly unknown. All ob- 
servers agree that the disease is directly contagious ; but it can not be very con- 
tagious if the hygienic influences be good. At least the results of our late epi- 
demics would imply this. In the Leipsic hospital, where at that time over two 
hundred and fifty cases were treated, and isolation could not be at all perfectly 
carried out, not one case of infection occurred. It is certain that the disease can 
be transmitted by direct inoculation with the blood of patients. This has been 
established by a Russian physician, by the experimental inoculation of healthy 
persons. Doctors have been repeatedly inoculated at the autopsy of those who 
have died of relapsing fever. The disease may likewise be transferred by inocula- 
tion to monkeys, while other mammals seem to enjoy an immunity from it. 

[The first cases of relapsing fever observed in this country were in Irish immi- 
grants coming over in the same vessel in the year 1844. At several periods since 
then more or less limited outbreaks traceable to immigration have occurred, but 
the disease has never acquired any foothold with us, and comparatively few physi- 
cians have ever seen it. So far as I can learn, only one case has ever been seen in 
Boston, and that was in the person of a physician from another city, who brought 
the disease with him and passed through it in the Massachusetts General Hos- 
pital.] 

Clinical History. — The stage of incubation lasts about five to eight days. It is 
only exceptionally that some slight prodromal symptoms present themselves just 
before the outbreak of the disease proper. As a rule, it begins suddenly, with a 
more or less pronounced chill and intense constitutional symptoms. There are 
violent headache, great languor, anorexia, and especially marked pains in the 
loins and extremities. The temperature rises rapidly, reaching generally 106° 
(41° C.) or higher as early as the first or second day. The skin is hot and dry, 
and usually quickly assumes a very characteristic dirty-yellowish color. In Leip- 
sic, we often saw herpes labialis, which seems, however, to have been rarer in 
epidemics elsewhere. The tongue becomes dry and thickly coated. Sometimes there 
is vomiting. The bowels are constipated, or there is a slight diarrhoea. The 
spleen becomes rapidly enlarged, being, as a rule, even larger than in typhoid or 
typhus. The liver is slightly enlarged. The chest presents the signs of a bron- 
chitis, generally moderate, but in exceptional instances severe. The pulse is 
much quickened. It is seldom that there are severe cerebral symptoms beyond a 
certain apathy and stupor. We have seen delirium tremens sometimes, in drunk- 
ards. A very characteristic symptom, already mentioned, is the marked hyperaBS- 
thesia of the muscles, especially in the calves. 

After these symptoms, accompanied by persistent and generally very high 
fever, have lasted five days to a week, there is a critical decline of temperature, 
with profuse sweating. The patient now improves so rapidly and decidedly that 
he thinks himself completely cured, and generally gives little credence to the 
physician's prophecy of a relapse. In rare but well-attested cases there has been 
really but one attack. The rule is that, after about a week, a second attack occurs, 
often a third after that, and, infrequently, even a fourth and fifth. In each of 
these, the above-mentioned symptoms are repeated more or less completely and vio- 



RELAPSING FEVER 



o5 



lently. As the only certain and constant sign of the recurring attacks (the 
so-called relapses) is a fresh rise of temperature, it will be well to consider their 
peculiarities at the same time that we describe the course of the fever. During 
the intervals of normal temperature the other objective symptoms of disease are 
usually absent, except an- evident splenic tumor, and, not infrequently, the peculiar 
pale-yellow hue. 

Course of the Fever (see Fig. 3). — The beginning of the fever in the first 
attack is, as we have said, almost always sudden, so that it may even in a few 
hours reach a considerable height. The fever lasts, as a rule, five to seven days, 
but not infrequently as short a time as three or four days, or as long as ten or 



1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 




Fig. 3.— Example of the temperature curve in relapsing fever. 



twelve days. During this time it may keep a tolerably uniform height, but 
oftener there are considerable remissions, which may even come to deserve the 
name of pseudo-crises. In such cases the temperature sinks in the morning to 
normal or even lower, so that we might believe the fever ended ; but in the even- 
ing the temperature rises again to its former level. These pseudo-crises are most 
frequent toward the end of the attack, but do occur sometimes in the very first 
days. The absolute height of the fever is, as a rule, very considerable. Tempera- 
tures between 105.5° and 106.5° (41° and 41.5° C.) are very often observed, and 
in themselves are not especially ominous in relapsing fever. The highest tempera- 
ture we have observed was 107.9° (42.2° C). Sometimes the temperature is more 
moderate (between 102° and 104°, 39° and 40° C). The fever almost always 
ends at the close of the attack by crisis, only rarely by a rapid, gradual decline. 
The crisis is often preceded by an especially great rise the evening before (per- 
tuvbatio critica) ; so that the subsequent fall of temperature is very considerable. 
It generally occurs at night, and is accompanied by profuse perspiration. The 
fall may amount to 9° or 10° (5° to 6° C). The temperature sinks almost 
always below normal, often as low as 95° (35° C.) or thereabouts. Once we saw 
it fall to 92.1° (33.4° C). 

To the first attack succeeds an interval during which there is no fever (apy- 
rexia), which lasts on the average about a week, sometimes a less time, and often 
a greater. The longest interval we have ever observed lasted seventeen days. 
During this interval the temperature, which, as a rule, is at first subnormal, rises 
to normal, and then generally remains there. Exceptionally there are slight 
evening exacerbations to above 100.5° (38° C). These may have no demon- 
strable cause, or may result from some complication, such as otitis, or a furun- 
cle. Then comes another change, and generally a sudden one, ushered in with a 



36 ACUTE GEXERAL IXEECTIOUS DISEASES 

chill, and a new rise of temperature, the beginning of the second attack or first 
relapse. During this attack the fever has the same general peculiarities as in the 
first attack. Generally the first relapse is briefer by a day or two than the first 
attack; but the reverse is sometimes true. We will add that we have observed 
not infrequently a rather high evening temperature (101.5°, 38.5° C.) for one 
or two days before the second attack began, as also before the third. 

Relapsing fever seems in many epidemics to have been made up of two attacks, 
so that not more than one tenth of the cases had a third attack. On the other 
hand, the majority of the cases in the last epidemic had two relapses. In these 
cases the rule was for the interval between the second and third attacks to be 
one or two days longer than the first apyrexia ; but earlier epidemics seem to 
have had the second apyrexia, if there was one at all, briefer than the first. The 
third attack is set down in all reported cases as decidedly shorter than either of its 
predecessors. It lasts generally two or three days. Exceptionally we have seen 
it persist for four or even six days. 

A fourth and even a fifth attack may occur, but only exceptionally. If they 
do happen, they are usually imperfectly developed, and often are limited to a 

fever of one day's duration. The more ac- 
curately and persistently we take the tem- 
perature during convalescence, the oftener 
do we find slight rises of temperature oc- 
curring at intervals late in the history of 
the case. These are probably to be inter- 
preted as final, rudimentary attacks. 

The Spirilli. — The number of cases of 
relapsing fever in which no spirilli can 
be demonstrated in the blood, if the exami- 
nation be accurate, has become so small 
that it can be disregarded, when we com- 
pare it with the much greater number of 
cases where such demonstration is made 
with ease and certainty. The best way is 
to get a drop of blood by pricking the 
skin, and examine it as it is, without mix- 
ing anything with it. Staining (with the 
basic aniline colors) is easy but unneces- 
sary. With any good dry lens of 400 to 500 diameters the spirilli are seen with 
perfect distinctness. It requires a little practice to make them out ; but this is 
easily obtained. Often the attention is first caught by little jogglings and mo- 
tions of the red blood-corpuscles, and then we see the delicate, narrow threads. 
Their length equals about three to six times the diameter of the red globules (Eig. 
4). They exhibit an active and almost continuous motion, like snakes. Often 
the whole thread bends upon itself, and then stretches out again. They are 
partly separate and partly tied up in knots composed of four to twenty individ- 
uals. The whole number visible in one field varies greatly in individual cases, 
and has no direct relation to the severity of the case. Often it requires long 
searching to find a few, while in other cases there may be twenty or more in the 
field at once. A very interesting fact is that their appearance in the blood de- 
pends upon the attacks of fever. On the first day of the attack we rarely find 
spirilli, and then only one or two. Epon succeeding days their number increases. 
Shortly before the end of the attack — that is, before the crisis — they generally 
disappear entirely ; but even after the crisis they have been found, exceptionally 
and in very small numbers. They have very often been found by the author as 
well as other observers during the pseudo-crisis described above, so that, after the 




Fig. 4.— Spirilli of relapsing fever in the blood. 



RE LAPS IX G FEVER 



87 



temperature has become normal, the presence of spirilli makes it very probable 
that another rise of temperature is impending. The spirilli have thus far 
been found in the blood only, in the catamenia, in bloody urine, or in blood 
coughed up from the lungs, and never in the organs or secretions (urine, milk, 
sweat, contents of herpetic vesicles). There can hardly be any doubt that the 
spirilli which appear in the separate attacks are to be regarded as separate gener- 
ations. As to their manner and place of development we have as yet no knowl- 
edge. In the final, rudimentary attacks, we find few if any. If the patient dies 
during an attack, they are to be found in the blood after death. Artificial 
cultivations have not been very successful; nor have pure cultures of them, 
to our knowledge, ever succeeded. Albrecht states that they will subsequent- 
ly develop in blood taken from a patient during the interval when he has no 
fever. 

The blood is otherwise modified during relapsing fever. We very often find a 
slight increase in the white corpuscles. There is often a noticeable abundance of 
very small bodies, so-called granular elements (Kornchenbildungen). The signifi- 
cance of these (the remains of white corpuscles?) is still doubtful. There are, 
finally, peculiar cells, rather large, with fat-granules. They were demonstrated 
by Ponfick in the venous blood, and are said to come from the spleen. We also 
find fatty-degenerated endothelium in the blood. 

Complications are on the whole rare, and mostly secondary. Important 
among these are troublesome ophthalmic disturbances, especially iritis and irido- 
choroiditis. Sometimes parotitis, laryngitis, or pneumonia occur. Epistaxis is 
a not infrequent complication. It is usually profuse and persistent, and it may 
even be dangerous. Sometimes there has been rather severe dysenteric trouble. 
In one case which ended fatally we observed a very peculiar intestinal lesion, 
consisting of hemorrhagic-necrotic foci in the colon and lower ileum. In severe 
cases acute hemorrhagic nephritis occurs with comparative frequency. At the 
autopsy an important and characteristic phenomenon is the wedge-shaped white 
spots which occur in the spleen, like infarctions. They have a clinical interest, 
as they may become the starting-point of pyemic conditions or of peritonitis. 
Splenic abscesses have been observed in a few cases. 

Variations in the course of the disease occur in this, as in all other acute 
infectious diseases. Eirst there are mild, abortive cases, in which the attacks 
are few and brief. Then cases have been described resembling intermittent fever. 
Of chief importance is that severe variety of relapsing fever first observed in 
Egypt by Griesinger, and described as " bilious typhoid." There is no longer any 
doubt about the proper classification of this disease, for spirilli have been proved 
to appear in it. and it has even been shown that its inoculation upon another 
person ( !) produces an ordinary case of relapsing fever. Bilious typhoid fever oc- 
casions successive attacks, like those of relapsing fever. The type is much more 
severe. As a rule, there appear marked icterus, grave nervous symptoms, haemor- 
rhages into the skin and mucous membranes; and the termination is frequently 
fatal. The autopsy shows a greatly enlarged spleen, often containing infarctions 
and abscesses, and in some cases hepatic abscesses, septic nephritis, and similar 
lesions. 

The prognosis of ordinary relapsing fever is on the whole very favorable. In 
the last epidemics the usual mortality was only two to four per cent. The fatal 
cases could some of them be laid to wretched nursing-. In the remaining portion 
death resulted from complications, such as pneumonia and nephritis. 

The treatment must as yet be purely symptomatic. Antipyretic treatment is 
generally needless, since the fever is relatively brief and often quite intermittent. 
Moreover, most patients can not well endure cold baths, because the muscles are 
so painful. As a rule, good nursing and proper food amply suffice. If the mus- 



38 



ACUTE GENERAL INFECTIOUS DISEASES 



cular pains are very violent, we may order chloroform liniment as an embroca- 
tion. Complications are to be treated on general principles. 

We are not acquainted with any remedy that can influence the disease itself 
or avert the relapses. Large doses of quinine, salicylic acid, etc., have been fre- 
quently employed for this purpose, but never with success. Lately there has 
been ascribed to calomel a favorable influence upon the general course of the dis- 
ease, and its use is said to diminish the number of attacks. We must await fur- 
ther evidence in support of this statement. 



CHAPTER IV 

SCARLET FEVER 

(Scarlatina) 

We now begin the consideration of those acute infectious diseases which are 
usually embraced under the name of the " acute exanthemata." In this group 
are reckoned, besides scarlet fever, measles, rotheln, small-pox, and varicella. The 
point which these diseases have in common is that in all of them is developed a 
characteristic eruption, of slight clinical significance in itself, in most cases, 
but of thoroughly characteristic appearance in each disease, and hence of essen- 
tial importance in diagnosis. A number of the acute exanthemata have this 
further point of mutual resemblance that they appear chiefly in children. These 
diseases are scarlet fever, measles, rotheln, and varicella. 

Etiology. — Infection with the specific scarlatinal poison occurs almost always 
by contagion, which takes place very readily. A single approach to a patient ill 
with scarlet fever may suffice to communicate the disease. There is no doubt that 
the disease may be transferred by objects which the patient has touched, such as 
linen, clothing, furniture, or toys. Persons who have been with the sick may be 
the means of transmitting the disease, although themselves unaffected. In Eng- 
land it has been thought that the contagium may be carried by milk. 

Numerous observations show that the scarlatinal poison is with great difficulty 
destroyed, and that it may keep its contagious powers for months ("tenacity"). 
We can thus see how difficult, how impossible, it may be in an individual case to 
point out the source of contagion. Scarlet-fever patients can communicate the 
disease certainly as late as the end of the desquamative period, or perhaps some- 
what longer. 

Details as to the manner of contagion, or as to the specific poison itself, are as 
yet unknown. All statements made in regard to finding alleged specific micro- 
organisms of scarlet fever are extremely doubtful. The exciting agent of scarlet 
fever must, however, be contained in the blood and in the contents of the miliary 
vesicles of scarlet-fever patients, for the disease has repeatedly been artificially 
produced in healthy persons by inoculation with these fluids. 

Predisposition to scarlet fever is far less universal than is predisposition to 
measles or small-pox. In families with several children often only one or two fall 
sick, while the rest escape, although equally exposed. As age increases, liability 
to the disease greatly diminishes, although there are cases of scarlet fever among 
adults. The majority of patients are between two and ten years of age. Scarlet 
fever is rare during the first year of life. It is an interesting fact that children 
with fresh wounds, either accidental or surgical, are especially liable to scarlet 
fever. An analogous and familiar fact is that women after delivery have a strong 



SCARLET FEVER 



39 



tendency to the disease.* As a rule, a person is attacked but once, so that, after 
the disease is over, an immunity from contagion is enjoyed; but there are excep- 
tions to this rule. 

Scarlet fever is now spread over the entire globe. In Germany there are 
almost always some sporadic cases in the larger towns, while from time to time, 
especially in autumn, there are more or less extensive epidemics in one place or 
another. There is considerable variation in the different epidemics of scarlet 
fever, as in many other infectious diseases, in the general character of the disease, 
and above all in the prevailing mildness or severity of the cases and the frequency 
of certain complications (nephritis, diphtheria), etc. 

Clinical History. — The period of incubation is not definitely known. Many 
observations seem certainly to indicate a short period of two to four days, but the 
incubation stage is perhaps often somewhat longer — four to seven days. There 
are hardly ever any decided prodromata. The disease begins rather suddenly, 
with fever, often introduced by chilliness, and sometimes by a well-marked rigor. 
There is almost invariably a painful, scarlatinal sore throat. A further symp- 
tom, in all cases of any severity, is cerebral disturbance, generally rather intense. 
There may be headache, dullness, uneasy sleep, delirium, and, in smaller chil- 
dren, sometimes even convulsions. A very frequent and characteristic early 
symptom is vomiting, which may be repeated. 

The characteristic rash usually appears as soon as the close of the first day, or 
on the second, and begins on the neck and on the chest and face, quickly becoming 
almost universal. The eruption consists at first of numberless small red points, 
crowded thickly together and soon united into a diffuse, intense, scarlet-colored 
erythema. The small and somewhat elevated points almost always correspond to 
the swollen hair-follicles. The diffuse redness is the result of an excessive hyper- 
emia of the skin, and vanishes completely on pressure. The skin as a whole 
seems slightly swollen and thickened. The back usually presents the most vivid 
tint. In the face there is generally pallor of the lips and chin, presenting a very 
striking and characteristic contrast to the bright-red cheeks. If some object 
like the end of a pen-holder be drawn over the red skin, there soon arise corre- 
sponding white lines, due to contraction of the blood-vessels. It is possible thus 
to make letters or pictures upon the back of the patient. We should add, how- 
ever, that this is not a peculiarity of the scarlatinal eruption, being seen in other 
erythematous eruptions. 

The rash persists for some three or four days, at first even increasing somewhat 
in vividness. It often appears more intense by artificial light than in the day- 
time. Meanwhile the severe general symptoms continue — the fever, the usually 
excessively rapid pulse, the cerebral symptoms, and the throat trouble. The spleen 
is often somewhat swollen, though seldom very large. Then the eruption begins 
to fade, the fever gradually ceases by lysis, the general condition and the difficulty 
in swallowing improve. With the end of the first week or the beginning of the 
second, the cases which run the typical course become fully convalescent. When 
the rash disappears, the epidermis usually begins to peel off, in a very character- 
istic way, in pieces of considerable size. The exfoliation upon the hands and 
feet is especially pronounced, and the little convalescents often amuse them- 
selves by peeling off the epidermis in strips. Cases which are apparently the 
mildest and most benign may have their convalescence interrupted by the oc- 
currence of a secondary scarlatinal nephritis. There is no sure prophylaxis 
against this. 

We will now pass on from this general summary to a more complete considera- 



* In puerperal cases genuine scarlet fever and septic diseases were formerly often confounded. 
(See Chapter XVIII.) 



40 



ACUTE GENERAL INFECTIOUS DISEASES 



tion in detail of general and local symptoms; and we shall see how manifold 
are the clinical phenomena presented by scarlet fever. 

1. Fever (see Fig. 5). — Although in a few undeveloped cases there is no fever, 
or scarcely any, almost all cases of any severity have high fever. It is only ex- 
ceptionally that severe cases are observed in which the bodily temperature is little 
if at all elevated. As a rule, the fever rises rapidly upon the very first day, cor- 
responding to the sudden onset of all 
the symptoms, to about 104° or 105° 
(40°-40.5° C). The next day it often 
becomes a little higher still, and then 
persists with but slight variations, as 
a rule, so long as the eruption is at its 
height. During this period a tempera- 
ture of 105° or more (40.5°-41° C.) is 
not infrequently observed. When the 
eruption fades, and the other symp- 
toms decline, defervescence occurs. 
This happens but rarely by crisis, and 
that in the slight attacks. It is almost 
always by prolonged lysis, as in ty- 
phoid, only more irregularly and more 
rapidly. If the fever lasts into the sec- 
ond week of the disease, it is almost 
always (though not without excep- 
tions) caused by demonstrable complications. The most frequent causes are the 
persistence of a severe sore throat, the occurrence of inflammatory changes in the 
cervical glands, or a purulent otitis media. In closing what we have to say about 
the fever in this disease, we would emphasize the fact that the pulse is often very 
rapid (140 to 160 a minute), even in comparison with the height of the tem- 
perature. 

2. The Throat. — The throat presents the most constant local lesion of scarlet 
fever. Sore throat is only in the rarest cases wholly absent; * but its form and 
intensity may vary extremely. The mildest variety is a simple, erythematous 
catarrh, without much swelling, but exhibiting usually a vivid and often punctate 
reddening of the soft palate and tonsils, the pharynx, and also the mucous mem- 
brane of the hard palate, frequently associated with enlargement of the little 
mucous follicles. Sometimes minute haemorrhages take place into the mucous 
membrane. In other cases the scarlatinal affection of the throat is from the start 
associated with considerable swelling of the parts, and especially of the tonsils, 
justifying the term " parenchymatous sore throat." Not infrequently small 
abscesses form in the lacunae of the tonsils ; or superficial spots of necrosis develop 
which leave behind them larger or smaller ulcers, and sometimes occasion con- 
siderable haemorrhage. There may even be a circumscribed gangrene of the 
tonsils. 

The most important, because it is also the most dangerous, of the affections 
of the throat resulting from scarlet fever is the so-called scarlatinal diphtheria 
— that is, a diphtheritic inflammation of the tonsils and soft palate. This usually 
develops on the third, fourth, or fifth day of the disease, replacing a simple in- 



* Absence of sore throat has been noted by others and by myself, especially in the scarlet fever of 
women in childbed. I suspect that the reason for this is that the infection does not enter in the usual 
way through the mouth, but from some wound due to parturition. On the other hand, it is to be noted 
that in the scarlet fever from wounds, when the infection follows an injury to the finger, etc, a sore 
throat occurs. 



123456789 




Eruption. 

Fig. 5.— Example of a normal scarlet-fever curve. 



SCARLET FEVER 



41 



flammatory condition of the parts. Whitish, dirty-colored spots develop on the 
tonsils, the arches of the palate, and the uvula. These rapidly increase in size, 
and cause a dry necrosis of the mucous membrane and subsequent ulceration. 
The process is a truly diphtheritic one — that is, there is an inflammation com- 
bined with an extension into the diseased tissues of a fibrinous exudation. 

It is especially characteristic of scarlatinal diphtheria that there is almost 
invariably a considerable swelling 1 of the cervical lymph-glands, except in those 
cases which die very quickly. It is true that the glands are usually somewhat 
enlarged in the milder forms of pharyngitis accompanying scarlet fever, but they 
seldom attain the size observed in the true diphtheritic process. In this there is 
an inflammatory and cedematous infiltration affecting of tern not only the glands 
themselves, but also the surrounding connective tissue, so that in severe cases the 
whole cervical region and the floor of the buccal cavity presents a firm and 
usually a very painful enlargement. It should be added that the severity of the 
throat symptoms and the extent of the glandular swelling are not always com- 
mensurate. Almost always the scarlatinal diphtheria is associated with a marked 
stomatitis, and very often also with a severe purulent or even diphtheritic rhinitis, 
although an invasion of the larynx (vide infra) is only exceptionally seen. 
At the alse of the nose and the corners of the mouth there are often superficial 
ulcers from this cause. Otitis is also a frequent complication of scarlatina (vide 
infra). 

The influence of the scarlatinal diphtheria upon the general condition of the 
patient is always considerable. Apart from the marked local discomfort, there 
is often a severe general septic condition. Grave signs of cardiac weakness (a 
very rapid, small pulse) are very apt to appear early. Moreover, cases of scarlet 
fever associated with pharyngeal diphtheria often show at the same time other 
severe septic complications (inflammation of several joints, simple or purulent 
inflammation of the serous membranes, nephritis, etc.). Many cases end fatally 
in a few days, while others pursue a more tedious course, lasting perhaps several 
weeks before death comes. These are often associated with pyemic processes in 
other parts of the body. 

With regard to the pathogenesis of the throat troubles seen in scarlet fever, the 
more simple forms are in all probability directly associated with the scarlatinal 
process — that is, they are direct sequences of the affection. In regard, however, 
to the severer forms, and especially to the diphtheritic variety, it is almost cer- 
tain that these are not a direct result of the scarlatinal poison, but are due to 
some secondary infection which occurs on the soil furnished by the primary scar- 
latinal angina. The severe necrotic disease of the mucous membranes and the 
secondary changes in the lymph-glands and other septic complications are due 
chiefly to streptococci (Lofner) ; but we are almost compelled to suppose that there 
is some intimate connection between the two varieties of infection, else why 
should this peculiar secondary disease, the scarlatinal diphtheria, be so often con- 
joined with scarlet fever? It seems to us certain that "scarlatinal diphtheria" 
should not without further evidence be identified with true diphtheria, in spite of 
the similarity of the anatomical (" diphtheritic ") changes. From a purely clin- 
ical standpoint the two present several important points of difference. In partic- 
ular the scarlatinal diphtheria, in contrast with the primary form of the disease, 
seldom spreads to the larynx. Laryngeal croup is therefore but rarely seen in 
scarlet fever. The severe dyspnoea which sometimes develops in the course of scar- 
let fever is probably caused by an inflammatory oedema of the glottis. Another 
important clinical distinction between genuine and scarlatinal diphtheria is that 
paralysis of the soft palate, the ocular muscles, and other parts is scarcely ever 
a sequel of scarlatinal diphtheria. On the other hand, however, it is easily con- 
ceivable that many similarities between the two diseases should exist, since 



42 



ACUTE GENERAL INFECTIOUS DISEASES 



severe secondary septic streptococcus infection may occur both in scarlatinal 
angina and in true diphtheria. It is also possible that in some cases an actual 
true diphtheria should appear as a secondary infection in scarlatinal angina. The 
reported cases of laryngeal croup after scarlet fever may thus be explained. All 
these conditions, which have been much discussed, will be made wholly plain 
when the accurate bacteriological investigations of individual cases become more 
numerous. 

3. We proceed by a natural sequence to the consideration of the affections of 
certain parts adjacent to the throat, troubles which must be regarded as chiefly 
the result of direct extension, or of a conveyance of the inflammatory process 
from the throat. 

The stomatitis we have already mentioned, as well as the disturbance in the 
neighboring lymph-glands and the surrounding tissue. Parotitis is not rare in 
severe cases. Of especial importance is the scarlatinal inflammation of the middle 
ear, which often results in permanent deafness. 

This inflammation usually arises at the time of desquamation, but it may occur 
earlier. It is either a simple catarrh, a purulent otitis media, or, in severe cases, 
an actual diphtheritic process. The deafness and earache are easily overlooked, 
as the other symptoms of the patient occupy the attention, so that the ear trou- 
ble is first recognized by the occurrence of perforation of the tympanum and sub- 
sequent purulent otorrhcea. After this declines there very often remains behind, 
as we have said, permanent deafness. Statistics have shown that four or five per 
cent, of all cases of deafness are referable to an attack of scarlet fever in child- 
hood. The otitis is seldom immediately dangerous, but yet cases of .purulent 
meningitis have been observed to follow it. 

We have already spoken of the purulent or even diphtheritic rhinitis which 
almost always accompanies the scarlatinal sore throat. In rare cases there may 
also occur a purulent conjunctivitis, which is most probably the result of a direct 
conveyance of inflammatory secretions. 

The tongue in scarlet fever deserves special mention. The first coating cleans 
off, and then the tongue usually presents a very characteristic appearance. It is 
diffusely reddened and covered with little elevations corresponding to swollen 
papiltee (strawberry tongue, scarlatinal tongue). 

4. The characteristic eruption, as developed in the great majority of cases, has 
been described above. It remains to describe certain variations from the usual 
appearances. 

First, the eruption may be rudimentary. It is then not pronounced, and visi- 
ble only on a limited portion of the body (face, trunk, or extremities). 

Variations from the type are not rare ; sometimes the papules are more strongly 
developed (scarlatina papulosa) ; very frequently there are little vesicles (scarla- 
tina miliaris). This latter form of the eruption appears by preference upon the 
trunk, but it may come also upon the extremities, and is often brought out by ex- 
cessive perspiration, or by wrapping up the patient too warmly. Many epidemics 
are noticeable from the frequent appearance of this miliary form. More rarely 
the rash has a spotted look, resembling the eruption of measles (scarlatina varie- 
gata). There may be minute ecchymoses, which are not very rare and not omi- 
nous. Well-developed cases of hemorrhagic scarlatina are, however, very danger- 
ous, because here the general infection of the system is almost always exceedingly 
severe, and probably due to secondary sepsis; and there is besides, as a rule, a 
general hemorrhagic diathesis. Other cutaneous lesions, especially herpes and 
urticaria, are not so very unusual in connection with the scarlatinal eruption. 
Furunculosis has been repeatedly observed after the rash fades. 

Desquamation generally begins as soon as the rash has completely disappeared, 
but it may not occur till a few days or even one or two weeks later. Its extent 



SCARLET FEVER 



43 



corresponds in general to the severity of the eruption, although extensive desqua- 
mation may follow a rudimentary eruption. It is seldom bran-like or furfura- 
ceous, as in measles. The rule is for it to be in lamellse, so that, as we have stated, 
quite large strips of epidermis may be detached entire. 

In rare cases an oedema of the skin appears after scarlet fever, which can not 
be shown to depend upon nephritis (vide infra), but which may perhaps be due to 
an abnormal permeability of the walls of the cutaneous blood-vessels following 
the eruption (hydrops scarlatinosus sine nephritide). 

5. Kidneys. — Next to the severer forms of throat trouble, the most important 
and dangerous complications are located in the kidneys. They may appear as 
early as the acme of the disease, as in many other 'infectious diseases. The urine 
lias a trace of albumen. In rare cases the amount of albumen may be consider- 
able. The appearance of the urine is generally not much changed, and the micro- 
scope reveals but few abnormal constituents. There are some white and red blood- 
globules, a few hyaline casts, sometimes one or two renal epithelial cells. This 
initial albuminuria very rarely gives cause for alarm. 

The genuine scarlatinal nephritis scarcely ever develops much before the end 
of the second or the beginning of the third week. Sometimes it comes even later. 
In one case under our own observation it did not begin till the thirty-third day of 
the disease. It may therefore be regarded to a certain degree as a localized re- 
lapse. It may be so mild as to cause no subjective symptoms whatever, so that it 
would be unnoticed if the urine were not carefully examined. On the other 
hand, it may be accompanied by the gravest symptoms, and may soon terminate 
fatally. It may follow either severe cases or the mildest, so that the rule should 
be to examine the urine in every case of convalescence from scarlet fever as often 
•and as carefully as possible. ~No exact statement can be made as to the fre- 
quency of this complication, for it is much more common in some epidemics than 
in others. 

The development of nephritis is often marked by a fresh rise of temperature. 
The elevation may be slight or it may reach 104° (40° C). According to our own 
experience, the fever often comes a day or two earlier than the changes in the 
urine. As the nephritis goes on, it is very often accompanied by a moderate 
fever with remissions. This fever may be almost wholly absent, especially in 
mild cases. The pulse generally becomes harder, and is sometimes quickened; 
but in many cases it will be slow, and it is sometimes irregular. Among other 
objective symptoms, the first to excite notice is generally a slight puffiness of the 
face, which is usually pale. The eyelids, particularly, present an evident oedema. 
In the milder cases this oedema remains limited, while in others it gradually 
increases in extent and degree, involving first, as a rule, the dependent parts of 
the trunk, and later the extremities. Severe cases develop a pronounced ana- 
sarca. There are then, usually, effusions into the serous cavities, especially ascites 
and hydrothorax. The latter is dangerous chiefly through disturbance of the 
respiration, particularly if it be associated with severe bronchitis or pneumonia 
(vide infra). Although in general the development of a universal dropsy is 
characteristic of scarlatinal nephritis, oedema may at times be wholly absent. 
On the other hand, it is noteworthy that the oedema may occasionally show a 
peculiar localization, especially in the mucous membranes (oedema of the con- 
junctivae, oedema of the ary-epiglottic folds with symptoms of laryngeal stenosis, 
oedema of the uvula and soft palate, etc.). 

The urine exhibits the most important changes (vide the section on renal 
diseases). These may be insignificant in the milder cases, but they are very pro- 
nounced in the severe ones. The amount is much diminished. Sometimes there 
will be for several days almost complete anuria. In cases of any severity the urine 
is turbid, dark, often evidently bloody, with increased specific gravity (about 1015 



44 



ACUTE GENERAL INFECTIOUS DISEASES 



to 1025), and containing a large amount of albumen. The sediment is generally 
abundant, and exhibits numerous hyaline casts of various lengths and diameters. 
To these may be attached red or white blood-corpuscles, detritus, granules of 
haematoidin, or bacteria. In cases of some duration the casts are often moderately 
fatty. Very frequently there are found noticeably long and broad waxy [fibrin- 
ous] casts, which are opaque and yellow. In many cases of scarlatinal nephritis 
the urine is peculiar in having very many white blood-corpuscles, either isolated 
or adhering to the casts. These undoubtedly originate for the most part in the 
kidneys. Red globules, some of them in the form of colorless rings, are found. 
They are usually present in small numbers, but may become more abundant, 
especially for a day at a time. We have seen a very haemorrhagic urine after the 
special albuminuria had disappeared. Renal epithelium is frequently seen, but 
not invariably nor in very large amount. 

Urasmic symptoms often develop in scarlatinal nephritis. They may be of all 
degrees of severity. They will be described in detail under diseases of the kidney 
(vide infra). The uraemia may be so severe as to cause convulsions, coma, and 
death ; but it is remarkable how often children recover from what seems to be the 
most pronounced uraemia. 

The duration of scarlatinal nephritis varies greatly according to its severity. 
In cases which run a favorable course, the urine is generally abnormal for two to 
four weeks, or even longer. There is sometimes a very slight albuminuria present 
for months without causing any symptoms. Death may be due to uraemia or 
more frequently it may come on with severe dyspnoea. The latter is due partly to 
dropsical conditions (hydrothorax, ascites), or often to a severe diffuse bronchitis 
or pneumonia accompanying the nephritis. Cardiac insufficiency also may be the 
cause of death. The transition of acute scarlatinal nephritis into chronic nephri- 
tis, especially into chronic contracted kidney, is rare, but it has certainly been 
seen both by ourselves and others. It is worthy of note that, after the nephritis 
has lasted some four to six weeks, beginning hypertrophy of the left ventricle can 
be detected by the displacement and strengthening of the apex-beat. Friedlander 
has demonstrated this early hypertrophy at autopsy. 

The anatomical changes of scarlatinal nephritis can be mentioned only briefly 
here. The forms vary. We often find the " large white kidney " — that is, a dif- 
fuse acute nephritis with fatty degeneration of the epithelium — and usually also 
more or less numerous haemorrhages. In other cases the kidneys macroscopically 
are apparently little altered, but we see in the cortex the gray, prominent, blood- 
less glomeruli, in which the microscope shows very marked changes (" glomerulo- 
nephritis " of Klebs and others). 

6. Joints. — When desquamation begins, or even earlier, pain and swelling 
may attack a certain number of the joints. This trouble was formerly called 
scarlatinal rheumatism, but now it is usually known as scarlatinal synovitis. It 
is generally mild and quite temporary, but, exceptionally, it may be severe and 
even purulent. Then it is usually a part of a secondary sepsis or a general 
pyaemia, as evinced by such other lesions as empyema, subcutaneous abscesses, 
jaundice, splenic tumor, nephritis, etc.; and they all seem to be caused by a sec- 
ondary infection with streptococci, etc. 

We have seen a few instances of excessive pain in the muscles of the thighs, 
accompanied by a moderate, diffuse swelling. 

7. Another important complication of scarlet fever is pneumonia. In severe 
cases lobular pneumonia sometimes appears as early as the first stage of the dis- 
ease; but it occurs more frequently in connection with the nephritis, when it 
may have the significance of so-called nephritic pneumonia (vide infra). The 
respiration may be very seriously embarrassed by it. Inflammations of serous 
membranes in the chest — viz., endocarditis, pericarditis, and pleurisy — are more 



SCARLET FEVER 



45 



rare. They may or may not be accompanied by disturbances in the joints 
(vide supra). Pericarditis, endocarditis, and myocarditis sometimes develop 
during scarlet fever, but it is usually hard to decide whether they are due 
to the direct action of the scarlatinal poison itself or to secondary septic com- 
plications. We refer the tendency to tachycardia or bradycardia, irregularity 
of the heart-beat, etc. (which sometimes last long after the scarlet fever), to 
myocarditic changes. Endocarditis may result in permanent valvular disease. 
Quite severe intestinal symptoms, such as diarrhoea, may appear. These 
are generally the result of a catarrhal inflammation of the intestinal follicles. 
Dysentery is less frequent. The enlargement of the spleen has been already 
mentioned. The liver is sometimes found to be considerably enlarged. A general 
moderate swelling of the lymph-glands (neck, axillae, groins) is usually present 
in scarlet fever at the time of the eruption. We usually find in the blood a 
pronounced leucocytosis which sometimes lasts long after the other morbid 
symptoms. 

Variations in the Course of the Disease. — The diversities of the clinical pic- 
ture in different cases of scarlatina will be understood when we consider the 
variety and number of the disturbances thus far cited. It is to be added that the 
general course of the disease may exhibit numerous peculiarities, of which it is 
hardly possible to give an exhaustive presentation. We will content ourselves 
with a cursory statement of the most important deviations from the typical 
course. 

1. Rudimentary Forms. — To this class, in which the disease does not reach a 
perfect development, belong first the cases of simple sore throat with no erup- 
tion, or at most an extremely faint and partial one (scarlatina sine exanthe- 
mate). Sometimes even the sore throat is hardly to be seen, and there is noth- 
ing but a brief and slight fever with mild symptoms of general disturbance. The 
recognition of these cases as scarlatinal is possible only when we consider their 
serological relation to other undoubted cases of scarlet fever. We had an excel- 
lent opportunity to observe them when the disease broke out in the children's 
wards of the hospital at Leipsic. The diagnosis is sometimes confirmed by a 
slight though evident desquamation, affecting the hands, feet, legs, and back, or 
by an acute nephritis, which may follow the mildest attacks of this sort. Many 
cases of acute nephritis, though apparently wholly spontaneous and primary, 
must be regarded as aetiologically scarlatinal. 

2. Rudimentary hut Pernicious Forms. — Under this head belong those attacks 
of scarlet fever in which the eruption is scanty or absent, while from the very 
start the most violent general symptoms appear. There is a very high fever, enor- 
mously rapid pulse, and delirium. Such cases must be the result of an uncom- 
monly severe general infection. They usually end in speedy death. Other cases, 
ending fatally in a few days, have a well-developed rash without other localized 
disturbances. 

3. Severe Forms with a more Protracted Course. — In these cases the long 
duration is not the exclusive result of especial complications, but is likewise due 
to the severity of the intoxication. One variety is the so-called typhoidal form of 
scarlatina, with persistent high fever and severe constitutional symptoms. An- 
other variety is the hemorrhagic form briefly mentioned above, in which there 
are extensive haemorrhages into the skin and into the mucous and serous mem- 
branes. This form may run an extremely acute course. Further, in all per- 
nicious forms, there may be severe local complications, particularly diphtheritic 
or gangrenous sore throat, inflammations of serous membranes, etc. Attacks 
of this sort are often not produced by the poison of scarlet fever alone, but by 
secondary complicating processes. While speaking of scarlatinal diphtheria it 
has already been pointed out that secondary infection of the system may result, 



46 



ACUTE GENERAL INFECTIOUS DISEASES 



principally originating from the diseased throat, and occasioning- sometimes 
grave septic conditions of the whole body, sometimes local disease of different 
parts. 

4. In extremely rare cases Relapses do occur. After the first illness a fresh 
eruption breaks out with all the other symptoms of scarlet fever. In anomalous 
cases, running a severe course, there is sometimes, at an advanced stage, a fresh, 
imperfect eruption (generally in spots), which Thomas has termed a pseudo- 
relapse. Probably this is usually a septic eruption. 

Diagnosis. — The diagnosis of scarlet fever is made in most cases from the 
characteristic eruption taken in connection with the other symptoms. We 
should, however, bear in mind that exceptionally other eruptions appear which 
exhibit the closest resemblance to that of scarlet fever. 1. After the use of 
certain drugs, especially atropine (belladonna), quinine, antipyrine, morphine, 
chloral; and likewise after the ingestion of crabs, fish, etc. 2. As a symptom 
of other infectious diseases, such as typhoid fever, small-pox; and, above all, 
in septic diseases {vide infra). In an uncertain or anomalous case, factors of 
importance for diagnosis are the aetiology (connection with other well-defined 
cases), the initial sore throat, and the eventual occurrence of desquamation or of 
a secondary nephritis. 

The prognosis must in every case be guarded. From what has been said of the 
course of the disease, it is evident that, even in cases which are at first appar- 
ently the most favorable, dangerous complications may appear. The commonest 
dangerous complication during the height of the disease is scarlatinal diph- 
theria, the commonest dangerous sequel is nephritis. 

Treatment. — The majority of those cases of scarlet fever which take a typical 
course will recover completely without our aid. In these the task of the physi- 
cian, so far as treatment is concerned, consists in arranging the details of hygiene 
and the general care of the patient. The sick-room should be cool and well ven- 
tilated and the diet rather strict, consisting mainly of milk. Broths and eggs 
may also be allowed. We should see that the skin and the mouth are kept clean. 
To change the linen frequently, if done with proper precaution, is not only 
permissible, but very desirable. Rubbing the skin with olive-oil, vaseline, etc., 
has some merit, and is especially to be recommended if the skin be harsh and dry 
after the eruption has faded. 

[From the moment that the disease is declared the patient should be thor- 
oughly anointed daily with carbolized vaseline, lard, or the like ; and this should 
be kept up until desquamation has ceased. Not only is the comfort of the 
patient promoted, but the danger of the spread of the infection is thereby 
greatly lessened.] 

The scarlatinal disease of the throat must be treated with the greatest atten- 
tion, the main duty of the physician in this regard being to prevent, if possible, 
the ingress of the above-mentioned secondary infection. It is therefore our 
opinion that in every case of scarlet fever the greatest pains should be taken 
from the very commencement of the disease to maintain complete disinfection 
of the mouth and throat. Larger children may use a gargle (two-per-cent. solu- 
tion of chlorate of potash, one- or two-per-cent. solution of carbolic acid). In- 
halations of carbolic-acid spray, dilute lime-water, etc., are also to be recom- 
mended where practicable. If there is prostration, or if the child be young or 
willful, we must cleanse the mouth and throat at short intervals, by means of a 
spray-apparatus, with disinfectants, such as boracic acid or permanganate of potash 
in solution. Sometimes it is a good plan to let the patient swallow slowly a half- 
teaspoonful of a solution of potassic chlorate (about 1 to 40), every half -hour or 
oftener, with the object of contributing to the local disinfection of the throat. If 
scarlatinal diphtheria nevertheless develops and the cervical lymph-glands begin. 



SCARLET FEVER 



47 



to increase further in size, there is reason to hope, according to the experience of 
Taube and Heubner, that parenchymatous injections into the tissue of the tonsils 
or the palatine arches may yet check the spread of the secondary infection. About 
6 minims (a Pravaz syringe half full) of a three-per-cent. solution of carbolic 
acid may be injected twice daily upon each side by means of a long hollow needle 
and a subcutaneous syringe. Catti recommends painting the affected parts with 
a l-to-1,000 solution of corrosive sublimate. Of the many other remedies ad- 
vised, we may add that the insufflation or dusting of the tonsils with powdered 
sugar is of advantage. In ordinary scarlatinal diphtheria we can expect no 
benefit from Behring's serum-therapy, but if there is a complication with true 
diphtheria a serum-injection is most advisable. 

If the nose be likewise affected, the chief thing to do is frequent cleansing 
and syringing while the head is bent forward. We should be on the watch for 
the possible occurrence of otitis. In this particular the physician is often guilty 
of sins of omission. Much harm may be averted by a prompt syringing of the 
ears, or, if need be, by insufflation of air into the middle ear, or paracentesis of 
the membrana tympani. 

Inflammation of the glands in the neck, if severe, is prone to pass on to sup- 
puration, and it must then be treated surgically. When the swelling has just begun, 
or is still moderate, we may try to cure it by rubbing in iodoform ointment (1 to 
15) two or three times a day. Ice is generally not so well borne as warm applica- 
tions (poultices or warm bran-cushions). 

If there be continuous high fever, accompanied by rather severe constitutional 
symptoms, a moderate employment of the cold-water treatment in scarlet fever 
is strongly to be recommended. The baths seldom need to be cooler than 81° to 
88° (22°-25° R.), and are to be employed two or three times daily, or oftener 
in severe cases. If the nervous disturbance be serious, or if the respiration 
be impaired, the patient should be douched with cold water during the bath. 
Instead of baths, wet packs may be used to advantage. Internal antipyretics, 
such as antipyrine, may usually be dispensed with, although in private practice 
we may be obliged to employ them. 

We must watch the condition of the heart carefully. When the pulse is very 
rapid we may use an ice-bag on the heart. When the heart begins to grow 
weak we may prescribe tincture of strophanthus, wine, etc., and the most efficient 
remedy for threatening collapse is injections of camphor. With mild scarla- 
tinal arthritis salicylate of sodium and antipyrine act well as palliatives, but in 
severe cases they, of course, do little good. 

We know of no means to avert the nephritis. In justice to himself, the physi- 
cian must always at the start point out the possibility of its occurrence, and must 
avoid as far as possible errors in diet or exposure to cold on the part of his pa- 
tient. He may thus escape blame. The treatment of the nephritis and its 
results is fully described in the section on renal diseases. The most important 
remedies are a mild diet and the use of warm or hot baths and packs. The other 
complications of scarlet fever must be treated symptomatically in the ordi- 
nary way. 

The patient must, as a rule, keep his bed three or four weeks, even if convales- 
cence be uninterrupted. 

[This injunction is rather extreme. Xephritis is as likely to follow a mild as a 
severe case, and occurs sometimes in spite of every precaution. The physician 
should use his discretion as to the length of time the patient is kept in bed, care- 
fully guarding against exposure to cold and imprudence in diet.] 

After desquamation is completed the skin should be thoroughly cleaned by 
warm baths. The disease is so dangerous that, whenever a case occurs in a fam- 
ily, isolation is absolutely demanded, and, if possible, all the other children should 



48 



ACUTE GENERAL INFECTIOUS DISEASES 



be sent away. If this advice be disregarded, we can reject all responsibility for 
any further cases and their results. 

[Scarlet fever is a disease at once so highly contagious and so common that it 
may be taken as the type of its class. Its hygienic treatment and the measures 
needful to prevent its spread consequently deserve more minute detail. 

The sick-room should be at the top of the house, if possible, and exposed to the 
south; every unnecessary article of furniture and all ornaments should be re- 
moved beforehand, carpets, curtains, and stuffed or upholstered furniture being 
included. A window should be kept open constantly, top and bottom; in cool 
weather a fire should be burning; in warm weather ventilation is furthered by 
placing a gas-burner or large kerosene lamp near the throat of the chimney. 
Outside the door of the sick-room a sheet moistened with a disinfectant solution 
should be carefully hung. Only those whose presence is absolutely necessary are 
to be allowed in the sick-room, and the physician, when his visit is completed, 
should pass directly out of the house. 

A convalescent should be kept away from all who are liable to contract or con- 
vey the disease until desquamation has entirely ceased. Several warm soap-baths 
should be given before the child emerges into every-day life, and it should finally 
be dressed in uncontaminated clothing. 

For further directions as to the disinfection of the room, the clothing, and the 
excreta, see pages 28-30.] 



CHAPTER V 

MEASLES 

(MorMUi) 

.^Etiology. — In contrast with the malignancy of scarlet fever is the compara- 
tively benign nature of measles, a disease of childhood which is but little feared 
even by mothers. It is so widespread, and the susceptibility to it is so universal, 
that measles passes for an almost unavoidable but comparatively insignificant an- 
noyance. Indeed, few escape it ; and probably the reason why adults have mea- 
sles so much less frequently than children is simply that most adults have already 
suffered from it in childhood. A second attack of measles in the same individual 
may occur, but it is certainly extremely rare. 

[In highly civilized countries measles has prevailed so long that it would seem 
that a relative resistance against the poison has been acquired. The frightful 
ravages of the disease when it was planted in virgin soil, as among the Fiji Is- 
landers not many years ago, apparently bear out this view. The susceptibility to 
measles is greater and more widespread than is that to scarlet fever — that is to 
say, fewer individuals reach adult life without having experienced an attack of 
the former than of the latter.] 

Measles generally comes in epidemics. Sporadic cases - are exceptional. In 
this respect measles differs decidedly from scarlet fever. The rapid spread of the 
disease when it has once broken out is a result of its great contagiousness. If one 
child in a family is attacked, the others almost always take the disease. The in- 
fection may be transmitted even by well persons and by means of articles with 
which the sick have come in contact, although this is not often the case. We are 
not yet acquainted with the specific poison of measles — although its existence 
is to be taken for granted — nor with the details of its transmission. Still it 
seems most probable that the poison is inhaled through the mouth and nose, 
and that this is the reason why its effects are usually first developed in the 



A 



MEASLES 



49 



respiratory passages (vide infra). The disease can be artificially produced by in- 
oculation of healthy children with the blood or liquid secretions of those suffer- 
ing from it. 

Clinical History. — The length of the stage of incubation is tolerably uniform. 
It is ten days to the beginning of the first symptoms, and thirteen or fourteen 
days to the breaking out of the eruption. These figures have been established by 
the observations of Panum, the opportunity having been afforded upon the first 
introduction of the disease into the Faroe Islands. As a rule, there are no espe- 
cial prodromata during the period of incubation except some slight elevations of 
temperature. At the end of ten days the initial stage * begins, generally sudden- 
ly, and with an abrupt rise of temperature to 102° or 104° (39°-40° C). At the 
same time the characteristic catarrhal symptoms appear: nasal catarrh (coryza), 
to be recognized by the abundant nasal secretion, the frequent sneezing, and 
sometimes also by nose-bleed; more or less severe conjunctivitis, characterized by 
photophobia, reddening of the eyes, and increased flow of tears; and, lastly, 
symptoms of a catarrh of the upper part of the respiratory tract, usually mod- 
erate, but nevertheless causing hoarseness and a slight cough. With all this 
the general condition is disturbed, the children are restless, have headache, and 
eat little. Symptoms of a mild sore throat are not infrequent, but are very far 
from being so prominent as in scarlet fever. 

These initial symptoms last, as we have said, three or four days. Then the 
eruption begins (stage of eruption). This is very often preceded for a day or 
two by a peculiar, usually spotted, reddening of the hard and soft palates, termed 
" eruption upon the mucous membrane." [Koplik, in 1898, called attention to 
an eruption of bluish-white specks, surrounded by a reddish area, upon the mu- 
cous membrane of the cheek and lips, occurring twenty-four to seventy-two hours 
before the cutaneous exanthem. Others confirm his observations and regard 
" Koplik's spots " as a great aid in early diagnosis. — V.] The true eruption of 
measles begins almost always in the face, on the cheeks, forehead, and around the 
mouth (contrasting with the characteristic pallor of the chin in scarlet fever), 
and spreads from there rapidly downward over all the rest of the body. The erup- 
tion consists at first of little papillae, corresponding to the follicles. These are 
soon surrounded by a pale-red, slightly elevated border, and in many cases become 
confluent. Perfectly flat elevations, of various sizes and of extremely irregular, 
dentated, roundish, or angular shape, develop. They are often so thickly crowded 
together as to touch one another, but usually limited portions of normal skin 
intervene between them. Within each raised spot the little follicular papillae 
remain visible. 

With the beginning of the eruption the fever rises, having been, as a rule, 
slight during the last days of the initial stage. It attains about 104° or 105° 
(40°-40.5° C). In thirty-six to forty-eight hours the eruption reaches its full 
development and its greatest extent. The fever and the catarrhal symptoms also 
persist for the same length of time. Sometimes we find a slight swelling of all the 
lymph-glands. Then follows a decline in the fever, usually rapid, and indeed 
almost by crisis, while the eruption after a short period of full development begins 
gradually to fade during the two or three days following. At the same time the 
catarrhal symptoms diminish. A more or less extensive desquamation of the 
epidermis begins, scarcely ever in large pieces as in scarlet fever, but in little 
scales, like bran. In eight or ten days, if the disease runs a normal course, the 
patient is fully convalescent. 

* We consider the term "initial stage" more correct than "prodromal stage. 1 ' The "prodromal 
symptoms" are the first slight symptoms which occur during the time of incubation of an infectious 
disease, while the symptoms presented by measles before the breaking out of the eruption are a part 
of the already developed disease. 
4 



50 ACUTE GENERAL INFECTIOUS DISEASES 

After this brief description of the usual course, we must consider more closely 
some of the symptoms and possible complications. 

The fever (see Fig. 6) of measles exhibits, as has been already implied, a toler- 
ably typical course. It begins with a rather marked and rapid rise upon the com- 
mencement of the disease. On the morning of the second day there is usually a 
marked remission, often to normal. In the last two days of the initial stage the 

fever is moderate, very rarely being so 
high as at the beginning. With the 
eruption there is a new, rapid rise, usu- 
ally higher than the initial one, so that 
we may well divide the fever into two 
periods — the prodromal fever and the 
eruptive fever. This latter is but brief 
and does not persist, as in scarlet fever, 
during the entire duration of the erup- 
tion. It falls by crisis when the rash has 
attained full development. There may, 
to be sure, be slight elevations of tem- 
perature during the next day or two; 
but, if the fever is considerable and per- 
sistent, it is always a sign that complica- 
tions have arisen, probably in the respir- 
atory apparatus. 

The eruption usually assumes the 
form described above, but may present 
manifold varieties. Sometimes its de- 
velopment is rudimentary. Sometimes 
it does not begin on the face, but on some other part of the body. This is generally 
regarded as a sign that the case will be anomalous in other ways as well. The 
individual spots may be smaller than usual, and may remain entirely separate 
from each other (morbilli papulosi). In other cases the eruption is so confluent 
(morbilli confluentes) that it resembles the eruption of scarlatina. The forma- 
tion of vesicles (morbilli vesiculosi) also occurs, but much more rarely than in 
scarlet fever. Hemorrhagic measles is also observed, but usually only in the 
form of small, capillary bleeding, and in cases that otherwise run a perfectly 
favorable course. Very rare cases have indeed been described, with a general 
hasmorrhagic diathesis and severe symptoms, resembling hsemorrhagic scarlatina. 
It is doubtful whether the " black measles " of the old writers was actually mea- 
sles at all. In addition to the proper eruption of measles, other eruptions some- 
times develop — such as vesicles, wheals, and pustules. 

The pulse is generally not so rapid in measles as in scarlet fever. Enlarge- 
ment of the spleen can be made out only to a slight degree, if at all. As a rule, 
we find no pronounced leucocytosis in the blood. 

The complications of measles are for the most part exaggerations or abnormal 
varieties and extensions of those troubles which are observed during the usual 
mild course of the fever. As in scarlet fever (vide supra), we often have to deal 
with the effects not of the original, but of secondary infection. Compared with 
the great majority of mild attacks taking the typical course, cases presenting com- 
plications of any severity are rare, and much less frequent than in scarlet fever. 
Epidemics are only now and then distinguished by unusual severity. 

Often quite serious eye-diseases are developed, particularly blennorrhagic con- 
junctivitis, keratitis, and iritis. 

Marked inflammation of the mucous membrane of the nose, throat, and lar- 
ynx may prolong the course of the disease. This is often merely an exaggera- 



1 2 3 4 5 6 7 8 




Initial Fever. Eruptive Fever. 

Eruption. 

Fig. 6.— Example of the temperature curve in 
measles. 



MEASLES 



51 



tion of the usual catarrh. Otitis media likewise sometimes occurs. A laryngitis 
of marked intensity, with considerable swelling of the parts involved, may pro- 
duce much discomfort, or even symptoms of stenosis ("false croup")- Actual 
croupous and diphtheritic lesions of the throat and larynx also occur (diphtheria 
of measles). This last is indeed much rarer than scarlatinal diphtheria, but it 
may have the same unhappy termination. It is worth mentioning that sometimes 
genuine laryngeal croup is observed in measles, unaccompanied by lesions of the 
pharynx. In all these affections secondary infection plays the chief part, as it 
does in scarlet fever (vide supra, page 41). 

It is, however, in the lungs that the most frequent and important of all compli- 
cations in measles occur. The usual mild bronchitis becomes very intense, ex- 
tends into the bronchioles (capillary bronchitis), and then results, for the most 
part, in a more or less extensive, lobular, catarrhal pneumonia (q.v.). Accord- 
ing to Koster, measles pneumonia rises from an inflammatory proliferation of 
nuclei about the small bronchi, and it usually invades the neighboring alveoli by 
continuity along the small branches of the pulmonary artery. It is then a " small 
nodular," but not strictly a lobular pneumonia. Measles pneumonia is to be 
diagnosticated when moist rales are heard in abundance over a large part of the 
chest, and when there is at the same time persistent fever and pronounced diffi- 
culty in respiration, with cough or dyspnoea. We get decided dullness on per- 
cussion only when the separate centers of infiltration are more than usually con- 
fluent. Genuine lobar, croupous pneumonia appears much less often than the 
lobular variety. It attacks one lobe, or several, is attended by high fever, and 
may end with a well-marked crisis. 

The foregoing pulmonary symptoms usually appear at the height of the dis- 
ease, and persist after the eruption fades. They may delay convalescence for 
weeks. In other cases measles will be seen at the start to run a normal course, the 
temperature will have already fallen, and then come new fever and the appear- 
ance of decided pulmonary disturbance. This is always to be regarded as a grave 
complication; and especially in feeble children it may lead to death, with the 
symptoms of impaired respiration or of constitutional exhaustion. At present 
we can not definitely state how far in measles pneumonia we have to do with the 
direct action of the measles poison itself or with secondary infection (strepto- 
cocci, diplococci, etc.). 

Marked intestinal symptoms sometimes appear, particularly an excessive diar- 
rhoea, due to intestinal catarrh. It is characteristic of measles that in severe 
cases such a diarrhoea may assume a pronounced dysenteric character, indicated by 
blood and slime in the dejections, symptoms which usually depend upon the devel- 
opment of follicular colitis with ulcerations. 

Now and then still other complications may present themselves, of which a full 
enumeration is impossible. Nephritis does occur, but far less often than in scar- 
let fever. A simple albuminuria during the acme of the disease is not infrequent, 
but as a rule it has no especial clinical significance. We should mention gangrene 
of the cheek, the so-called noma, as a complication, which is very rare but appar- 
ently characteristic. 

Peculiarities in the course of the disease are much rarer in measles than in 
scarlet fever. Yet we see, on the one hand, unusually mild or rudimentary 
cases, in which either the rash or the other local symptoms are remarkably slight, 
and on the other hand, abnormally severe cases. These latter are distinguished 
by the unusual height or persistence of the fever, by the severe constitutional and 
nervous symptoms, and further by the early appearance of complications. Such 
cases have been termed "typhoid measles." We have already mentioned the 
severe form of hsemorrhagic measles. 

We should notice the clinical relation which measles bears to two other in- 



52 



ACUTE GENERAL INFECTIOUS DISEASES 



fectious diseases — to whooping-cough and tuberculosis. Measles and pertussis 
(q. v.) may follow each other in the same individual at a short interval, some- 
times one and sometimes the other taking the initiative ; epidemics of the two dis- 
eases prevail with comparative frequency at the same time. Tuberculosis is like- 
wise to be mentioned as an important sequela of measles. In these cases it is 
probable that the children have a tubercular focus smoldering somewhere in 
the body (lymph-glands, lungs) before the attack of measles which kindles it and 
aids its further extension. The measles may also, of course, excite a predisposi- 
tion to infection with tubercle bacilli. 

The diagnosis of measles, as of the other acute exanthematous diseases, is 
based chiefly upon the eruption, but we must also regard, of course, other symp- 
toms which may be present (fever, catarrhal symptoms). Personal experience does 
more to sharpen the perception than can the fullest descriptions. We can merely 
suspect the disease during the initial stage unless an epidemic prevails. If, 
beside the characteristic catarrhal symptoms, the above-mentioned eruption on 
the mucous membrane of the palate exists, the diagnosis becomes tolerably cer- 
tain. We should consider that eruptions similar to that of measles appear in 
other diseases, more especially in rotheln, scarlet fever, typhus fever, in the begin- 
ning of small-pox, and sometimes in secondary syphilis. Furthermore, we need to 
exclude eruptions due to drugs, especially antipyrine, and also turpentine, balsam 
of copaiba, etc. In doubtful cases we shall be enabled to form a decided opinion 
by the other symptoms, and, above all, by the further course of the disease. 

Prognosis. — We have already remarked how favorable in general the prog- 
nosis is, but we must here repeat that all epidemics do not exhibit the same 
benign character, and that in every case the physician must bear in mind the pos- 
sibility of complications, and particularly the danger of severe pulmonary dis- 
turbances. 

Treatment. — The patient should in general be kept somewhat warmer than in 
scarlet fever. Even in what seem to be the mildest cases the child should be 
kept in bed till desquamation is over. The sick-chamber is to be somewhat dark- 
ened, on account of the photophobia which usually exists at first. In this way, 
normal cases run on favorably without any especial therapeutic interposition. 
The catarrhal symptoms, however, should always be heeded, since to disregard 
them may lead to their becoming aggravated. The chief requisite is cleanliness. 
At regular intervals the eyes, the nasal cavity, and the mouth should be washed 
out with lukewarm water. 

If, despite all this, certain disturbances appear in a worse form than usual, or 
if complications develop, these must receive especial attention. Severe eye trou- 
bles should be treated according to the usual ophthalmological practice. The 
treatment of croupous trouble in the throat or larynx will be fully described in a 
later chapter. For the pulmonary complications, lukewarm baths, combined if 
need be with rather cool douches, constitute the most effectual remedy. Cold 
packs are also very efficient. These we shall speak of later in more detail in the 
chapter on catarrhal pneumonia. The chief task of the physician in the treat- 
ment of measles is, however, to hinder as far as possible the appearance of compli- 
cations. We are not acquainted with any internal remedies for the lung troubles 
which are at all trustworthy. In rare instances the excessive accumulation of 
mucus in the bronchi requires the administration of an emetic. As expectorants 
we may try ipecac, liquor ammonii anisatus, etc. If considerable intestinal dis- 
turbance arises, we must employ small doses of opium, calomel, tannalbin, or sub- 
nitrate of bismuth. We hardly need to say that, whatever else is done, the 
strength of the patient should be kept up as much as possible by giving wine, 
broths, milk, eggs, etc. For at least two or three weeks after the disease has 
ended, the child must be very carefully watched. 



ROTHELN 



53 



As the disease is usually so mild, prophylaxis is not very strenuously at- 
tempted. If one child in a family is attacked, it is probably already too late to 
isolate the others, and it is even an advantage to the family to have all the chil- 
dren finish at once what they will hardly be able eventually to avoid. We would 
make an exception in favor of isolation if the disease prevailed in a severe 
form. 

[It is not customary with us to insist so strongly upon isolation and thorough 
disinfection as in scarlet fever, but the tendency of the present day is toward a 
wide application of the principles of preventive medicine. It is certainly of no 
advantage to a child to contract measles. Delicate children, especially those 
with tubercular predisposition, should be carefully guarded against it ; and, even 
if it is decided that it is not worth while to attempt to confine the disease to one 
member of a family, every precaution should be taken against infecting other 
families. Under suspicious circumstances, consequently, children are to be kept 
away from school and from contact with others. 

If there is any reason to fear the development of tuberculosis, every possible 
hygienic means should be employed in order that full vigor may be regained.] 



CHAPTER VI 

ROTHELN" 

{German Measles) 

Rotheln is a disease similar to measles, but distinct from it, although formerly 
often confounded with it, and perhaps with scarlet fever as well. The observa- 
tions of Steiner, Thomas, and others leave now no room to doubt that these dis- 
eases are distinct, for epidemics occur in which all cases present the characteristic 
peculiarities ascribed to rotheln. But the best proof is that children who have 
had rotheln are not infrequently attacked by genuine measles later. It may in- 
deed be very difficult in an individual case to decide which disease is present ; but 
that rotheln does exist, as an independent form of disease, can be denied by those 
alone who have never seen it. 

After an incubation of about two or three weeks the disease begins with 
the appearance of the eruption, which is usually noticed first in the face. 
Initial symptoms (cough, sneezing, etc.), preceding the eruption, either are 
wholly absent or at most last for half a day. The eruption is decidedly like 
that of measles, but its individual spots are smaller. They are seldom larger 
than small peas and circular, being only exceptionally as dentated and irregular 
in outline as are the maculae of measles. They appear on the whole face, the 
head, the trunk, and the extremities, are pale red (sometimes deep red), only 
slightly elevated, and are not apt to become confluent. In rare instances, 
small vesicles develop upon the macules. The soft palate sometimes exhibits, 
as in measles, a faint macular eruption at the beginning of the disease. 
After two to four days the eruption fades. There is usually no decided desquama- 
tion. 

Other symptoms of disease than this eruption are slight. Fever in many 
cases appears to be entirely absent. As a rule, there is for a day or two a little 
elevation of temperature, reaching 102° (39° C.) at most, Tokens of a moderate 
catarrh of the conjunctiva, the nasal mucous membrane, the throat, and the 
larynx are also observed — viz., photophobia, nasal discharge, and cough. Often, 
the cervical lymph-glands are more or less swollen. The constitutional disturb- 



54 



ACUTE GENERAL INFECTIOUS DISEASES 



ance is generally so slight that the child can hardly be kept in bed. Important 
complications hardly ever occur. 

The prognosis of rotheln is therefore perfectly favorable, and the employment 
of any special treatment is needless. 



CHAPTER VII 

SMALL-POX 

( Variola. Varioloid) 

.ZEtiology. — Small-pox has been known for centuries, although formerly often 
confounded with other diseases.* It is one of the most dreaded acute infectious 
diseases, and in earlier times it has destroyed thousands in its pestilential prog- 
ress. It was the discovery of the possibility of prophylactic inoculation, and the 
ever-increasing spread of this precautionary measure, which first robbed the dis- 
ease of some portion of its terrors. 

Numerous statements have been made about the occurrence of micro-organ- 
isms in the variolous eruptions on the skin and mucous membranes, but we are 
compelled to say that we are not yet acquainted with the specific, organized poison 
of small-pox, however strongly justified we may be in assuming its existence. 
Bacteria can in fact easily be demonstrated in the eruption of variola, but most 
of them come from the surrounding atmosphere, and have no relation to the spe- 
cific variolous processes. The foci of bacteria found in the internal organs (liver, 
spleen, kidneys) are also due, as their discoverer, Weigert, himself supposed, to the 
secondary ingress of other varieties of micro-organisms, and are not directly asso- 
ciated with the variolous process, the diseased condition of the skin furnishing a 
ready entrance for infectious matter. 

Predisposition to variola, except as diminished by vaccination (vide infra), is 
universal. The disease may appear at any age, even in utero. Women are 
believed to be especially liable to it during pregnancy and child-bed. It is said 
that persons ill with another acute infectious disease, such as scarlet fever, 
measles, or typhoid fever, are, for the time being, tolerably secure from infection 
with small-pox; but this rule certainly has exceptions. The same individual 
rarely takes the disease a second time. 

A case of variola is always the result of transmission of the poison to a healthy 
person from one who is already ill with it. The specific poison is most abundant 
in the diseased portions of the body and in the pus of the suppurating pocks, 
as well as the crusts and scales which are left when these have dried up; but 
the disease is also contagious in its earlier stages, before the pustules develop, 
and even, according to a few observations, during the stage of incubation. Cer- 
tainly the variolous poison is very volatile— that is, it is prone to disseminate 
itself through the air in the neighborhood of the patient. In order to catch the 
disease it is not necessary to touch the patient, but merelv to remain in his vicin- 
ity. In many cases we can not, however, determine with exactness the mode of 
transmission, since the contagion may either be direct or by means of objects and' 
utensils with which a patient has come in contact — for example, the soiled linen. 
The dead body also is capable of transmitting the disease. In general, numerous 
instances point to a considerable " tenacity " in the poison. The precise manner 



* The very name small-pox (petite verole) is significant of its confusion with syphilis, which was 
termed the " great pox." 



SMALL-POX 



55 



of infection is not yet known. It is most probable that the poison is drawn into 
the lungs with the inspired air. 

It has been demonstrated that the disease can be transmitted to healthy per- 
sons by direct inoculation of the contents of the variolous pustules. It is stated 
that monkeys and other animals may be successfuly inoculated in the same way. 
Whether inoculations with the blood of the sick will reproduce the disease is not 
yet settled. The secretions (saliva, sweat, urine, and milk) do not apparently 
contain the infectious matter. 

Course of the Disease. Variola and Varioloid— The stage of incubation lasts 
as a rule thirteen to fourteen days, sometimes a somewhat shorter time. During 
this period prodromal symptoms are absent or insignificant. 

The disease itself begins suddenly with what are usually very characteristic 
initial symptoms — rigor, fever, headache, and intense pain in the loins. It is only 
in comparatively few cases that one or another of these symptoms is slight or 
wanting. The constitutional symptoms may be very severe — a dry tongue, stupor, 
wakefulness, delirium. The fever continues intense for some days. The pulse is 
much quickened. There is almost total anorexia, and often there is vomiting. 
There is constipation, or, more rarely, diarrhoea. Frequently there is a slight sore 
throat, and sometimes a slight bronchitis. The spleen is enlarged in most of the 
severe cases, and the urine often has a trace of albumen. In women, menstrua- 
tion occurs in a remarkably large number of cases. The proper variolous eruption 
does not at once appear, but from the second day other characteristic efflores- 
cences are not rare. These are termed the initial rash of small-pox. We may 
find either a diffuse or macular erythema, extending in varying degree over the 
trunk and extremities (especially on the extensor surface), or a hemorrhagic 
eruption with small spots, appearing by preference upon the hypogastrium and 
the inner surface of the thighs (in the so-called femoral triangle of Simon) or on 
the lateral surface of the trunk and on the upper arm. The erythema soon dis- 
appears, but the hemorrhagic spots can be seen longer. Both forms of the initial 
eruption may be combined. 

The initial stage, just pictured, lasts usually three days. Severe symptoms 
occurring at this time do not exclude the possibility that the further course of the 
disease may prove favorable, while mild symptoms are of good omen. 

At the end of the third or on the fourth day the temperature makes a decided 
fall, and the regular variolous eruption begins to be developed upon the skin — the 
stadium eruptionis. During this period an evident difference among the separate 
cases becomes manifest. This distinction can not indeed be always drawn with a 
narrow line, but it is noticeable enough to justify the establishment of two types 
of variolous disease. We refer to the division into a severe form (variola vera), 
and another, mild form (varioloid). The variola proper has a well-developed 
eruption with many pustules, and, as a result of this, a second stage of fever 
(stadium suppurationis) . Varioloid has a much more scanty eruption, and little 
or no suppurative fever. We must now discuss these two forms separately. 

Variola Vera 

The eruption almost always begins in the face and upon the hairy scalp, ap- 
pearing somewhat later on the trunk and arms, and last of all upon the legs. 
It begins in the form of little red dots and spots, which develop in about two days 
to small papules (stadium floritionis) . If the hand be passed over thickly set and 
well-developed papules of variola, a peculiar soft, satin-like feeling is perceived. 
On the points of these papillae a little vesicle forms. This keeps growing larger 
and larger, its contents becoming turbid and purulent, till at last, on the sixth day 
of the eruption and the ninth of the disease, the development of the genuine pus- 
tule of variola is complete (stadium suppurationis). The pustule usually presents 



56 



ACUTE GENERAL INFECTIOUS DISEASES 



upon its summit a little dimple (umbilication), and is surrounded by a red 
border or " halo." Where the pocks are especially close together, as in the face, 
the skin between them is diffusely swollen, and the consequent burning and pain 
are excessive. The countenance becomes much disfigured. Often the eyes can 
not be opened because of the oedema. The hands also are apt to be intensely 
affected, especially the back of the hands, and also all parts which have previously 
been injured in any way (pressure or friction of clothing, etc.). On the trunk 
the pustules are very rarely as close together as on the face and hands. It is 
worthy of note that often new eruptions of pustules keep appearing for two or 
three days. 

At the same time with the eruption upon the skin, or even somewhat earlier, a 
perfectly analogous efflorescence develops upon the mucous membranes. The 
chief places for its appearance are the mouth and throat, the tongue, the soft pal- 
ate, the nasal cavity, also the larynx, the trachea, and the upper part of the oesopha- 
gus. In the vagina and rectum it is rare and scanty. In this mucous efflores- 
cence, however, there are no proper pustules, but small, superficial ulcers. These 
result from the maceration of the uppermost layers of the mucous membrane. 
They sometimes become confluent. The annoyance produced by this eruption in 
the mouth and throat is, of course, very great. The pocks in the larynx manifest 
themselves by hoarseness, and occasionally by symptoms of stenosis. 

As we have said, the beginning of the eruption is the signal for a noticeable 
fall in the temperature; but in true variola the fall does not reach the normal, 
or only temporarily. The other symptoms likewise remit, especially the head- 
ache and lumbar pain. When, however, the suppuration begins, the fever rises 
once more, and there are fresh symptoms of constitutional disturbance. This is 
the time for the dreaded attacks of delirium, during which the patient must be 
vigilantly watched, lest some untoward event happen. Now, too, complications 
may arise (vide infra). 

On the twelfth or thirteenth day of the disease the pustules begin to dry up 
(stadium exsiccationis) . The purulent contents of the pustules, part of which 
have burst, form yellow crusts, the swelling of the skin subsides, and, a few 
days later, the crusts and scabs begin to fall off. With the beginning of desic- 
cation, the fever declines; the local as well as the constitutional symptoms 
become daily slighter, and convalescence follows. The healing of the pustules is 
frequently accompanied by an extremely troublesome itching. After the scabs 
have been cast off, the skin presents pigmented spots, which persist for months. 
Wherever the cutis vera has itself been destroyed by the suppuration, a scar is 
inevitable. Thus arise the familiar scars (pitting) of small-pox, which continue 
visible through life. Very often, after the end of the disease, there is almost 
complete alopecia. The hair often grows again, but not always. 

Varioloid 

The distinction between varioloid and variola vera is not in kind, but in de- 
gree. Varioloid is only a milder form of variola. There is, as we have already 
said, no sharp boundary-line between the two. Varioloid is 'most often observed 
in those whose susceptibility to the variolous poison has been diminished by 
vaccination (vide infra). 

As above mentioned, the behavior of the disease during its initial stage will 
not permit us to decide positively whether variola or varioloid will be developed. 
It is true that if the symptoms be especially mild, we may guess that it will be 
varioloid ; and, likewise, the appearance of the initial erythema already spoken of 
is regarded as a favorable omen. 

Shortly after the pocks begin to appear, the decision can almost always be 
made with certainty. In varioloid the eruption is rather scanty. It is often 



SMALL-POX 



57 



irregular, and does not by any means always begin, like that of variola, in the 
face, but often on the trunk. The individual pocks are in no way different from 
those of variola ; but it often happens that they do not pass through all the regu- 
lar stages to full suppuration, but undergo resolution before this occurs. Such 
cases, in which there is nothing beyond papillae or vesicles, are sometimes spoken 
of as variolois verrucosa seu miliaris. The scantiness of the eruption and the 
limited amount of suppuration have for their corollary an absence, or at least a 
very slight development, of the suppurative fever. 

When the eruption appears the temperature usually falls by crisis to the 
normal level and remains there. The desiccation may begin as early as the 
eighth or tenth day of the disease, so that the whole duration of varioloid is con- 
siderably shorter than that of variola. Grave complications are very exceptional. 
The pocks may develop upon the mucous membranes, but here, too, they are 
scanty and not very vigorous. 

Course of the Fever, Symptoms presented by Separate Organs, and 

Complications 

1. Fever (vide Fig. 7). — In the initial stage, as we have said, the temperature 
rises rapidly as a rule, with a pronounced rigor; and during the first days it very 
often reaches 104° to 106° (40°-41° C). It sinks on the third to the sixth day, 
when the first papillae develop, and then, in the case of varioloid, falls rapidly to 
normal, and remains there. In variola the decline is slower and less complete; 
and with the beginning of suppuration the temperature begins to rise again. The 
violence of this suppurative fever is usually in direct proportion to the severity of 
the eruption. It has manifold fluctuations, but seldom lasts, in severe cases, less 



2 3 4 5 6 7 ft 9 10 11 12 13 14 15 16 17 18 




Initial Fever Suppurative Fever. 

Eruption. 

Fig. 7. — Example of the temperature curve in true small-pox. 



than a week. Temperatures of 104° (40° C.) and higher are common. The fever 
declines by lysis. In case of approaching death, the temperature may be ex- 
tremely high, even reaching 108° or 109° (42°-43° C). 

2. Shin. — We have already described the macroscopic appearance of the erup- 
tion. It remains to mention briefly the histological phenomena. The first de- 
monstrable changes are in the cells of the deeper layers of the rete Malpighii. As 
a result of the variolous infection, the cells perish, are swollen by the lymph 
which escapes from the papillary blood-vessels, and transformed into flaky, 
homogeneous masses without nuclei ("coagulation necrosis" of Weigert). The 
lymph becomes more and more abundant, and crowds the cells farther and far- 
ther apart. These are thereby finally changed into threads and membranes, 



58 



ACUTE GENEKAL INFECTIOUS DISEASES 



forming' a distinct net-work in the vesicle. This explains why, if such a vesicle 
be pricked, its entire contents are never discharged at once. Great numbers of 
white corpuscles escape, along with the lymph, from the blood-vessels, and finally 
render the contents of the original vesicle purulent. Proliferative processes occur 
in the surrounding epithelial cells, which are still intact, and thus the margin of 
the vesicle becomes elevated, while the dead portion in the center sinks in. Thus 
the pock becomes umbilicated. If a portion of the papilla itself suppurates, a scar 
must be left on healing. If the process remains limited to the epithelium, com- 
plete regeneration takes place, and the skin reassumes its normal appearance. 

Certain secondary complications, which sometimes attack the skin, remain to 
be mentioned: abscess, phlegmon, erysipelas, gangrene, and bed-sores. None of 
these are due directly to the specific variolous intoxication. 

3. Respiratory Organs. — The disturbances here are in part symptoms of the 
specific process of the disease, and in part secondary. The frequent occurrence of 
secondary symptoms in small-pox is easy to understand (compare the chapter on 
lobular pneumonia). Of the primary symptoms, we should mention genuine 
pocks in the larynx, the trachea, and the larger bronchi. As sequels to these, 
more or less severe secondary disorders are very frequent : laryngeal ulcerations, 
which may even lead to laryngeal perichondritis and oedema of the glottis ; diffuse 
bronchitis; lobular pneumonia, often of great extent, due to the inhalation of 
solid matter into the lungs, and frequently accompanied by pleurisy. It should 
be especially noticed that lobar, croupous pneumonia is not rare. Whether this 
be likewise secondary, or a direct result of the variolous poison, is not yet known. 

4. Digestive System. — The genuine pocks often develop, as stated, in the 
mouth and pharynx, and likewise in the upper part of the oesophagus. They are 
not observed in the mucous membrane of the stomach or intestines. The active 
diarrhoea sometimes seen depends upon catarrh of the intestine. Dysentery is 
rare. The eruption in the mouth and throat may result in severe secondary trou- 
bles, purulent otitis, parotitis, pharyngeal diphtheria, etc. The spleen is almost 
always considerably enlarged, and often the liver also, but in a less degree. 

5. Circulatory System. — Pathological changes in the heart are rare, if we 
except the slight parenchymatous degeneration of its muscular fibers, common to 
almost all severe infectious diseases. Sometimes there is a slight endocarditis 
(q. v.), which is probably secondary. Pericarditis is rather more frequent. 

6. Organs of Special Sense. — Genuine variolous pustules occur upon the eye- 
lids and the conjunctiva. Later in the disease there may be keratitis, iritis, or 
choroiditis. 

We have already mentioned the relative frequency of aural disturbances, par- 
ticularly purulent otitis media. 

7. Articular swelling may appear in the suppurative stage. The shoulders and 
knees are most apt to be attacked. Periostitis also occurs. 

8. Nervous System. — We find no pathological changes corresponding to the 
severe nervous derangements manifested during the disease. After the small-pox 
is over, spinal diseases sometimes occur, with either paralysis or ataxia. Westphal 
has shown that they are caused, in some cases, by numerous disseminated centers 
of inflammation in the spinal cord. Encephalitic processes have also been ob- 
served in small-pox, and in some cases neuritic paralysis. 

9. Albuminuria is quite common in severe attacks, but genuine nephritis is a 
very rare complication. In pregnant women attacked by small-pox abortion or 
premature labor is very apt to occur. If a living child be born, it usually dies 
soon after birth. 

Anomalies in the course of the disease are manifold. We will not speak of 
the two typical forms already considered. There are abnormally mild cases, with 
scarcely any initial symptoms, or with an obscure eruption, or with no eruption at 



SMALL-POX 



59 



all (febris variolosa sine exanthemate). In such cases a correct diagnosis is pos- 
sible only at the time an epidemic prevails, and by the aid of the attendant sero- 
logical circumstances. There are also abortive cases in which the first symptoms 
are severe, but which recover with remarkable rapidity. 

The abnormally severe cases are more important. First, there is the confluent 
variety. This is merely the typical process in its completest development. The 
initial symptoms are themselves generally very severe, and are followed, without 
any considerable remission of the fever, by the eruption of hundreds of pustules. 
The skin of the face and hands is one continuous area of suppuration. The local 
discomfort is extreme, as is also the intensity of the fever and of the constitu- 
tional symptoms. The nervous system suffers most. There is at the same time 
an unusually abundant eruption upon the mucous membranes. The occurrence 
of the above-mentioned complications affecting the various organs of the body is 
frequent. Death is a common result; or, if recovery takes place, it may be 
delayed by tedious sequelae. 

Hemorrhagic small-pox is the worst anomalous form. The name is applied 
to several different varieties. In the first place, any variolous eruption may be- 
come more or less hsemorrhagic, and yet the general course of the disease not be 
essentially altered. Such cases are more common among elderly people, cachec- 
tic persons, and drunkards. Secondly, there is a very severe form of small-pox, 
which is generally quickly fatal. The initial stage is marked by the unusual 
severity of the symptoms. The abundant eruption soon becomes hsemorrhagic, 
and there are also ecchymoses in the mucous membranes and the internal organs. 
This has been called black small-pox, and by Curschmann variola hemorrhagica 
pustulosa. 

There is another form of hsemorrhagic variola, different from these but linked 
to them by transitional varieties. In it the acute hsemorrhagic diathesis develops 
during the initial stage. Death almost always occurs before the regular variolous 
eruption. This most frightful form is usually termed purpura variolosa. That 
it is small-pox is proved by its serological relations alone. Otherwise it would be 
impossible to distinguish it from certain other acute septic disorders. It is prone 
to attack the youthful and vigorous. Chills, headache, and pain in the loins are 
the first symptoms, just as in ordinary cases. Cutaneous ecchymoses appear as 
early as the second or third day. They increase in area so rapidly that one can 
almost see them grow. They are most extensive in the hypogastric region. There 
are also ecchymoses in the eyelids, the conjunctiva, the mouth and pharynx, and, 
as the autopsy discloses, many in the internal viscera. The constitutional symp- 
toms are most severe, and the patient seldom survives the fifth or sixth day of the 
disease. 

Diagnosis. — The certainty with which we can make the diagnosis of small-pox 
in any well-developed case is equaled by the difficulty of deciding about it during 
the beginning of the disease, or even during the beginning of the eruption. At 
this period diagnosis may be impossible. When the variolous eruption is in pro- 
cess of development, it may be confounded with typhus fever, with that form of 
measles in which the papillse are prominent, with syphilitic eruptions, and with 
certain forms of erythema exsudativum, just breaking out. We can not here 
fully discuss all the factors which should be considered in making this diagnosis. 
It is important not to regard the cutaneous appearances alone, but to note all the 
other symptoms besides. But it is often necessary to watch a doubtful case for 
some time before a diagnosis can be established. 

Prognosis. — The facts which are of greatest weight in prognosis have already 
heen emphasized. We may repeat that during the initial stage the prognosis^ of 
any individual case can seldom be determined. If the first symptoms are mild, 
or if the initial erythema appears, the case is regarded hopefully. The abundance 



60 



ACUTE GENERAL INFECTIOUS DISEASES 



of the eruption has an influence upon the severity of the disease. Circumstances 
peculiar to the individual are also important — e. g., age, constitution, or alcoholic 
habits. We have already called attention to the danger of confluent small-pox, 
and to the almost absolutely fatal prognosis in the genuine hemorrhagic variety. 
The mortality varies greatly in different epidemics; on the average it may be 
taken at about fifteen to thirty per cent. Beyond doubt, the introduction of 
vaccination has decidedly lessened the fatality of the disease by diminishing 
the frequency of the severe forms. 

Treatment. — 1. Prophylaxis — Vaccination. — As in all contagious diseases, 
isolation is of little avail unless complete. This fact has led to the erection in 
late years of small-pox hospitals. All utensils used by the patient, and his cloth- 
ing, bedding, and the like, should be most carefully disinfected. The best method 
is to employ a high degree of heat— viz., 240° to 250° (115°-120° C). 

These precautionary measures are employed in many other diseases as well, 
but for small-pox we are acquainted with a special method of prophylaxis. It is 
founded upon a fact which is the most remarkable within the domain of the infec- 
tious diseases. We refer to prophylactic vaccination. It must long ago have 
been remarked that a person who has had the disease once, enjoys, to a large 
degree, immunity from any fresh infection. This suggested the idea of exposing 
children purposely to contagion, so as to insure them from small-pox for the rest 
of their lives. The actual inoculation of small-pox is said to have been long 
practiced in India and China. In the year 1717 it was employed by Lady Mary 
Wortley Montagu, of England, upon her own son, and with success. Unfortu- 
nately, however, the inoculated small-pox proves fatal in many instances; and, 
being itself contagious, it serves to spread the disease still further. Then ap- 
peared an article written by the English surgeon, Edward J enner, in 1798. This 
informed the medical profession of a fact already known to the rural population 
of his native place, but which Jenner first established scientifically, and recognized 
in all its importance. There sometimes occurs a disease similar to small-pox upon 
the teats and udder of the cow, called variola vaccina. It is apparently a local 
trouble, and it can easily be inoculated upon the skin of human beings. Vaccine 
pustules will be developed upon the spot inoculated. These almost invariably 
heal without any great constitutional disturbance ; but the person vaccinated pos- 
sesses the same immunity from small-pox as if he had had small-pox itself. This 
statement of Jenner's was soon confirmed upon every side. The result is the con- 
tinually spreading custom of prophylactic vaccination. In some countries it is 
enforced by law, and it can be opposed only by ignorance or by lamentable 
prejudice. 

To explain exactly how vaccination can protect against small-pox in this way 
is still beyond our powers ; but vaccination has at present lost much of its former 
enigmatical character, since we know that a similar immunity can be produced 
in almost all infections by inoculation with attenuated or altered virus (see the 
chapters on malignant pustule, diphtheria, tetanus, pneumonia, etc.). This anal- 
ogy has become the more certain since there is no longer any doubt, according to 
recent observations (Fischer and others), that vaccinia is, in fact, only a form of 
small-pox rendered milder and modified by transmission to animals. If we in- 
oculate a calf with the contents of a fresh small-pox vesicle from man, typical vac- 
cinia is produced. With the contents of this vaccine vesicle children can be 
inoculated without any danger, and they are no longer susceptible either to vac- 
cinia or small-pox. 

We can mention only the most important of the details relating to vaccination 
and the method of its performance. Only exceptionally do we vaccinate witk 
the contents of a human vaccine vesicle ("humanized lymph"), but we almost 
invariably use animal lymph from vaccine vesicles of calves. This is now ob- 



SMALL-POX 



61 



tained in large quantities and put on the market. The process of vaccination is 
to make three shallow incisions, 3 or 4 centimetres apart, in the skin of the upper 
arm, and to introduce the vaccine-lymph into them. The surrounding tissue 
becomes swollen in three or four days. In seven or eight days the vaccine vesicles 
are well developed, if the disease takes its normal course. Next they become 
purulent, and then dry up, and finally, on healing, leave the familiar scar behind. 
The whole process occupies about three weeks. If the vaccination fails, or is but 
partially successful, it must be repeated after a few months. The protective 
power of vaccination does not last indefinitely, and therefore re-vaccination is 
necessary every five or six years. The first vaccination of children usually takes 
place when they are three or four months old. If they are feeble we wait longer, 
unless small-pox is prevalent. 

It must be confessed that vaccination is not without its dangers. The little 
cutaneous wound made by it may lead, like any other, to sepsis or to erysipelas. 
The latter has been called vaccination-erysipelas. But such misfortunes are ex- 
tremely rare. The not uncommon " vaccine roseola " deserves especial mention. 
It appears first upon the arm vaccinated, and spreads over the rest of the body ; 
but it is not a serious matter. It is of course possible, by especially bad luck in 
the use of human lymph, that other diseases, among which syphilis is of chief 
importance, may be inoculated along with vaccinia ; but this is a very rare occur- 
rence — much more so than the enemies of vaccination pretend. If the physician 
exercise proper care in the selection of the person from whom to take humanized 
virus, it can be entirely avoided. 

[The incubation stage of vaccinia being shorter than that of small-pox, the 
prompt vaccination of an unprotected individual who has been exposed to infec- 
tion should always be practiced, if possible; oftentimes the severe disease may 
thus be prevented.] 

2. The treatment of small-pox is purely symptomatic. When the disease has 
once begun it is too late for vaccination to have any influence upon its further 
course. During the initial period we may advantageously employ cool baths to 
diminish the fever and alleviate the constitutional symptoms. An ice-bag will 
relieve the headache. We must not let the lumbar pains lead us to any but a 
cautious use of local irritants, for the pocks come out in greater abundance upon 
such portions of the skin as have been in any way irritated. If the disease proves, 
during the stage of eruption, to be varioloid, there will be no further need of 
special treatment. Good nursing and proper food will suffice. 

The true small-pox, on the other hand, demands the interposition of the physi- 
cian. He must strive to guard the regular course of the disease in the skin and in 
those portions of the mucous membrane which are accessible from being disturbed 
by secondary inflammations; for we have no doubt that the ruptured pustules 
furnish a most easy ingress to septic impurities from the surrounding atmosphere, 
so that later, when there is extensive suppuration of the skin, or analogous and 
severe disturbance in the mucous membrane, it is impossible to discriminate 
between the effects of the small-pox itself and those due to the secondary suppura- 
tion. If we were able to have the whole process go on " antiseptically " we 
should certainly have made an important advance in therapeutics. Indeed, the 
methods of treatment which have been up to this time recommended fulfill this 
indication up to a certain point, e. g., painting the skin with tincture of iodine, or 
with a strong solution of nitrate of silver — methods formerly much in vogue. 
Schwimmer's suggestion seems still better. He recommends, from the beginning 
of the eruption, the use of a paste made as follows : Acid, carbol., parts 4 to 10 ; 
ol. olivse, 40 ; cretse prseparat., 60. M. et ft. pasta mollis. This is spread on pieces 
of old linen and laid upon those parts where the eruption is apt to be worst — viz., 
the forearm, hand, and leg. The face is covered with a mask, having holes corre- 



62 



ACUTE GENERAL INFECTIOUS DISEASES 



sponding- to the mouth, nose, and eyes. The applications are changed every 
twelve hours. Under this treatment the local distress is said to be diminished, 
suppuration slight, and healing comparatively rapid. The pain and sense of ten- 
sion in the skin are often relieved by cold applications, or by simple ointment or 
oil. Under Hebra, in Vienna, continuous warm baths were employed in severe 
cases with great success. 

The treatment of the affected mucous membrane in small-pox must also meet 
the indication above mentioned. The most thorough disinfection of the mouth 
and pharynx must be aimed at. The means to be used are careful washing and 
gargling with solutions of chlorate of potash (1 to 30), carbolic acid, borax, per- 
manganate of potash, or liquor f erri chloridi. The eyes, if they need it, must also 
be appropriately treated. As to all other complications, cool baths are relatively 
the most useful remedy. They can be given without difficulty. The chief indica- 
tions for them are severe pulmonary or nervous symptoms, or continuous high 
fever. Internal antipyretics, such as quinine or antipyrine, are also employed. 
Violent nervous disturbances, such as delirium, sometimes require the cautious 
use of narcotics. There is nothing to add as to the treatment of malignant hem- 
orrhagic small-pox, for, as we have said, such cases are unfortunately almost 
hopeless. 



CHAPTER VIII 

VARICELLA 

( Chicken-pox) 

Varicella is truly one of the diseases of childhood. Adults very rarely have it. 
It is contagious, and often comes in epidemics. 

The stage of incubation does not last over thirteen to seventeen days. The 
disease begins with the appearance of vesicles, the size of a pea or a little larger, 
usually having a small red areola, and varying in number from ten to one hun- 
dred or more. The trunk usually bears the greater part of the vesicles, while the 
extremities have few. The face is frequently the seat of a considerable number, 
and sometimes there are a few upon the hairy scalp. There may be a vesicle here 
and there upon the mucous membrane of the mouth or palate. There are seldom 
any prodromata. Slight symptoms of fever may attend the eruption itself. The 
eruption is usually over in a few days, although there may be repeated crops, so 
that we often see fresh vesicles by the side of others which are drying up. Each 
individual vesicle heals quickly, and the pustulation seen in small-pox is here ex- 
ceptional. The course of the disease is completed in a week or ten days. Most 
children feel perfectly well the whole time, although there may be in rare cases 
pain in the limbs, anorexia, and a slight coryza. A severe complication is hardly 
ever seen. An unusual event is a mild nephritis. 

Exceptionally, the disease may be rudimentary, with a varicelloid roseola and 
no formation of vesicles. On the other hand, some cases present quite severe con- 
stitutional symptoms and a high fever, even reaching 105° (41° C.) temporarily. 
In most cases, however, as we have said, the child is so slightly disturbed that a 
physician is hardly thought necessary. 

The diagnosis is almost always easy. Formerly varicella was often con- 
founded with small-pox, and to this day the followers of Hebra, in Vienna, for 
some inconceivable reason, maintain the identity of the two. That they are essen- 
tially distinct is shown (1) by the epidemics of the two appearing entirely separate 
from each other, (2) by the fact that having one does not give immunity from the 



ERYSIPELAS 



63 



other, and (3) by the uniform failure of attempts to produce variola by inoculat- 
ing varicella, or vice versa. Still, we must bear in mind, in order to avoid mis- 
takes, that many dermatologists class the mildest cases of small-pox as varicella. 
Those who devote themselves to general diseases are probably all now convinced 
that varicella is a separate disease. 

The prognosis is perfectly good. There is usually no special treatment neces- 
sary, but young children should be kept in bed till the eruption has dried up. 



CHAPTER IX 

ERYSIPELAS 

(St. Anthony's Fire) 

etiology. — Erysipelas is a peculiar inflammation of the skin, recognized by 
redness, swelling, and pain. It has the peculiarity of spreading gradually, by 
direct extension, from its point of origin over a larger or smaller portion of the 
body. The cause of this inflammation, as was first shown by Fehleisen, is a local 
infection by the streptococcus pyogenes and its further extension in the skin. 
The exciting agent of erysipelas is then bacteriologically identical with the strep- 
tococcus which is the cause of phlegmonous suppuration, severe septic infection, 
etc. The reason why in the individual case 
erysipelas develops, and not some other strep- 
tococcus disease, is the special variety of in- 
fection and the further spread of the strepto- 
cocci in the deeper lymphatics of the skin, 
and in part perhaps the special " virulence " 
of the infecting germs. 

The former distinction between " trau- 
matic " and " idiopathic " or " exanthe- 
matic " erysipelas can no longer be rigidly 
maintained. Every erysipelas is in a certain 
sense traumatic, since infection with strepto- 
cocci can not occur through the unbroken skin, 
The so-called " idiopathic " erysipelas is dis- 
tinguished from " wound erysipelas " (in 
which, of course, we include puerperal erysipe- 
las, erysipelas of the newborn starting from 
the umbilical wound, etc.) only by the fact f ig . s.— The cocci of erysipelas. xTOO. 
that in the former the infection takes place in Section through a lymph-vessel in the skin, 
small, insignificant wounds of the skin which 

are easily overlooked. Such an erysipelas occurs chiefly in the face and head, and 
the following description of the symptoms refers chiefly to this facial erysipelas. 
Most of these cases of erysipelas arise from little excoriations, cracks, and scratches 
about the nose or ears, or more rarely about other parts of the face or scalp. A 
previous coryza, by the accompanying slight erosions about the nose, sometimes 
gives the opportunity for an attack of erysipelas, but sometimes the infection oc- 
curs in the mucous membrane of the nose or pharynx; then we have a primary 
erysipelas of the mucous membrane, which extends through the nasal passages and 
finally appears on the external surface of the nose. 

Facial erysipelas is most apt to attack the young, and seems to be somewhat 
more frequent in women than in men. The laity erroneously regard catching cold 




ACUTE GENEKAL INFECTIOUS DISEASES 



and getting frightened as frequent causes of the disease. If we except the pre- 
disposing causes above mentioned — viz., coryza, slight scratches, cuts, etc. — we 
usually find no cause of which we can feel certain. Often endemic influences are 
important. It has been long known that traumatic erysipelas can get so secure 
a footing in particular hospitals or wards that every wounded person treated in 
them is in danger of this disease; but the apparently idiopathic variety is some- 
times remarkably frequent in particular places (barracks, etc.). Several mem- 
bers of one family may likewise have facial erysipelas simultaneously. In nearly 
all such cases the sufferers are infected from some common source, for direct 
contagion is certainly exceptional; but patients with open wounds should never 
be put near erysipelas cases, because here the risk of infection can not be wholly 
excluded. Direct inoculation can, however, as has been proved, convey the dis- 
ease from a patient to other persons or to animals. 

In contrast with the behavior of many other infectious diseases (typhoid 
fever, measles, scarlet fever, small-pox, etc.), erysipelas is peculiarly apt to attack 
the same individual over and over again. There are persons who have facial 
erysipelas about every one or two years, and ten to fifteen times. Often the 
explanation of this apparently lies in some chronic disease — e. g., chronic 
ozsena, chronic eczema of the nostrils or ears — which makes infection easy, 
but in other cases no cause can be discovered. Of course when erysipelas 
afflicts the same person a number of times the individual attacks gradually be- 
come milder. Marasmus seems to predispose to erysipelas. At least we have 
observed that erysipelas occurred with relative frequency, in the Leipsic hos- 
pital, in patients suffering from the last stages of phthisis or cancer, or similar 
diseases. 

Clinical History. — In many cases the first subjective symptoms are simultane- 
ous with the cutaneous swelling, and these are chiefly local. There is pain and a 
sense of tension in the skin. Soon subjective symptoms of fever also appear, such 
as general malaise, anorexia, headache, and sometimes vomiting. In other cases 
the disease starts with more violent constitutional symptoms : there is an initial 
rigor, with violent headache and great languor. The local erysipelatous swelling 
appears almost at the same time with these general symptoms or sometimes a few 
days later, either because the local inflammation is at first slight or because 
it is not noticed, as in the scalp when the hair is very thick. In rare instances the 
disease begins with sore throat. We saw three almost simultaneous cases of facial 
erysipelas in one family, in which a severe sore throat lasted for four or five days 
preceding the appearance of the cutaneous disorder. We have seen a number of 
similar cases since and believe that they are due to a true erysipelatous angina — 
that is, to an erysipelas of the soft palate which extends through the nostrils to 
the external skin. In cases of erysipelas which follow a coryza we may assume, 
as stated above, that there is an erysipelas of the nasal mucous membrane pre- 
ceding the erysipelas of the skin. 

The erysipelatous process in the skin is almost always circumscribed at first. 
It usually starts on the nose, less often upon the cheek, the ears, or the hairy scalp. 
The skin becomes considerably swollen, grows red, smooth, 1 and shiny, and feels 
hot. The redness and swelling keep spreading. There is usually a sharp, elevated 
ridge, perceptible to sight and touch, separating the diseased from the still healthy 
portion of the skin. As long as the erysipelas is spreading, we see stretching out 
from its border, or somewhat removed from it, small red streaks and spots which 
gradually increase in area and intensity, and finally coalesce. Any decided fold in 
the skin may hinder for a time the extension of the disease. The naso-labial folds 
are particularly apt to limit it. The border of the hairy scalp frequently forms a 
terminal line; but the whole scalp may be attacked, the inflammation stopping 
only when it reaches the nape of the neck. The boundary of the erysipelas in the 



ERYSIPELAS 



65 



hairy scalp can usually be quite accurately determined by palpation (swelling and 
local tenderness). 

It is only in a relatively small number of cases that it spreads farther yet, 
attacking the back, the arms, and the anterior surface of the trunk, or even 
extending to the feet. This is known as erysipelas migrans. The facial erysipelas 
may be healed long before the disease ceases to extend over the other parts of 
the body. When the spreading process is about to cease, the inflammation 
usually becomes decidedly milder, appears only in isolated spots, and finally 
stops completely. In most cases, only the face, the ears, and a part of the scalp 
are attacked. 

It is not a rare thing for vesicles or bullae to form in the portions of skin 
attacked. Such cases are called erysipelas vesiculosum or erysipelas bullosum. 
The serum may change to pus in these blisters, and then we have erysipelas 
pustulosum. Exceptionally the infiltration of the skin becomes so intense as to 
result in a localized necrosis or gangrene — erysipelas gangrenosum. The parts 
most apt to be attacked by this are the eyelids, where abscesses sometimes form. 

Microscopic examination of the skin shows a marked hypersemia of all the 
blood-vessels and a very considerable infiltration of both the skin and the subcu- 
taneous connective tissue with serum and cells. In those parts where vesicles are 
formed there are many dead and disintegrated epithelial cells in the rete Mal- 
pighi. In the parts where most streptococci develop there may also be necrosis 
of the deeper layers of the skin. We have already said that there may be many 
streptococci in the lymphatics of the skin, but they are found only in the first 
fresh stages of the inflammation. When the inflammatory exudation has reached 
its full height, the streptococci have usually wholly disappeared. As a rule we 
find only a few or no streptococci in the contents of erysipelas vesicles. 

The inflammation in any one spot usually ends four or five days after it has 
made its appearance there. There is apt to be much attendant desquamation. 
The face is often left with a finer complexion than it had before. 

The other symptoms, of which the constitutional disturbance and the fever are 
chief, correspond pretty closely to the severity and extent of the cutaneous lesion. 
It is comparatively seldom that this correspondence does not exist. 

The fever in facial erysipelas usually rises rapidly at first, and to a considerable 
height. We have seen but few cases where the high fever was delayed till a day 
or two after the skin was attacked. The temperatures observed in erysipelas are 
often extreme: 106° (41° C.) is not at all rare. The highest we ever saw was 
107.2° (41.8° C). While the erysipelas continues or is spreading, the fever is sel- 
dom continuous, nor are the remissions insignificant. Pronounced intermissions, 
even down to normal, are very frequent, but are followed again by a rapid and 
great rise of temperature. The fever may terminate with a genuine crisis. In 
intense cases of considerable extent, or in erysipelas migrans, the termination 
is more apt to be by a more or less gradual lysis. We have seen the cutaneous 
inflammation in erysipelas migrans still extend itself a little, in a rudimentary 
form, after the fever had completely ceased. 

The headache is often intense, and seems to result not merely from the inflam- 
mation of the scalp but from disturbances of the circulation in the underlying 
parts, or more probably from the action of a toxine. Other severe cerebral 
symptoms are also relatively frequent. The patient may be very restless, excited, 
and wakeful. At night there may be mild or even violent delirium; or there 
may be decided stupor. All these symptoms are in chief part due to the general 
intoxication caused by the infection ; but they also justify a surmise, as we have 
said, that there is a circulatory derangement in the meninges and the brain itself, 
resulting from the inflammation of the scalp. In drunkards, delirium tremens is 
not infrequent. 

5 



66 



ACUTE GENERAL INFECTIOUS DISEASES 



One of the most constant symptoms in facial erysipelas is gastric and intestinal 
disturbance. There is usually complete anorexia. The tongue is thickly coated. 
Vomiting is frequent, not only at the beginning but during the course of the dis- 
ease. There is constipation ; or there may be quite severe diarrhoea. There is no 
pathological lesion known corresponding to these clinical symptoms. The spleen 
is usually moderately swollen. In all severe cases we find in the blood a pro- 
nounced leucocytosis (16,000 to 18,000 leucocytes in a cubic millimetre). Strep- 
tococci are not found in the blood. 

The entire duration of the disease varies greatly in different cases. A very 
light case may get well in a few days. Most cases of average severity last a week 
or ten days. Erysipelas migrans may continue for many weeks. We have sev- 
eral times seen a relapse come on after a number of days of complete apyrexia. 
Either the face would be once more attacked, or some portion of the skin which 
had previously escaped. 

Local complications are comparatively rare and insignificant in erysipelas. 
The lymphatic glands of the throat and back of the neck are very frequently 
somewhat swollen, but seldom attain great size. Bronchitis and lobular pneu- 
monia may develop in severe cases, but are not at all characteristic. Some ob- 
servers call attention to the occurrence of pleurisy, endocarditis, and pericarditis ; 
but these complications also are very rare. The spleen is usually slightly swollen. 
Sometimes there is an icteroid hue. The urine frequently contains a small 
amount of albumen, and in severe cases of erysipelas acute hasmorrhagic nephritis 
is not so very rare, but it almost always disappears entirely. The albuminuria 
usually disappears a few days after the fever. Swelling of the joints has been 
repeatedly observed. It is more frequent in the severe surgical forms of erysipelas, 
which are combined with universal septic and pysemic conditions of the system. 
Purulent meningitis may complicate an erysipelas located in the head, but it is 
very rare. We should be exceedingly cautious about asserting its existence even 
when the cerebral symptoms are very pronounced. 

Cutaneous complications are relatively frequent. We have seen herpes labialis 
quite often, and a number of cases of urticaria. Of much greater importance are 
the cutaneous abscesses which occur in severe cases. These are due to a phleg- 
monous or even gangrenous inflammation of the connective tissue. Their most 
frequent seat in the face is the eyelids, as already stated ; and in that case the eye 
may itself be endangered. At the close of severe cases of erysipelas migrans, 
numerous abscesses may develop in the skin of the trunk and extremities, delay- 
ing convalescence. Since, as we have said, the streptococcus of erysipelas is abso- 
lutely identical with the streptococcus pyogenes, all purulent inflammatory com- 
plications of erysipelas are to be referred to the local or metastatic action of 
the original infectious germs, but erysipelatous nephritis is probably of purely 
toxic origin. 

The diagnosis of erysipelas is almost always easy when once the cutaneous 
lesion has developed. Phlegmonous inflammation of the skin and lymphangitis 
are to be eliminated ; but this is always possible, with proper care. After a single 
examination, we may confound it with acute facial eczema bf great severity, or 
even with a marked urticaria. Chief attention should be paid to the characteristic 
border of erysipelas and to its manner of extension. In erysipelas beginning in 
the hairy scalp the local inflammation may easily be overlooked, being completely 
masked by the severe general symptoms. 

The prognosis of facial erysipelas, when it attacks a healthy person, is very 
favorable. In drunkards a severe case may be complicated by delirium tremens, 
and the issue be unfavorable. We saw one case end fatally because of gangrene 
of the eyelids, followed by purulent inflammation of the orbital connective tissue. 
Erysipelas migrans may so exhaust the powers of feeble patients as to become 



DIPHTHEKIA 



67 



dangerous. The prognosis of surgical erysipelas is relatively more unfavorable, 
but it can not be considered here. 

Treatment. — The treatment of ordinary erysipelas of the head and face, 
which is the main question here, is purely symptomatic. The large number of 
remedies recommended (tincture of iodine, nitrate of silver, iodoform, ichthyol, 
carbolic acid, collodion, etc.) shows that they can not any of them materially 
influence the morbid process. It is easy to be deceived about their efficacy, as most 
cases are relatively benign. We therefore usually content ourselves with powder- 
ing the affected skin or covering it with oil or vaseline to relieve the tension, and 
also with putting on an ice-bag if the patient likes it. We have found no proof 
that we can limit the advance of the disease mechanically by applying firm ad- 
hesive plaster to the boundary of the erysipelas, etc. We can expect no specific 
action from internal remedies (PirogofPs camphor cure, liquor ferri sesquichlo- 
rati, etc.). 

Apart from alleviating the local discomfort, some other symptoms occasionally 
demand special consideration. Severe headache and other severe nervous symp- 
toms may be relieved by the local use of cold or by antipyrine and similar remedies. 
With high temperature cool baths or antipyretics internally may be used with 
benefit, but in general the fever does not often demand energetic treatment, since 
in erysipelas, as we have said, considerable spontaneous remissions of temperature 
often occur. When there are marked gastro-intestinal symptoms we may pre- 
scribe hydrochloric acid, opium, etc. 

Only when there is a true migrating erysipelas and the disease spreads over the 
body should we try more energetic methods. Heuter recommended subcutaneous 
injections of a two-per-cent. solution of carbolic acid a little way from the edge 
of the erysipelas. Although this method is certainly rational, we have usually 
seen no striking results from it. It seems more effective to scarify the erysipela- 
tous skin and then wash it with a corrosive-sublimate solution, as lately recom- 
mended. In the severe cases the main point, after all, is to maintain the patient's 
strength by nursing and food. If cutaneous abscesses form, they should be opened 
promptly, when they usually soon heal. 



CHAPTEE X 

DIPHTHERIA 

(DipMheritis. Croup. Cynanche contagiosa) 

iEtiology and General Pathology. — Clinically, "diphtheria" means a certain 
well-characterized, specific, acute, infectious disease, the chief visible lesion of 
which is a croupous-diphtheritic inflammation of the pharynx and upper air-pas- 
sages. In a purely pathological sense, however, the terms " croupous " and " diph- 
theritic " have a broader meaning. They denote a certain form of inflammation 
which may occur in the mucous membrane of almost any part of the body. It is 
frequent in the intestine and bladder. There is great diversity in the causes 
which may produce it. 

The pathological characteristic of every croupous-diphtheritic inflammation 
consists in the formation of a fibrinous exudation. This may either be a croupous 
membrane, which is grayish white, rather firm and elastic, and which can be lifted 
off with comparative ease from the mucous membrane upon which it rests, or it 
may be a diphtheritic infiltration with necrosis of the tissues. Here the exudation 
is more or less deeply imbedded within the proper structure of the mucous mem- 



OS 



ACUTE GENERAL INFECTIOUS DISEASES 



brane itself. There is no essential difference between croup and diphtheria ; diph- 
theritic inflammation is the severer form of the disease, croupous inflammation the 
milder. In diphtheria the fibrinous exudation is preceded by a necrosis of the 
epithelium and of the underlying tissues of the mucous membrane as well, while 
in the case of croupous exudation the necrosis is limited to the epithelium. The 
croupous membrane never rests upon an intact mucous surface, but replaces the 
epithelium, which has already been totally or in very large part destroyed. Elaky 
remnants of the epithelium, no longer nucleated, are sometimes found in the 
meshes of the fibrine. The preceding destruction of the epithelium is essential to 
the occurrence of fibrinous, croupous inflammation. The fibrinous exudation can 
be formed in those places only where the cause which excites the inflammation 
kills the epithelium at the same time. It is still undecided whether or in what 
degree the epithelium takes part in the formation of the croupous membrane. 
Most pathologists hold that the material for the fibrine comes from the fibrinogen 
of the inflammatory matter which transudes through the walls of the vessels, and 
also from the disintegrated migratory white blood-globules. These last are 
abundant throughout the deposit itself, and still more numerous in the entire 
tissue of the mucous membrane beneath the croupous or diphtheritic exudation. 
If recovery takes place in croup, all that is needed after the exudation has been 
cast off is the renewal of the epithelium, which can be accomplished through the 
exclusive agency of the remnants of epithelium left along the borders of the dis- 
eased spot. In diphtheria, however, the entire necrotic portion of mucous mem- 
brane must slough off, a line of demarkation being formed, and cicatricial tissue 
replaces the necrosed portion. 

The above is a bare outline of the present views about croupous and diph- 
theritic inflammations. They have been reached gradually through the labors of 
E. Wagner, Weigert, and others. We have not yet touched upon the serological 
factors; but what precedes renders it evident how manifold they may be, for 
many causes which destroy the epithelial layer of the mucous membrane, and at 
the same time promote inflammation, may excite croup. We have mechanical 
causes, such as impacted fasces, gall-stones, renal calculi; chemical irritants, 
caustics, like ammonia and the acids; and, finally, a number of specific, infec- 
tious, disease-producing poisons. Among these is the specific poison of diphtheria 
proper. 

There has been no doubt for a considerable period that true pharyngeal diph- 
theria could be produced only by a specific organized cause. To demonstrate this, 
however, has been thus far extremely difficult, for there are in the diseased parts 
a great number of diverse micro-organisms, originating in the mouth and throat, 
and really secondary to the diphtheritic process ; and, although they of course are 
entirely different from the specific " diphtheritic bacteria," it is very hard to 
separate them. Nevertheless Lofner has of late succeeded in solving the ques- 
tion of the origin of diphtheria in an apparently decisive way. Erom numerous 
investigations by Roux and Yersin, Heubner, and others, there can scarcely be 
a doubt at present that the specific diphtheria bacillus is a form of bacillus char- 
acterized by a definite and particular granular formation, a club-like swelling at 
the ends, and special methods of growth on blood-serum. The diphtheria bacilli 
are found only on the diseased portion of the mucous membrane or the point 
of inoculation, and never in the blood or the internal organs. This fact is of the 
greatest pathological significance, and it has been established not only for diph- 
theria in man, but also for experimental diphtheria in animals. In pharyn- 
geal diphtheria they are found chiefly on the under surface of fresh false mem- 
brane. The severe general symptoms of diphtheria, however, except when due to 
secondary infection (vide infra), depend upon the poisonous chemical action of 
certain substances produced by processes of metabolism in the bacilli. Little 



DIPHTHERIA 



69 



that is definite is known, however, as to the precise chemical nature of these 
" toxines." 

We may accept it as a fact that the diphtheria bacilli or their spores reach 
the pharyngeal cavity directly through the inspired air or in some other way, 
and there, in case they attach themselves to the mucous membrane and increase, 
produce diphtheria. In a few rare cases they seem to be inhaled into the larynx 
at once, and to excite there a "primary laryngeal croup" (vide infra). The 
source of the infection is always to be referred ultimately to another case of 
diphtheria, but the way in which the disease spreads can not always be traced in 
detail. In many cases, of course, a direct (" contagious ") transmission of the 
poison is evident, as from coughing, or the many cases of the disease in physi- 
cians and nurses from sucking the croupous membrane out of the tracheotomy 
tube in children, etc. If several children in one house fall sick, as often hap- 
pens, we may here suspect a direct transmission of the disease, although it is 
also possible that in such an event several cases may arise from the same source 
of infection. We do not yet know positively how far the diphtheria bacilli can 
lead an independent existence outside of the human body (the earth, the floors 
of dwellings, etc.). It seems certain that the infection can be carried from one 
person to another by some intermediary, by clothing, linen, toys, and other objects 
to which the diphtheria poison clings. The resistance of the latter to external in- 
fluences — temperature, drying, etc. — is very considerable. After complete recov- 
ery from diphtheria, virulent diphtheria bacilli may be found in the oral cavity 
for a considerable time. This is particularly to be noted on account of its prac- 
tical importance. We must mention, in conclusion, that attention has lately been 
called to the possibility of the transmission of diphtheria from sick animals 
(hens, doves, calves, [cats] ) to man, since diseases resembling diphtheria undoubt- 
edly occur in the domestic animals mentioned. 

Diphtheria, as is well known, is a disease chiefly of childhood, but some 
cases, and even very severe ones, may occur in adults. In advanced life the dis- 
ease is very rarely seen. In large cities sporadic cases occur from time to time, 
but the disease often takes on an epidemic character. At such times some places 
appear to be much more subject to the disease than others. 

[While it seems in the highest degree probable that the poison is usually purely 
local at the start, cases occur which suggest that constitutional infection through 
the pulmonary blood-vessels may precede the local manifestations. Infection 
through the alimentary canal is not probable, though its occurrence can not be 
positively denied. 

There are still points in the aetiology and pathology of this affection which are 
involved in obscurity. Much has been said and written in this country and in 
England about the relations of filth and diphtheria. That filthy surroundings 
contribute a soil favorable to the development of the poison, and at the same time 
diminish the resisting power of the human organism, can not be doubted ; but, as 
long as the parasitic theory of infectious diseases prevails, sewer-gas and the like 
must be classed among the predisposing or accessory causes. 

Some of the frightfully virulent epidemics of diphtheria in sparsely settled 
country districts and on the Western plains are difficult to explain under the 
theory that each case is mediately or immediately the result of a previous case; 
these difficulties will, however, doubtless be cleared away in time.] 

Clinical History. — The incubation is rather brief, seldom exceeding two to five 
days. The disease itself almost always begins with general malaise, headache, 
fever, and pain on swallowing. Little children, however, often do not complain 
of this last symptom, and in older children the sore throat may not be very 
troublesome at first. It is therefore a very important rule for the physician to 
examine the throat carefully in every child who presents ill-defined general symp- 



70 



ACUTE GENERAL INFECTIOUS DISEASES 



toms. If diphtheria is beginning-, we find redness of the soft palate, and more or 
less swelling of the tonsils. Upon the inner surface of the latter, and perhaps 
upon the arch of the palate and the uvula also, are spots covered with a grayish- 
white coating, which is quite firmly adherent to the mucous membrane. They are 
less frequent at first upon the posterior wall of the pharynx and the hard palate. 
Their extent varies greatly in different cases. In the mildest they are chiefly 
confined to the tonsils, attacking the soft palate or the tonsillar surface of the 
uvula but little if at all. In severer attacks the spread of the false membrane 
during the first days of illness is rapid. Almost invariably there is a very early 
and considerable swelling of the lymph-glands at the angle of the jaw. The con- 
stitutional symptoms persist. The children are restless. There is complete an- 
orexia, and frequently vomiting. The temperature-curve is not typical. It is 
irregular, but is often rather elevated. In true diphtheria such high tempera- 
ture, 104°-105° (40°-41° C), as is common in follicular tonsillitis, is certainly 
exceptional. On the other hand, fever may be slight or almost absent, even in 
the worst cases. The pulse is very rapid. The urine may have a trace of 
albumen. 

In mild cases the local and constitutional symptoms remain moderate ; and at 
the end of a week or ten days there is decided improvement, with rapid convales- 
cence. In severe cases, however, dangerous symptoms appear, perhaps early; the 
croupous inflammation involves neighboring organs, or a severe constitutional 
condition is developed. 

The diphtheria very frequently extends into the nose. This " diphtheritic 
coryza," though not in itself dangerous, is usually a sign that the case is a severe 
one. The inflammation of the nasal mucous membrane may be simply muco- 
purulent (from secondary infection with streptococci?), but it may also be 
croupous. It is betrayed by the abundant purulent discharge. Excoriations and 
superficial ulcers are usually soon produced at the edge of the nostrils. There 
may be nose-bleed. 

A much more dangerous complication is the extension of the croupous inflam- 
mation into the larynx. This creates a mechanical hindrance to respiration, 
which proves fatal in a great many cases, as the child's larynx is so small. For- 
merly " croup " — i. e., croupous inflammation of the larynx — was regarded as a 
different disease from diphtheria. Many specialists in children's diseases still 
maintain this view ; but it is in direct opposition to all anatomical, clinical, and 
^etiological facts. We grant that there are cases where the pharynx is slightly 
affected, while the croupous inflammation of the larynx is extreme ; and once in 
a great while the diphtheritic infection results in croupous laryngitis and trache- 
itis alone, the pharynx escaping disease. Still the proposition that there are two 
distinct diseases, " croup " and " diphtheria," is absolutely untenable. In the 
overwhelming majority of cases the throat is first affected and then the larynx. 
We should also consider how easily slight lesions in the pharynx may be over- 
looked, especially if located upon the posterior surface of the soft palate or upon 
the epiglottis. Cases of what is called " ascending croup," in which the laryngeal 
affection precedes the appearance of the disease in the pharynx, are, to say the 
least, very exceptional. 

Hoarseness is usually the first indication that the diphtheria has attacked the 
larynx. Then follows the peculiar, harsh, ringing, " croupy cough," so dreaded by 
the parents, and, finally, there are signs of beginning laryngeal stenosis. Respira- 
tion is not much accelerated, but is labored, and the accessory muscles of respira- 
tion are called more and more into action. The child becomes more restless and 
anxious. Its face grows pale and livid. Even in children who can make no 
definite statement as to their subjective sensations these symptoms which we 
have mentioned are very noticeable. The chief cause of the dyspnoea is undoubt- 



DIPHTHERIA 



71 



edly the mechanical stenosis due to the croupous deposit. Paralysis of the laryn- 
geal muscles may perhaps be a factor. If portions of the false membrane become 
partially detached, they may act like valves, being sucked in at each inspira- 
tion, and pushed aside by the current of expired air. If greater stenosis occurs, 
respiration becomes noisy, resembling snoring. Inspiration, particularly, is pro- 
longed and " sawing," and is attended by marked depression of the larynx toward 
the sternum. An important diagnostic point is the drawing in during inspiration 
of the supra-sternal region, the epigastrium, and the lower part of the sides of the 
thorax. This is the direct result of the obstructed flow of air into the lungs. As 
the lungs do not expand enough to correspond to the inspiratory dilatation of the 
thorax, the parts mentioned are forced in by atmospheric pressure. The degree of 
dyspnoea may vary at different times. The false membrane may be loosened and 
coughed up, rendering respiration easier for a time, till fresh exudations or dis- 
placements of membrane cause renewed distress. Recovery is still possible. The 
membrane may be expectorated and no more be formed. Unfortunately, this 
happy termination rarely occurs. In most cases the symptoms of suffocation in- 
crease more and more, respiration grows quicker and more superficial, and the 
child becomes more and more stupefied by the excess of carbonic dioxide in the 
blood. The pulse gets very small, rapid, and irregular. There are mild convul- 
sions and then death. 

The autopsy in these cases usually discloses that the croupous inflammation 
has extended into the larger bronchi or even into the smaller. The lumen of the 
bronchioles may be almost completely occluded by false membrane. This croup- 
ous bronchitis gives rise to no especial auscultatory phenomena during life, 
so that often we suspect it rather than diagnosticate it. Its clinical signifi- 
cance, however, is very great, since, even in adults, it may cause death by suffoca- 
tion without any especial stenosis of the larynx. If it is present, respiration may 
not be materially relieved in spite of tracheotomy. 

Beside the dangers attendant upon the local extension of the diphtheritic 
inflammation, the general intoxication of the body must be regarded as the second 
most important circumstance in our general estimate of the disease. As men- 
tioned above, the diphtheria bacilli produce an extremely poisonous toxine, which 
enters the circulation and which may give rise to the severest symptoms. Our 
knowledge of human diphtheria is not yet so far advanced that we can state posi- 
tively what particular symptoms are due to this intoxication, but, special attention 
must be called to the fact that the general symptoms are often very slight, in spite 
of extensive local croupous inflammation. On the other hand, where the local dis- 
ease is relatively slight, severe general symptoms sometimes occur which may 
justly be referred to this diphtheritic intoxication. Among these severe general 
symptoms are somnolence, which may increase to complete sopor, an increase in 
the pulse to 120 or 140, progressive cardiac weakness, and collapse. The con- 
ditions are different in those cases which are termed septic diphtheria. Here 
the local disease in the pharynx usually has a special appearance : instead of the 
croupous deposits we see a deeper-seated necrotic destruction of mucous mem- 
brane covered with a foul-smelling, greasy, purulent deposit (" gangrenous diph- 
theria"). In such cases the lymph-glands in the neck are almost always much 
swollen. The tongue is dry and fissured, and a stinking secretion runs from the 
nose. The temperature is usually not very high, but the pulse is very rapid and 
small. In these cases there is certainly a secondary septic infection, probably 
in most cases from streptococci, as in scarlatinal diphtheria (vide supra). Gen- 
eral septic intoxication and secondary septic inflammation are now mixed with 
the original disease, and, as we have said, it is often hardly possible to trace in 
an individual case the precise origin of the morbid condition. 

These considerations must also be borne in mind in our study of the symptoms 



72 



ACUTE GEXEKAL INFECTIOUS DISEASES 



manifested in other organs in diphtheria. We mnst first mention the direct local 
extension of the original specific diphtheritic process to the neighboring parts. We 
have already said that the nose, larynx, trachea, and bronchi are often involved, 
but the dense squamous epithelium of the oesophagus and the mucous membrane 
of the stomach, which is protected by its secretion, are very rarely affected. We 
must add, however, that diphtheria often extends to the Eustachian tube and mid- 
dle ear, and also to the anterior part of the oral cavity (gums, lips), and through 
the nose to the lachrymal canal and the conjunctiva. The latter may also be 
affected by the direct conveyance of the infectious matter by the finger, etc. 
In a similar way diphtheria may sometimes involve the external genitals (in 
girls) or any accidental wounds or injuries of the skin, such as blistered sur- 
faces, etc. 

Of the internal organs, the lungs, heart, and kidneys demand chief attention. 
In the lungs, beside croupous bronchitis, pneumonia often develops in severe cases. 
This is usually a lobular catarrhal pneumonia, more rarely lobar croupous pneu- 
monia. Although we can not absolutely deny that the pneumonia may some- 
times be of a true diphtheritic nature, the majority of cases of pneumonia de- 
veloping in diphtheria must certainly be classed as secondary affections, due to 
the inhalation and development of secondary agents (probably streptococci), 
which may readily take place. After the original diphtheria has disappeared the 
secondary lobular pneumonia may long prevent recovery or even cause a fatal 
termination of the illness. The condition of the heart in diphtheria is of especial 
importance, because severe functional impairment, probably of toxic origin, is 
common. Even when the fever is slight the pulse may sometimes be very rapid, 
small, and often irregular. An abnormal slowness of beat is much rarer. It is 
especially to be borne in mind that even in apparently mild cases there may be 
^ery dangerous cardiac weakness. Even during convalescence we repeatedly see 
audden death which must be regarded solely as "heart-failure." The autopsy 
shows that gross disease of the heart is very exceptional in diphtheria, but degen- 
eration of the muscular fibers and little interstitial myocarditic foci of secondary 
origin are often found in severe cases. It is at present quite impossible to esti- 
mate the actual clinical significance of these anatomical changes, since it is at 
least probable that disturbances of the innervation of the heart cause the car- 
diac weakness as much as these lesions of the cardiac muscle. 

Since nephritis is especially common in septic diphtheria, it is hard to decide 
whether it is due to the primary disease or is to be considered a secondary compli- 
cation. Its clinical significance is not very great, since it neither materially 
modifies the general picture nor has any definite bearing on the result of the 
disease. (Edema, uraemia, etc., are only rarely seen in diphtheritic nephritis. 
The macroscopic changes in the kidney are usually very slight. Microscopically 
we find the various degenerative conditions of acute nephritis (vide infra). 

The Nervous Sequelae of Diphtheria. — The convalescent from diphtheria is 
liable to be attacked by certain nervous sequelae. Of these, diphtheritic paralysis 
is the most important. It appears about one or two weeks after the throat trouble 
ceases, or perhaps earlier, and it is quite as likely to follow mild cases as severe 
ones. It attacks the soft palate by preference. The voice becomes nasal and 
deglutition difficult. The naso-pharjmx is imperfectly cut off during the act of 
swallowing, and with each attempt liquid regurgitates through the nose. Usually 
the pharyngeal mucous membrane is hypoaesthetic at the same time, and de- 
prived of its reflex excitability. There may also be paralysis of the vocal cords 
upon one or both sides, and this again is frequently combined with anaesthesia of 
the mucous membrane of the throat. There may be paralysis of the ocular mus- 
cles, of which those controlling accommodation are most apt to be affected, render- 
ing the vision for near objects imperfect. Paralysis of the muscles of the trunk 



DIPHTHEKIA 



73 



and extremities is least frequent, but it may be very extensive. Sometimes sev- 
eral of these parts are paralyzed simultaneously. Thus we see quite often paral- 
ysis of the soft palate and of the muscles of accommodation combined. In some 
cases there is well-marked ataxia of the lower limbs with or without paresis. 
This renders the gait very uncertain and tottering, the tendon reflex is almost 
always abolished, while sensation is affected slightly if at all. Very rarely diph- 
theria is followed by contracture of the hands or other parts, by difficulty in artic- 
ulation and paresis of the bladder. A paralysis of the pharynx is sometimes left 
behind, so that the children have to be fed for weeks through an oesophageal tube. 
It is a remarkable fact that not only in almost every case of the nervous dis- 
orders which we have mentioned, but often also in individuals who have entirely 
escaped them, there may be no patellar reflex after diphtheria for weeks or even 
months. With regard to the pathological state, it is probably a degenerative con- 
dition of the corresponding peripheral nerves, not only in the post-diphtheritic 
paralysis, but also in the cases of post-diphtheritic ataxia (see the chapter on mul- 
tiple neuritis). These degenerations are probably due to the poisonous chemical 
action of certain toxines which are produced directly by the vital processes of 
the diphtheria bacilli. It is therefore of great interest to note that paralysis 
has been produced experimentally in animals by the action of diphtheritic toxine 
by Eoux and Yersin and others. The prognosis of all the nervous sequelse of diph- 
theria is very favorable, and even in severe cases complete recovery usually takes 
place in the course of a few weeks or months. This is in harmony with the periph- 
eral nature of the disease. But there is one paralysis which is highly dangerous — 
that of the heart, as already mentioned. It may occur suddenly during convales- 
cence. Probably it is analogous to the other nervous derangements, and the 
result of degeneration in the [nuclei or] fibers of the pneumogastric. 

Diagnosis. — The physician will seldom fail to recognize a case of actual diph- 
theria if he pays proper attention. The characteristic patches and the severe gen- 
eral and local symptoms make the diagnosis certain. It is much more common to 
mistake other forms of sore throat, particularly in adults, for diphtheria. The 
most deceptive are follicular and necrotic tonsillitis (vide infra). We must not 
suppose that every white spot upon the tonsils is diphtheritic, and we must speak 
of " diphtheria 93 only when there is an actual croupous inflammation in the phar- 
ynx with a true membranous deposit. The practiced eye can usually distinguish 
at the first glance the plugs of pus limited to the follicles of the tonsils, which are 
usually multiple, and also the slight and superficial necrosis of mucous membrane 
limited to the tonsils in necrotic angina. Of late, it has often been proved by 
bacteriological examination that in these tonsillar affections there are no diph- 
theria bacilli, and that they therefore are not true diphtheria. 

We must add, however, that there are light forms of true diphtheria in which 
the pathological changes assume a milder form, resembling the tonsillar affections 
just mentioned. In such cases we are therefore certainly justified, especially 
in dealing with children, in bearing in mind the necessary precautions, but in our 
opinion the physician should never alarm the family by the justly dreaded word 
" diphtheria " without sufficient reason. 

An absolutely definite diagnosis between diphtheria and the other tonsillar 
diseases can be made only by bacteriological examination. This is at present 
still too difficult a matter in diphtheria to be within the scope of every physician, 
but the constantly increasing number of good bacteriological laboratories renders 
it possible for almost every physician to obtain bacteriological examination of 
the suspected deposit in doubtful or important cases. An experienced clinician 
can usually make a correct diagnosis and prognosis even without a " culture." 

[When the membranes are confined to the nose, the diagnosis may be more or 
less difficult ; but it is especially in cases in which the nasal mucous membrane is 



74 



ACUTE GENERAL INFECTIOUS DISEASES 



involved that we encounter great swelling of the glands at the angles of the jaw. 
There is also apt to be a thin, acrid, bloody, or sero-purulent discharge. 

Jacobi states that while diffuse pharyngeal injection may or may not point to 
imminent diphtheria, marked local congestion is either traumatic or diphtheritic. 
An examination of the urine should never be neglected in doubtful cases : in diph- 
theria a trace of albumen is very common; in simple or follicular sore throat 
albumen is very rare, if indeed it occurs at all.] 

Prognosis. — The dubious prognosis of true diphtheria is universally known, 
even by the laity. The very fact that the best-developed and healthiest children 
so often fall victims to it associates the name diphtheria with the saddest mem- 
ories. There are indeed many mild cases which recover in a week or two, and 
severer ones which end happily in three or four weeks ; but in most cases, where 
the process extends into the larynx, or the symptoms of a severe constitutional in- 
fection occur, the prognosis must be regarded as very serious. Only recently, 
however, since the introduction of the serum treatment, has the prognosis even 
of severe diphtheria become considerably more favorable. Formerly, before the 
serum treatment, it was regarded as a relatively favorable result if one half of the 
children with diphtheria in the hospitals, on whom tracheotomy was done, re- 
covered! Sixty or seventy per cent, of the children operated on often died. At 
present, however, the mortality of the tracheotomy cases, treated at the same 
time with serum, has fallen to about twenty-five per cent., and these are only the 
severe cases in which the serum treatment was begun late. The improved prog- 
nosis under the serum treatment appears much more favorable if we compare the 
whole number of cases and the death-rate of diphtheria before and after the in- 
troduction of this treatment (Heubner, Widerhofer, Baginsky, etc.). 

In general, diphtheria is to be regarded as the more serious the younger the 
child is. In later childhood, after the eighth or tenth year, the number of dan- 
gerous cases is much less. The description of the symptoms shows sufficiently 
what the dangers of the disease are. and how they are to be recognized. TTe 
would state once more that, even in apparently mild cases, the danger of sudden 
paralysis of the heart, though fortunately rare, always demands the greatest 
caution. 

Treatment. — Up to a short time ago it was impossible to say anything in re- 
gard to any generally recognized treatment of diphtheria which was really effect- 
ive, but very recently a method of treatment has been discovered, chiefly by 
the important and interesting investigations of Behring and Roux, which de- 
serves to be called an actual specific. If further observations confirm the pres- 
ent results, this treatment is one of the most brilliant and triumphant medical 
acquisitions. 

Behring found, in continuing the important discoveries of Pasteur, Buchner, 
and others, that certain protective matter (" antitoxine ") was formed in the 
blood-serum of those animals (sheep, goats, horses, etc.) which had been infected 
with artificially weakened cultures of diphtheria bacilli. If the animal survive 
the milder infection, it is less sensitive to a severer infection, and, finally, by 
continued inoculation, it may even become completely immune to the severest in- 
fection. The blood-serum of such immune animals can now be used in the treat- 
ment of diphtheria in man. The treatment is simple, and consists in injecting 
the serum under the skin of the child who has diphtheria by means of a carefully 
disinfected syringe. The best places for injection are the anterior chest wall or 
the thigh. Since the amount of serum to be injected is usually about five cubic 
centimetres, we should use a special syringe which is not too small. The best are 
made like a Pravaz syringe with an asbestos packing. It is to be understood that 
the injections must be made with the strictest aseptic precautions. There are 
three different preparations of serum in the market, varying according to the 



DIPHTHERIA 



75 



strength of their immunizing action. In fresh and milder cases we inject Serum 
I ("600 units of antitoxine in severer and more advanced cases, especially if 
there be any signs of disease in the larynx, we use at once Serum II (" 1,000 units 
of antitoxine "), or even Serum III. According to the severity of the case, or 
according to its course, we repeat the same injection or a -weaker dose of the same 
once in the next twelve to twenty-four hours. In many cases of moderate severity 
a single injection of Serum II sufhces. The favorable action of the serum is 
shown chiefly by the fact that the affection does not extend after the injection. 
The existing croupous deposit is thrown off in the course of the next four or 
five days. 

The serum injections have no injurious action. Urticaria sometimes occurs 
after an injection, but it has no serious significance. There is no proof that 
albuminuria and post-diphtheriuc paralysis are seen oftener in cases treated 
with serum than in other cases. TTe need not explain further that-the serum must 
be ineffectual in severe septic diphtheria. Taking everything into consideration, 
it is therefore the duty of the physician, in accordance with our present knowl- 
edge, to use the serum in every case of true diphtheria in children. At present 
it is, of course, impossible to pronounce a final judgment on the whole question; 
but it seems beyond a doubt that we physicians are standing on the threshold of 
an entirely new era in the treatment of infectious diseases. 

It is of the greatest practical importance that the serum treatment be begun as 
early as possible. The most favorable results are seen in children treated on the 
very first days of the disease. [In merely suspicious cases, therefore, it would 
seem wise to administer the antitoxine at once, and thus give the patient the 
benefit of the doubt. — V.] Local treatment of the affected places in the phar- 
ynx at the same time is unnecessary. We would, however, emphasize the impor- 
tance of a general cleansing and disinfection of the whole oral cavity by gargling 
and rinsing with dilute solutions of potassic chlorate, salicylic acid, corrosive sub- 
limate (1 to 3,000), etc. Inhalations may also be used, with caution, for the same 
purpose. It is also very important to watch the child's nutrition carefully in 
order to keep up the strength. Milk, egg's, meat juice, small quantities of wine, 
etc., are most advisable. 

Since the introduction of serum-therapy all the former methods of treatment 
have been quite superseded. This is especially true of the many previous attempts 
to limit the morbid process and cause it to disappear by local disinfection. The 
practical difficulties in carrying out any really effective local treatment have 
always prevented the general recognition of the value of caustics, painting, etc. 
Xevertheless some remedies, even up to the present time, are still recommended 
as efficient, especially liquor ferri sesquichlorati (pure or diluted), dabbing with 
a l-to-1,000 sublimate solution, etc. 

Of the many internal remedies which were formerly tried we can mention 
only chlorate of potassium and iodide of potassium. The former remedy may still 
be recommended and may be given in teaspoonful doses of a solution containing 
1 part to 30 or 40 of water. 

[The tincture of the chloride of iron is much used in this country in the treat- 
ment of diphtheria, and appears to be of real service ; but it must be given in large 
doses. The following prescription is recommended by Jacobi. whose experience 
has been very large, for a child of two years : 

Tinct. ferri chloridi oij; 

Potas. chlorat gr. xx; 

Glycerin, pur §j ; 

Aquas 5 T - 

M. S. : Teaspoonful every fifteen, twenty, or thirty minutes. 



76 



ACUTE GENERAL INFECTIOUS DISEASES 



Turpentine is better as an inhalation than by the stomach ; a teaspoonf ul or two 
of the oil can be poured in water kept at the boiling- point by an alcohol-lamp. 
The whole air of the room is thus charged with the remedy. No drug should be 
used with disorders the stomach. Tablet triturates containing one one- thou- 
sandth of a grain of corrosive sublimate can be allowed to melt in the mouth with 
the greatest freedom, and seem sometimes to exert a distinctly beneficial local 
action. The dose is, however, too small to secure the systemic effects of the drug 
unless the case is a mild one and free from notable dysphagia.] 

If the larynx is attacked, and if, in spite of the serum treatment, the conse- 
quent laryngeal stenosis threatens to cause suffocation, tracheotomy is our only 
resort. It is never indicated by the disease itself nor by the severity of the case, 
but only by persistent obstruction of the larynx. It is therefore not invariably 
easy to decide whether tracheotomy is called for in any particular case. If the 
general condition be bad and respiration already impaired, it is often very diffi- 
cult to determine whether laryngeal stenosis exists. Tracheotomy will be of no 
avail if the croup has already extended to the bronchi, or if the dangerous condi- 
tion of the patient is due to the severity of the constitutional infection or to 
incipient paralysis of the heart. We have already said that, since the introduc- 
tion of the serum treatment, the prognosis of diphtheria has become better even 
in the tracheotomy cases. How tracheotomy is performed, and in what the after- 
treatment consists, must be learned in the text-books on surgery, where we will 
also find the necessary description of the so-called intubation of the larynx. 

Intubation, as devised by Dr. O'Dwyer, is a procedure which makes a distinct 
advance in the treatment of laryngeal stenosis. In permitting the free access of 
air to the trachea, intubation may save life without resort to the serious operation 
of tracheotomy ; or it may tide over a time until tracheotomy becomes absolutely 
necessary or until the consent of the parents can be obtained to the use of the 
knife. In hopeless cases it may promote euthanasia. 

If severe pulmonary symptoms occur in diphtheria, we should use first of all 
wet packs of the whole body or tepid baths with cool affusions. Such cutaneous 
stimulation refreshes and enlivens the whole nervous system, and we should there- 
fore try it also in the severe cases with secondary septic infection. In septic 
diphtheria we must also pay especial attention to the condition of the heart. So 
far as is possible we should try to avert the threatening cardiac paralysis by stimu- 
lants, such as wine, camphor, and strophanthus. 

The nervous sequelae of diphtheria are best treated with the constant current. 
As an internal remedy, iron is good, and also nux vomica or strychnine. The last 
may be given subcutaneously, if desired, in doses of gr. eV -3V (grm. 0.001-0.002). 

The prophylaxis of diphtheria demands that every child with diphtheria be 
absolutely isolated from healthy children. Behring [and many others^ believe 
that a healthy child may be positively protected from infection by diphtheria for 
two or three weeks by the injection of a small dose of serum — the whole or one 
half of Dose I — that is, about three hundred units of antitoxine. It is, of course, 
very hard to judge of this, and for the present, therefore, it must be left to the 
individual judgment of the physician in what cases he will try prophylactic injec- 
tions of serum. 

[Diphtheria is a disease which involves commonly much exhaustion, and too 
much stress can hardly be laid on the importance of administering the maximum 
amount of nourishment in the most assimilable and easily swallowed forms from 
the start. 

It is also important to give stimulants early in most cases, not waiting for 
signs of exhaustion. Enormous quantities of brandy can often be given to small 
children without the slightest toxic effect. No general rule can be laid down; 
the requirements of each case must be studied and met. 



INFLUENZA 



When painful deglutition interferes with nutrition, peptonized milk, eggs, 
brandy, and the like, must be given by the rectum. Rectal alimentation and 
stimulation and feeding with the oesophageal tube are also to be resorted to in 
cases of post-diphtheritic paralysis of the oesophagus.] 



CHAPTER XI 

INFLUENZA 

{La Grippe) 

Influenza is a specific, acute, infectious disease which is especially distin- 
guished by the occasional enormous extent of its epidemics. While often years 
and decades pass without any especial attention being called to the disease, sud- 
denly cases of it will appear with such frequency that the largest part of the 
population is attacked, and the disease may better be described as pandemic than 
epidemic. Pandemics of influenza can be traced back with certainty into the six- 
teenth century. In the present century the influenza during the years 1830-33 
traversed almost all of Asia and of Europe, then later there appeared numerous 
smaller epidemics, but these aroused general attention so little that the disease, 
upon its last pandemic appearance in the winter of 1889-90, was almost unknown 
to many physicians. Since that time the disease seems never to have wholly 
disappeared, as a few cases, and occasionally small groups of cases, are constantly 
seen. 

.ZEtiology. — The organized agents of influenza are still not positively known, 
but R. Pfeiffer has invariably found in the bronchial secretion of patients with 
the " catarrhal form " of influenza (vide infra) a definite form of very small 
bacilli with rounded ends which stain darker than the central portion. These 
bacilli, which are either free in the mucus or in the pus-cells, are very probably 
of significance as a cause of the disease. The influenza bacilli very soon die if 
dried, and also if put in water. 

In all probability the infection is usually due to inhaling the germs. The 
bacilli seem to appear at certain times over an immense territory, so that they 
or their spores are scattered everywhere through a large extent of country. 
Many observations upon the appearance of the disease in isolated institutions 
(convents and the like) render it very probable that the poison may also be 
carried by a person suffering from the influenza to another in regions pre- 
viously unaffected. Nevertheless, this contagious manner of spreading plays no 
great role in comparison with the direct infection from the outer world, this latter 
mode being everywhere possible during an epidemic of influenza. 

There is scarcely any N reason for speaking of especial predisposing causes of 
influenza, inasmuch as at the time of a well-marked epidemic the overwhelm- 
ing majority of the population are attacked, both the healthy and the diseased, the 
vigorous and the feeble. Sex certainly makes no difference, and age only to this 
extent, that the disease is seen more rarely in little children under one year of age 
than in older children and adults. That catching cold has no special ^etiological 
significance is evident from the fact that influenza often appears in patients who 
are already sick in bed. 

It should finally be mentioned that animals also, and in particular horses, may 
be attacked by the influenza; but, nevertheless, it is as yet a doubtful question 
whether all the diseases in animals which are described under this name are actu- 
ally identical with genuine influenza. 

Symptoms and Clinical History. — The best general idea of the extremely 
manifold symptoms of the disease will be obtained if we bear in mind that the 



78 



ACUTE GENERAL INFECTIOUS DISEASES 



influenza causes both a marked infectious (or toxic) general constitutional dis- 
turbance of the body, and also certain local lesions with local symptoms. The 
clinical picture therefore varies greatly according to the predominance of one or 
the other group of symptoms, and also according to the special form of the local 
disease. 

The onset of influenza is generally rather sudden. As a rule the marked cases 
begin with rather high fever, ushered in with a chill, violent headache, marked 
constitutional depression, and usually considerable pain in the back and loins. 
The weakness of the patient may be so great that, even if a vigorous individual, 
he will at once take to his bed. Severe nervous symptoms, such as stupor and de- 
lirium, are exceptional. Sometimes, but not very often, there is initial vomiting. 
The backache is often associated with pains in the muscles and joints. Oppressive 
pain in the eyes is quite characteristic also. This is particularly felt upon moving 
the eyeballs, and therefore is probably located in the external muscles. The spleen 
is occasionally somewhat swollen, but any great increase in its size is excep- 
tional. 

If the clinical symptoms as the case progresses are mainly limited to the above- 
named constitutional symptoms — fever, languor, headache, pain in the muscles — 
we may speak of a " typhoidal form " of the disease. Usually, however, certain 
local symptoms put in an early appearance, and it is especially the respiratory 
apparatus which is attacked. The precise symptoms vary considerably in different 
cases. Sometimes the upper portion of the respiratory tract, the nose, larynx, and 
trachea are involved ; sometimes, from the start, the smaller bronchi. In the first 
instance there is marked coryza or hoarseness, in the other case there is cough, 
due to a dry bronchitis, which can be easily detected upon auscultation, and which 
involves especially the lower portion of the lungs. If these local symptoms out- 
weigh the constitutional, the case is described as belonging 1 to the " catarrhal 
form " of influenza. 

Sometimes the influenza is localized in the digestive apparatus. This " gas- 
trointestinal form " is much rarer than the catarrhal. In this case, in addition 
to the more or less strongly characterized constitutional symptoms, there is 
marked disturbance of the stomach and intestines, as shown particularly by 
nausea with persistent vomiting, diarrhoea, abdominal pain, etc. In one case 
we observed jaundice. TTe may also mention in this connection the appearance 
of an initial pharyngitis. 

The pains in the back, loins, and extremities already mentioned may persist 
with unusual violence, and this peculiar form of the disease is known as the 
" rheumatoid." The muscles and the muscular attachments are probably the chief 
seat of these pains, which may be so violent that the patient is unable to lie com- 
fortably, and sometimes keeps up a continual moaning. The loins, in particular, 
may be the seat of most acute pain, also the upper arms, the knees, the thighs, and 
the eyes. Objective changes in the painful parts, such as swelling of the joints, 
are scarcely ever seen, nor are the nerve-trunks as a rule especially sensitive to 
pressure. The painful muscles are usually weaker than normal. 

The grouping of the clinical varieties of influenza under the four forms al- 
ready named affords a general idea of the manifold symptoms of the disease, but 
this division into separate forms must not be carried out too strenuously, for in 
reality many cases of the disease occur which present transition forms and com- 
binations of the various groups of symptoms. Moreover, in all the forms a dis- 
tinction must be made between mild and severe attacks, for in influenza, just as 
in most other infectious diseases, there are many rudimentary and mild cases as 
well as the fully developed ones, and some could not be properly interpreted but 
for the presence of the epidemic. 

The duration of the disease is best determined by the duration of the fever. 



INFLUENZA 



79 



In the very mildest cases there may be no fever whatever, or simply a slight 
evening rise of temperature. As a rule, there is a moderate fever, between 
101.5° and 103° F. (38.5° and 39.5° C), although higher temperatures even to 
104° F. (40° C.) and more are not infrequent. In the beginning of every severe 
attack the fever rises abruptly. After a duration of several days (four to seven) 
it may fall again in a manner approaching a crisis. More frequently, espe- 
cially when there exists diffuse, catarrhal trouble in the lungs, the fever ends by 
lysis. With comparative frequency there are found to-be noticeable deviations 
in the temperature curve ; thus, for example, the high fever of the onset sinks on 
the second or third day, to be followed by an almost afebrile period of one or two 
days, whereupon a marked rise of temperature ensues. With this change in the 
temperature there are usually also corresponding variations in other symptoms. 

We see, then, that the duration of simple, uncomplicated influenza is in the 
mild cases about three or four days, in the severer cases about seven to ten days. 
To be sure, we should also consider in this connection that convalescence is often 
surprisingly slow, so that the after-pains (as it were) of the disease are felt for 
weeks. These consist, for instance, in a certain degree of debility, and in pain- 
fulness of the muscles. Sometimes also there are complete relapses, so that di- 
rectly or a short time after the disease has ended the symptoms begin anew. The 
special form of the disease may change in this case, so that, for example, the re- 
lapse of an influenza with predominant constitutional symptoms assumes the pro- 
nounced catarrhal form. Again, during the same epidemic it is not very rare for 
a patient to suffer from two attacks of influenza separated by a considerable inter- 
val of time. 

Complications and Sequelae. — While all the symptoms of influenza which we 
have thus far described are the direct effects of the original pathogenic cause, the 
majority of the frequent complications are undoubtedly dependent upon the in- 
gress of secondary infection. The system when attacked by influenza is greatly 
exposed to these secondary influences, and almost all the dangerous and tedious 
cases of influenza become such only because of a mixed infection of this sort. 
This is particularly true of the lungs, in which secondary disease occurs most fre- 
quently — sometimes even in the first days of illness, but also in other cases later. 
The conditions here are similar to those seen in measles and whooping-cough. 
The simple, mild catarrh belongs to the original disease; the severe pulmonary 
affections are, however, invariably secondary complications occasioned by new 
pathogenic influences. These influences are not always the same. According to 
the investigations of Kibbert, Finkler, and others it is chiefly the pneumonia dip- 
lococcus and the streptococcus which are the true excitants of the secondary pneu- 
monia seen in influenza. These cases of pneumonia are either extensive catarrhal 
pneumonia especially affecting the lower lobes, or more rarely croupous pneu- 
monia with its characteristic sputum. We must also add that the influenza 
bacilli themselves may excite a lobular pneumonia, which shows a marked puru- 
lent character. If pneumonia be added to influenza, the former overshadows the 
whole picture. The patient is oppressed for breath, has a severe cough with pro- 
fuse expectoration, looks pale or cyanotic, and suffers from high fever. These 
symptoms persist for two or three weeks, and then gradually abate. It is in this 
way that influenza becomes dangerous for elderly and feeble or sickly persons. 
With noticeable frequency, pleurisy with effusion is conjoined with the influ- 
enza pneumonia. The exudation is generally serous, but exceptionally it is puru- 
lent. 

Complications in other organs are less frequent. We would make especial 
mention of purulent otitis media and keratitis and other severe diseases of the 
eye. We have several times observed acute nephritis, but this has always pursued 
a mild course. Among cutaneous eruptions herpes labialis is a frequent phenome- 



80 



ACUTE GENEKAL INFECTIOUS. DISEASES 



non in all forms of influenza, even the milder. Other exanthems, such as urticaria 
and roseola, are much less frequent. Many of the complications named may con- 
tinue even after the fever and all other symptoms have ceased, so that they must 
be regarded as sequelae. This is particularly true of the diseases of the ear and 
eye and of persistent bronchitis, but only rarely of a pneumonia assuming the 
chronic form. An important and for the patient a troublesome and painful 
sequel is furunculosis, especially if some of the boils are located in the axilla or 
near the anus. Very often neuralgic pains in the distribution of the trigeminus 
or in the course of the sciatic or other nerves will persist for a considerable time 
after the influenza has ceased; but these pains may sometimes be located in the 
muscles; thus, for example, the frequent, persistent, and troublesome pain in the 
eyes. In a few cases more severe nervous sequelae, such as spinal symptoms and 
psychoses, have been seen after influenza. A special form of acute hemorrhagic 
encephalitis (vide infra) has been thought to have a relation to influenza. 

Diagnosis. — The diagnosis of influenza is in general not difficult if one has to 
deal with a well-marked case at the time of an influenza epidemic. The charac- 
teristic initial symptoms of fever, headache, and pain in the loins are to be con- 
sidered first of all. Their onset is much more rapid than, for example, in typhoid 
fever. Later on the pain in the various muscles as well as the catarrhal symp- 
toms are the most characteristic phenomena. 

Uncertainties and errors in diagnosis may arise from the fact that, on the one 
hand, we are disposed at the time of an epidemic to call almost all the catarrhal 
and indefinite mild affections we see " influenza," while, on the other hand, when 
there is no epidemic, we can not positively distinguish the sporadic " cases like 
influenza " from the ordinary acute febrile bronchitis, etc. It is indeed very 
possible, a priori, that different morbid agents may produce similar mild acute 
diseases of the accessible mucous membranes. In such cases, with pronounced 
general symptoms, high fever, etc., we must often be content with the diagnosis 
of " infectious " laryngitis, bronchitis, etc., without being able to decide defi- 
nitely whether the case is to be classed setiologically with influenza or not. At 
any rate in practice we should not abuse the diagnosis of influenza. 

Prognosis. — For an individual who is healthy and vigorous, influenza is not a 
dangerous disease, even in its severer forms; for elderly persons or invalids it 
may, however, be a serious affection. Patients with heart disease or pulmonary 
disease, or those suffering from chronic nervous troubles, sometimes succumb to it ; 
so that the general mortality at the time of a great epidemic of influenza is 
always considerably increased. The above-enumerated pulmonary complications 
are by far the most dangerous ; less often is a fatal termination caused by general 
or cardiac weakness. The above-mentioned nervous sequelse are also to be con- 
sidered in prognosis. 

Treatment. — No specific remedy for the disease is known. Many physicians 
maintain that the exhibition of calomel at the beginning of the attack decidedly 
shortens its course, but confirmatory experience is wanting. In general we must, 
therefore, pursue a purely symptomatic method of treatment. For the initiatory 
fever, the headache, and the pain in the loins, antipyrine is sometimes a good 
remedy, and the same may be said also of phenacetine, antefebrine, and especially 
salipyrine. These drugs are also prescribed for the persistent pains in the mus- 
cles which come on later. Soothing liniments and ointments may be employed, 
with friction, for the same purpose. The treatment of the pulmonary complica- 
tions is according to the established methods. Morphine is mainly used for the 
troublesome cough. Apomorphine, senega, and other expectorants may be em- 
ployed, and, if indicated, external remedies such as an ice-bag or dry cupping. 
If the patient becomes very feeble, stimulants such as [strychnine], champagne, 
and strophanthus are demanded. 



DYSENTERY 



-1 



CHAPTER XH 
DYSENTERY 

etiology. — By " dysentery " is meant a disease of the colon, which, appears 
sporadically, but more often in epidemics; it is excited by infection with, an 
organized pathogenic poison, about which we have as yet no definite knowledge ; 
and the infection is probably at first a local one. From the investigations of 
various men, especially Kartulis, it seems very probable that a certain form of 
amoeba must be regarded as the cause of " endemic tropical dysentery." At least 
in endemic dysentery we almost invariably find, both in the stools and in the 
walls of the dysenteric intestinal ulcers and in the dysenteric abscesses of the 
liver, many amoebae (amoeba coli), which are never found in any other intes- 
tinal affection. Dysentery may also be artificially produced in cats by means of 
faeces containing amoebae. In dysentery as it occurs in Germany, however, we do 
not apparently find amoebae in the stools as a rule, although even in Germany 
Quincke and others have described certain cases of " acute enteritis " (" amoebic 
enteritis ") in which there were a large number of amoebae. The question of 
the excitants of dysentery therefore needs further investigation, and it is not 
impossible that several intestinal affections with different aetiology have thus 
far been included under the name of dysentery, especially in the tropics. The 
true home of dysentery is in warmer and tropical countries, where the disease is 
much more violent and widespread than here. Eor example, the mortality 
among the soldiers of the Anglo-Indian army due to dysentery is said to be at 
times thirty per cent, of the entire number of deaths. In our climate most of 
the epidemics occur at the end of summer and in autumn. Endemic influences 
are certainly important. The special conditions in some places are evidently 
very favorable for the development and dissemination of dysenteric germs, and 
there are other places equally unfavorable. There can be no other explanation 
of the immunity of some localities contrasting with the great prevalence of the 
disease in others. How infection occurs we do not yet know. Many observations, 
especially in southern countries, support the idea that the germs may be taken 
into the system by drinking water. Dysentery does not seem to be directly 
contagious; but that it can be spread through the medium of the faecal dejections 
of the sick — e. g., from privies, chamber-vessels, and bed-linen — is very probable. 
Many cases were formerly referred to catching cold or to some error in diet ; but 
we must, of course, regard these merely as predisposing influences. 

The objective pathological lesion of the colon, in all severe cases, consists in 
a pronounced croupous-diphtheritic inflammation. The remarks as to the general 
pathology of such inflammations made in the preceding chapter are equally ap- 
plicable to the analogous dysenteric inflammation. In this case, too, there is first 
a destruction of the epithelium and then the formation of a fibrinous exudation 
occupying its place, and penetrating down into the tissue of the mucous mem- 
brane itself. At the same time there is an intense purulent infiltration of the 
mucous and submucous tissue, accompanied by extensive ecchymoses. In the 
most virulent cases the macroscopic appearances are marked thickening of the 
whole wall of the intestine, congestion of the serous layer, and the conversion of 
the inner surface into a mottled, dark-red, irregularly roughened area of ulcera- 
tion. The disease may be confined to the rectum and the sigmoid flexure, but in 
severer cases it involves the entire colon as far as the ileo-caecal valve, or even 
extends to the lower portion of the ileum. Besides this severe form of diph- 
theritic or even gangrenous dysentery, there is a milder variety, termed catarrhal 
dysentery. In this the mucous membrane is found in a state of intense purulent 
6 



82 



ACUTE GENERAL IXFECTIOUS DISEASES 



inflammation, with ecchymoses. Even here little masses of croupous exudation, 
which can be torn off, have replaced the epithelium; but they never form con- 
tinuous layers of great extent. There is no sharp boundary-line between the two 
forms, the milder catarrhal-croupous and the severer diphtheritic dysentery. 
Xumerous transitional and combined varieties exist. 

We must remark, in conclusion, that precisely the same anatomical changes 
as are presented in true dysentery may result from other causes. Important 
among these is persistent fsecal impaction in the rectum, which, by a purely 
mechanical effect upon the epithelium, may excite a diphtheritic inflammation in 
the mucous membrane. And any severe constitutional disease whatsoever, such as 
typhoid fever, measles, small-pox, septicaemia, or phthisis, may be attended by a 
so-called " secondary dysentery." This is most frequent in hospitals. Whether 
it has the same aetiology as genuine dysentery is uncertain. 

Clinical History. — Throughout the entire illness the most prominent symp- 
toms are intestinal. There may be first of all some slight irregularity of the 
bowels for a few days, and then appears a moderate diarrhoea. The stools are at 
first feculent, although thin, and number two to six daily. After a few days 
the discharges increase in frequency, and become extremely characteristic. 

The stools are very frequent, occurring ten to twenty, and even sixty or more, 
times, in twenty-four hours. In severe cases there may be a distressing and almost 
constant desire to evacuate the bowels. After every operation, and to some extent 
during it, there is tenesmus attended by intense burning pain in the anus. The 
stools soon lose their usual feculent character in great part if not entirely. They 
become scanty, so that not more than about half an ounce is evacuated each 
time. For the most part they usually consist of a sero-mucous fluid, in which 
are suspended numerous shreds and particles of varying size. These are blood- 
stained bits of mucus, little coagula of blood, and necrosed pieces of mucous mem- 
brane. One or another of these constituent parts may predominate, so that there 
may be slimy, purulent, or bloody stools, or all sorts of combinations of these 
varieties. We often find, besides, a few small masses of faeces, usually covered 
with mucus. We sometimes see numerous clumps of mucus, resembling sago or 
frog's spawn ; they are probably mucous casts of the follicles. Under the micro- 
scope the greater part of the dysenteric discharge is seen to consist of pus-corpus- 
cles and blood. There are also cylinder epithelium and an enormous amount of 
detritus, and the bacteria of putrefaction. A purely dysenteric stool has no bad 
odor, except that in the worst cases of gangrenous dysentery the discharges become 
blackish and extremely offensive. 

The rectal tenesmus may be accompanied by a cramp-like pain during micturi- 
tion. There are often violent attacks of colic. The abdomen is Usually rather 
tense, and tender on pressure along the line of the colon, but without tympanites. 
The anus may be red, inflamed, and excoriated. Gastric symptoms are on the 
whole infrequent, if we except the complete anorexia which exists in all severe 
cases. Sometimes there is repeated vomiting. Occasionally hiccoughs prove dis- 
tressing. The tongue usually has a dry, greasy coating. 

The symptoms just depicted last about a week or ten days. If the case is of 
much intensity, the general condition is also greatly affected. The patient seems 
much collapsed, and is very languid and feeble, with a small and rapid pulse. 
The skin becomes cool and rough, the voice weak and hoarse. There is pain in 
the muscles. The patient wastes away. The temperature has little that is char- 
acteristic or typical. In many cases there is no fever at all, and the temperature 
may even be subnormal. In most cases, however, there is an irregular fever 
seldom exceeding 10-4° (40° C), and having remissions. 

In the worst cases the general weakness may increase more and more, and 
death occur; but with us a favorable termination is much more frequent. The 



DYSEXTEKY 



83 



distress gradually diminishes, the stools assume more and more of a feculent char- 
acter, the patient becomes stronger, and after one and a half to three weeks con- 
valescence is established. It may be a long while, however, before a patient com- 
pletely recovers from a severe attack. A third possibility is the transition of the 
acute into a chronic dysentery. In this the symptoms of a chronic colitis, usually 
attended with cachexia, may persist for months and years. 

Mild, rudimentary forms of dysentery also occur, presenting no severe intes- 
tinal symptoms, and recovering at the end of a few days. In these cases, too, 
great sensitiveness of the intestine to disturbing influences frequently persists for 
quite a long time after the illness. There may be exacerbations of the disease, and 
relapses. 

Complications of dysentery, localized in other organs, are rare, at least in 
epidemics here. In tropical dysentery abscess of the liver is comparatively com- 
mon. It is dependent upon metastatic processes from the portal radicals. In 
some cases abscesses of the lungs and of the brain may follow abscess of the liver. 
Inflammation of the serous membranes or of one or more joints may also occur. 
If paraplegia follows it may be referred either to secondary myelitis or to poly- 
neuritis. Dysentery is also said to occur in connection with a " general scorbutic 
diathesis," but to all appearances this is usually a " septic " complication. The 
dysenteric ulcers rarely lead to perforation and consequent peritonitis. 

The diagnosis is seldom very difficult. It is based exclusively upon the intes- 
tinal symptoms and the character of the stools. It is only the cases of secondary 
dysentery which occur in the course of other severe diseases that are likely to 
escape observation. 

The prognosis is mainly influenced by the character of the epidemic, which, as 
we have said, is in our climate usually benign. There may be danger, particu- 
larly to elderly people, from bodily weakness and collapse. 

Treatment. — Prophylaxis demands that the isolation of the patient and the 
disinfection of the stools be as complete as possible. The healthy must be very 
careful during an epidemic not to catch cold, and to avoid errors in diet, for 
experience shows that an opposite course predisposes to the disease. 

The patient must be kept warm, and must not leave his bed, even if the attack 
be mild. The diet must be rigorous. If the strength is fair, thin porridge, milk, 
and broths suffice for some days. To a feebler person we should give somewhat 
stronger nourishment from the start, e. g., eggs, peptonized meat, and wine. Most 
patients bear liquids that are lukewarm better than those which are cold. 

As to drugs, the habit of almost all experienced physicians is to give at first a 
mild laxative. Although opium does not usually control the diarrhoea and tenes- 
mus at all, it is the rule for decided improvement to follow the exhibition of the 
laxative. During the first days, or, if need be, later, we give two to four table- 
spoonfuls of castor-oil daily. If this medicine is very disagreeable to the patient, 
we can replace it by a strong infusion of rhubarb (10-100). In southern countries 
large doses of calomel (gr. x to xv, grm. 0.5-1) are customary, and are highly 
praised by the physicians there. Further on in the disease we may content our- 
selves with giving mistura amygdala? ; or we may administer bismuth in the fol- 
lowing mixture: Bismuthi subnit. vel salicylate grm. 5; mucilaginis acacia?, 
syrupi simpl.. aa 15; aqua? destil.. 120 — to be shaken before taking. If the dis- 
ease should get worse again, however, we should always try a laxative. 

Emetics at the beginning of the disease are often employed in the tropics, but 
seldom with us. Ipecacuanha (radix antidy sent erica) , given in large doses of fif- 
teen to thirty grains (grm. 1-2), is even regarded by many as a specific. Among 
antiparasitic remedies, naphthalin (gr. viij, grm. 0.5, thrice daily) and salol (one 
to two drachms, grm. 4.0-8.0, a day) have been especially recommended. Numer- 
ous attempts have been made at local treatment by enemata. Xo brilliant results, 



84: 



ACUTE GEXEEAL INFECTIOUS DISEASES 



however, can be claimed for any of these methods or medicines. A decided pallia- 
tive effect can be obtained from the injection of thin starch to which twenty or 
thirty drops of laudanum have been added. Suppositories of cocoa butter con- 
taining extract of opium often mitigate the tenesmus. Other injections are recom- 
mended, each to measure gij to iijss. (grm. 60-100), and to contain either argenti 
nitrat., gr. j to vj (grm. 0.05-0.30), or plumbi acetat., gr. ij to viij (grm. 0.1-0.5), 
or potassii chlorat., gr. xv to xx (grm. 1-1.5), and especially tannin (three in- 
jections a day of a warm 0.5-per-cent. solution). In severe cases we may also try 
high injections of solutions of tannin as in cholera (vide infra). Many other 
solutions are used. The success of this treatment is, however, dubious. In all 
cases the margins of the anus must be protected from inflammation by frequently 
washing and anointing the skin. 

The treatment of weakness and collapse is by the usual stimulants — wine, 
ether, camphor, and the like. In chronic dysentery the main point is to persevere 
in a strict control of the diet. We may exhibit astringents, such as tannin and 
columbo. Subnitrate of bismuth is also given, and nitrate of silver and acetate of 
lead. And in these chronic cases a long-continued and thorough use of rectal 
irrigation with fluids containing some mild astringent or disinfectant may have a 
good effect. 

[Sporadic dysentery is a self-limited disease, and, as has been shown by Flint, 
runs its course within ten days without medication. Treatment, however, adds to 
the comfort of the patient and shortens the course. It is not customary with us 
to use daily laxatives. If there is any doubt as to whether the intestines have 
been emptied, a saline should be given, the action of which should be followed by 
opium in sufficient doses to allay pain and tenesmus. Subsequent action of the 
bowels is best obtained by simple large enemata. In weak persons castor-oil is to 
be preferred to salines. 

In epidemic dysentery active treatment is much more important. Laxatives 
are contra-indicated by sero-sanguinolent dejections or by asthenia, but enemata 
can be freely used. Stimulation is often required; nutrition must be carefully 
looked after, such articles being chosen as are digested and absorbed by the 
upper portions of the intestinal tract, leaving as little residue as possible to pass 
on to the inflamed colon. Opium is often demanded and tolerated in large doses, 
and astringents, such as the acetate of lead, gallic acid, and the pernitrate of iron, 
are of service. 

In acute dysentery the patient should be instructed not to yield to the desire to 
go to stool if he can help it, and tenesmus can often be much diminished by 
simple irrigation of the lower bowel with water, which may be warm or cold, 
whichever the patient finds more agreeable. 

Chronic dysentery is one of the most difficult maladies with which we have 
to deal. In its treatment a sea voyage, or removal for at least some months to a 
climate other than that in which the disease originated, is of far more value than 
drugs. 

Amoebic Dysentery 

The amoeba coli, first found by Losch in the stools of a dysenteric patient, has 
received very careful study at the Johns Hopkins Hospital, and forms the subject 
of a most exhaustive and valuable monograph by Councilman and Lafleur. 

The living organism is readily seen, and recognized especially by its active 
amoeboid movements on the warm stage of the microscope. If the faeces contain 
small gelatinous masses, these will be found to provide the most fruitful field 
for search. The numbers of the organisms vary widely in different cases, and even 
in the same case, from day to day. They are said to be present in this form of 
dysentery alone, and have been found in secondary abscesses of the liver and the 



CHOLERA 



85 



lung, alike after death and during life. They should be sought for in all obstinate 
cases with dysenteric symptoms. 

The prognosis is uncertain, and the cases are apt to drag along with exacerba- 
tions and remissions of the symptoms; but recovery does take place. There is 
notable danger of the formation of secondary abscesses, in which event re- 
covery is hardly to be hoped for. The only treatment which seems to have been 
of much service — beyond a general hygienic and supportive regimen — consists in 
the use of copious injections into the intestinal canal of solutions of quinine, 
in the strength of one to one thousand or even five thousand. Losch found that 
contact with a solution of the latter strength for one minute suffices to kill the 
amoeba?.] 



CHAPTER XIII 

CHOLERA 

(Asiatic Cholera) 

Historical Remarks. — The home of genuine Asiatic cholera is India. The first 

epidemic in that country with which we are accurately acquainted occurred in 
1817. This was very widespread. The disease was probably endemic there at an 
earlier period. In the next few years the cholera extended in all directions, and 
reached Astrakhan by way of Persia. Between 1830 and 1832 the disease made its 
first great epidemic progress over Europe. Invading all European Russia, it 
reached Germany in 1831, and Erance and England in 1832. Then came many 
smaller epidemics up to 1838, when there was a complete cessation till 1846, in 
which year the disease, again starting from Asia, overspread Europe. There have 
in later years been epidemics in many places, but we can not here enter into the 
particulars of them. During the war of 1866 there were many cases of cholera in 
Germany, and from 1883 to 1886 Italy, Erance, and Spain were visited by the dis- 
ease. In August, 1892, cholera broke out suddenly and very unexpectedly in 
Hamburg, where within three months about 18,000 persons were attacked by the 
disease, and over 7,600 died of it. 

iEtiology. — Some time ago it had become evident that the real cause of cholera 
consists in the infection of the system by a specific micro-organism. Koch was, 
however, the first to succeed in the search for the poisonous agent. He was in 
charge of the scientific expedition sent out by the German Government in 1883 to 
Egypt and India for the purpose of investigating the disease. Koch found in the 
intestines of all the victims of cholera whose bodies he examined a certain kind 
of micro-organism which he named the comma bacillus. It is shorter than the 
bacillus of tuberculosis, but somewhat thicker, and it is usually bent in the shape 
of a comma, or even like a semicircle (see Fig. 9). In pure cultures the comma 
bacilli grow into long spiral threads, resembling the spirilli of recurrent fever. 
Examined in a liquid, the individual bacilli are seen to make vigorous move- 
ments. This mobility is probably dependent upon the thin, filiform fibers at the 
ends of the comma bacilli discovered by Loffler. 

The comma bacilli flourish best at a temperature between 86° and 104° (30° 
and 40° C). Below 61° (16° C.) they cease to grow, but they are not killed even 
by a greater degree of cold. The free access of oxygen is desirable but not abso- 
lutely indispensable to their growth. They multiply very rapidly in liquids — e. g., 
broth or milk — and they may, under favorable circumstances, retain their vitality 
for many weeks, while they can be readily destroyed by desiccation. In this again 
they resemble the genuine spirilli, which can maintain their existence only in 



86 



ACUTE GENERAL INFECTIOUS DISEASES 



fluids. It is necessary that the nutrient material have an alkaline reaction. On 
neutral or acid material the growth of the comma bacilli ceases entirely. The 
characteristic features of pure cultures can not be described in detail here, but 
we may observe that the nutrient gelatin is slowly liquefied by the bacilli. Noth- 
ing definite is yet known as to the occurrence and the formation of permanent 
spores. 

There can now be no doubt that the sole cause of cholera is infection by the 
comma bacilli. It has been shown that in every case of genuine Asiatic cholera 
the comma bacilli are present in the intestine, and that they are never found 
under any other circumstances. Even the last postulate which was needed to 
show their pathogenic significance has been fulfilled. Rietsch and Nicati, followed 
by Koch himself and others, have succeeded in producing cholera in a guinea-pig 
by introducing into its duodenum or into the contents of the stomach previously 
made alkaline, pure comma bacilli. 

Investigation as to the origin of cholera must, therefore, now meet this culmi- 
nating question: Under what circumstances and through what channel do the 

comma bacilli penetrate into the human 
system, and in what manner do they there 
excite the characteristic processes of the 
disease ? There can be no doubt that among 
Europeans, and probably everywhere except 
in India, the cholera is invariably imported. 
It is equally certain that the dejections of 
"Ail J r 'h ' $^'1 \\ cholera patients, which are rich in comma 

I'J'h) '/ ^ [/ Mfo //J bacilli, are the chief if not the only agent 

by which the disease is spread. The bacilli 
which escape into the outer world with the 
stools find abundant means to prolong their 




'» u'"(' ' \ existence. They continue their growth 

iyjl j J /' ^/ \ \\ upon moistened bed-clothes, or in water 

y~ J If // '(/ j which contains a sufficient amount of or- 

/ / / hi ' ganic substances, or in food, such as fruit or 

« milk, or in moist earth; and the ways by 

Fig. 9.— (From Koch.) Comma bacilli from which they can in turn enter the system of 

a cholera dejection which had lain for two i i - i i i • •.*?•<• 

days on a wet cloth. The S-shaped bacilli a healthy human being are minute m num- 
are at a. 600 diameters. ber> It is eagy to -understand why certain 

persons — e. g., laundresses and nurses — are 
more liable to infection than others; and it is equally intelligible that the spread 
of the disease should often bear a relation to certain outward circumstances. 
The fact has long been a familiar one, that the cholera almost always progresses 
along the world's most frequented highways, and that it never travels faster than 
the means of human intercommunication render possible. This is important, 
because it shows plainly that the germs of the disease are not disseminated by 
currents of air. It is easy to understand that the distribution of the disease 
should sometimes correspond with that of water destined for personal use. The 
experience of the last few years has again proved most clearly that the drinking- 
water is the chief, although of course not the only, source for the dissemination 
of cholera. If an extensive water-supply is contaminated by comma bacilli, as 
was the case in Hamburg, the disease may suddenly break out in a place with great 
severity. Sporadic cases usually arise from the use of a contaminated stream 
which is used for drinking only by a small number of men (sailors, etc.). 

A man falls sick with cholera, of course, not simply from swallowing the 
cholera bacilli, but because the bacilli remain in the intestine and multiply. It 
is safe to assume that many men swallow comma bacilli at the time of a cholera 



CHOLERA 



87 



epidemic without falling sick at all, or without any but the slightest disturb- 
ance, because the comma bacilli are at once destroyed by the acid gastric juice 
or they develop in the intestine only in small numbers or perhaps in an attenuated 
form. In the last epidemic at Hamburg comma bacilli were sometimes found in 
the solid stools of healthy men, who were in close contact with cases of cholera, 
and also in the stools of men who had a very mild " cholera diarrhoea." These 
facts are extremely important. They lead to a correct estimate of the infection 
experiments repeatedly practiced of late on human beings, and, on the other 
hand, they have a great practical significance in regard to the danger of trans- 
mitting cholera. 

These theories may be brought into harmony with the observations collected 
by Pettenkofer, which go to show a connection between the dissemination of 
cholera and the character of the soil. The character of the soil can evidently 
influence the dissemination of the cholera bacilli in various ways. The conditions 
of the water in springs, etc., may depend very materially upon the character of 
the surrounding soil. The epidemiological facts especially emphasized by Petten- 
kofer are : 1. Certain places are immune, especially those lying in a rocky terrain. 
2. The frequency of cholera (as of typhoid fever, vide supra) corresponds with 
variations in 1he ground-water. 

Most cholera epidemics happen in the summer months. Liability to the dis- 
ease is very widespread, although some remarkable exceptions are seen. Sex is 
unimportant. Age has more influence. The disease occurs in sucklings, but, as 
a rule, is more rare among children than among adults. Elderly people are 
very apt to take the disease, while of typhoid fever the opposite is true. Most 
authors lay great stress upon predisposing causes. Among these, taking cold 
is not so important as are errors in diet and mild attacks of gastro-intestinal 
catarrh, which are shown by numerous observations to predispose strongly to the 
disease, because the acidity of the gastric contents is thus diminished, and the 
retention of comma bacilli in the intestine is thus facilitated. The stage of incu- 
bation seldom lasts over one to three days at most. 

Clinical History. — In cholera, as in most acute infectious diseases, the inten- 
sity of the illness varies between the extremes of mildness and severity, so that 
usually a correct interpretation of the mildest cases is rendered possible only by 
the fact that an epidemic exists and by the discovery of comma bacilli. These 
insignificant cases are called simple choleraic diarrhoea. The symptoms are 
those of a violent acute intestinal catarrh; the dejections are watery, rather 
large, painless, and number about three to eight in twenty-four hours. There 
is considerable malaise, complete anorexia, and thirst, and there may already be 
indications of severer choleraic symptoms — vomiting, slight pains in the calves 
of the legs, and diminished secretion of urine. Many cases recover after a few 
days or a week, but in others the first mild diarrhoea is succeeded, at the end of 
about one to three days, or rarely later still, by a severe attack of cholera. In 
such cases we speak of a " premonitory diarrhoea of cholera." 

The mild form is succeeded in a gradual transition by the cases designated 
as " cholerine." Cholerine exhibits the symptoms of a violent, rather sudden 
cholera morbus. It often begins at night. To the diarrhoea, which now and then 
displays even at this time the characteristics of pronounced cholera, vomiting is 
soon added. The accompanying constitutional symptoms are rather severe. 
There is great languor and depression. The voice grows weak, the extremities are 
cool, the pulse is small and accelerated, painful cramps occur in the calves of the 
legs, the urine grows scanty and perhaps albuminous. The whole attack lasts 
about a week or two, before recovery is complete. The course of the disease is 
not infrequently varied by repeated improvements and relapses. 

From these cases of medium severity there is again a continuous line of tran- 



88 



ACUTE GENERAL INFECTIOUS DISEASES 



sition to the pronounced severe form of cholera. Statistics as to the frequency 
of the separate forms can not be given, since many of the milder cases escape 
observation. 

The true attack of cholera may begin suddenly with the severest symptoms. 
As a rule, however, it is preceded, as already stated, by a first stage of brief pre- 
monitory diarrhoea. This, after one to three days, is replaced with equal sudden- 
ness by the severe symptoms of the second or " algid stage," or " cholera asphyxia." 
Its first symptoms are the abrupt appearance of great bodily weakness, chilliness, 
and vertigo. The characteristic gastro-intestinal symptoms soon declare them- 
selves. 

The diarrhoea grows very violent. At short intervals there are copious painless 
dejections, which at first retain somewhat of a feculent character, but very soon 
present a characteristic resemblance to rice-water, gruel, or whey. A single 
stool will measure a little less than half a pint (grammes 200). The stools 
have no color and almost no odor. They are watery, and usually deposit a finely 
granular, grayish-white sediment upon standing. Their reaction is neutral or 
alkaline. Only one or two per cent, is solid matter, with a little albumen and 
a relatively large amount of sodic chloride. In many severe cases the dejections 
contain more or less blood. The microscope reveals epithelium, triple phosphate, 
and numerous micro-organisms. Of these last a part are the comma bacilli, 
and a part are bacteria of putrefaction, etc. 

These excessive evacuations are but very rarely absent. They are more apt 
to fail if death occurs at the end of a few hours — cholera sicca. 

[In cholera sicca the intestines after death contain the characteristic rice- 
water material which, perhaps owing to paralysis of the muscular coat, was not 
expelled during life.] 

The appearance of the diarrhoea is soon followed by frequent though rarely 
distressing vomiting. The vomitus consists in part of ingested liquids and in part 
of an actual transudation through the mucous membrane of the stomach and 
intestine. Hiccoughs may accompany and follow the emesis. 

In addition to these prominent digestive symptoms of vomiting and profuse 
diarrhoea there are complete anorexia and excessive thirst. The tongue has a 
thick, dry coat. The abdomen is usually flat and soft, or it may be concave and 
hard. Sometimes we may feel fluctuation in the intestines, due to their being 
filled with fluid. There is not much real abdominal pain; what there is, is de- 
scribed as a " feeling of heat and pressure " around the umbilicus. 

At the same time very severe symptoms develop in other organs. The circu- 
latory system is chiefly affected. 

The action of the heart may be stimulated at the beginning of the attack. 
The patient complains of palpitation and great precordial anxiety. After a brief 
time, however, cardiac weakness appears, and continually increases. The action 
of the heart becomes very weak, and the heart-sounds feebler and feebler. The 
pulse at the wrist grows very small, and is usually somewhat accelerated. In a 
severe case the pulse vanishes completely after a few hours. 

This collapse of circulation makes itself quickly evident in the appearance of 
the patient. The face and extremities grow cool, and then ice-cold; the complex- 
ion becomes partly livid and partly a bluish gray ; the lips are almost black. The 
surface temperature may fall below 95° (35° C), while in the rectum febrile tem- 
peratures may often be observed, reaching 102° (39° C.) and higher. The eye and 
cheek grow very hollow, the skin becomes wrinkled, and loses all its elasticity. 
The voice grows hoarse and feeble (voice of cholera). Respiration is laborious 
and superficial. The mind may remain unclouded to the end, but usually there is 
great apathy, and all acuteness of perception is destroyed. Only a few patients are 
restless and excited. Reflex action is much impaired. 



CHOLEKA 



89 



One characteristic symptom is the cramps in the muscles. These are usually 
very painful, and consist in tonic contractions of the muscles, particularly those 
of the calf of the leg, but also those of the toes, thighs, arms, and hands. The 
cramps occur spontaneously or upon the least provocation, last a few minutes, and 
recur at short intervals. The precise reason of their occurrence is not yet known. 
It may be the effect of poison (vide infra). They can be observed in other severe 
acute diseases, although most marked in cholera. They sometimes occur in chol- 
era morbus. 

In a well-developed attack of cholera there is almost invariably oliguria or 
anuria. The urine, if any be secreted, is concentrated, with abundant sediment, 
and it very often contains albumen. In many cases not one drop of urine reaches 
the bladder for days, and this condition persists till death or recovery. 

The symptoms thus far depicted, if taken as a whole, represent the algid stage, 
which seldom lasts more than one or two days. In many cases death occurs 
during this period. It is ushered in by the tokens of extreme general prostration, 
and may take place after a few hours, or more frequently in the second half of the 
first day. But in other cases the " stage of reaction " succeeds. This may be a 
true compensatory period, leading directly to convalescence. The evacuations 
become less frequent and more feculent, and the vomiting ceases. The pulse 
becomes stronger, the cyanosis and coolness of the extremities diminish, and an 
abundant perspiration is not infrequent. After a few days urine is again ex- 
creted. This is almost invariably quite albuminous, and usually contains casts 
and red blood-globules. If convalescence be uninterrupted, however, the urine 
very soon becomes perfectly normal, and after a week or two recovery is to be 
regarded as complete. 

Departures from this favorable course of the stage of reaction are frequent. 
Eecovery may be interrupted by repeated relapses into the previous condition, 
sometimes with a fatal result; instead of convalescence, there is developed a 
severe third stage, usually with fever. This stage ordinarily bears the generic 
name of cholera typhoid, although it is subject to manifold variations in its clin- 
ical symptoms as well as its exciting causes. 

Cholera typhoid may present an actually typhoidal general condition with 
severe fever. There is a considerable elevation of temperature, headache, and 
dullness. The pulse is full and rapid, the face flushed. The skin, particularly 
that of the extremities, sometimes presents the so-called choleraic eruption, in the 
form of an erythema, roseola, urticaria, or the like. This variety of cholera 
typhoid ends after a few days in recovery, or else passes into one of the following* 
conditions. 

A second form of cholera typhoid is distinguished by the development of the 
most diverse local inflammations. Thus, there may be a severe dysenteric or diph- 
theritic inflammation of the small and large intestine, attended by offensive puru- 
lent and bloody stools. Pneumonia is also possible, as well as purulent bronchitis, 
diphtheritic inflammation of the larynx, pharynx, bladder, and female genitals, 
parotitis, and sometimes erysipelas and pyaemia. And when we consider that, 
besides all these conditions, the usual intestinal symptoms, or those of choleraic 
nephritis, may exist also, it is evident how varied the clinical picture may be. 
The development of these local affections frequently lays the foundation for 
numerous sequelae. 

Choleraic nephritis gives rise to the third or uraemic variety of cholera typhoid. 
The secretion of urine is almost suspended. The region of the kidneys is some- 
times sensitive on pressure. The little urine that is still passed contains numer- 
ous casts, albumen, and frequently renal epithelium and white and red blood-glob- 
ules. Somewhere toward the end of the first week, or possibly earlier, there are 
grave nervous symptoms, to be regarded as uraemic : first there is headache and 



90 



ACUTE GENEKAL INFECTIOUS DISEASES 



vomiting, then sopor and coma, or delirium and convulsions. Most of these cases 
are fatal. 

Pathology and Pathogenesis. — We are now acquainted with the manifold 
symptoms and varieties of the disease. If we seek for the pathological changes 
which control the process, and endeavor to find some correspondence between 
them and the symptoms, we shall be disappointed. At least, in its early stages, 
cholera is merely a severe local disease of the intestine. We find the serous layer 
of the coils of the small intestine rose-red from congestion. The mucous mem- 
brane is in a state of catarrhal inflammation : it is swollen, reddened, and at first 
covered with a layer of tough, transparent mucus; but very soon an abundant 
transudation flows into the canal, so that the intestinal coils are filled with a large 
amount of clear fluid, looking like rice-water or gruel, and so devoid of bile 
as to indicate the suspension of its secretion. The signs of inflammation of 
the mucous membrane now grow more pronounced. The solitary follicles and 
Peyer's patches become swollen, with edges of a vivid red, and frequently there 
are many small ecchymoses in the mucous membrane. The extensive desquama- 
tion of the epithelial lining of the intestine has also been regarded as important, 
because it was regarded as in part the cause of the copious transudation. Still 
it may be questioned whether the desquamation is not, at least to some extent, 
a post-mortem change. In yet later stages of the disease the intestinal trouble 
very frequently assumes a croupous-diphtheritic character. The surface is ne- 
crosed and ulcerated in many places, and the contents of the intestine are no 
longer colorless, but sanious and bloody, with a foul odor. 

Otherwise most of the post-mortem lesions correspond to what was obvious 
at the bedside. The muscles exhibit an early and persistent rigor mortis, and fre- 
quently contract in such a way as to throw the corpse into some unusual posture. 
All the internal organs are remarkably dry, pale, and anaemic. The left ventricle 
is contracted. The blood lies mostly in the large veins, the right side of the 
heart, and the cerebral sinuses. It is thickened, is but little clotted, and is said to 
resemble the juice of bilberries or huckleberries. The spleen is not enlarged — an 
exception to the rule in infectious diseases. The kidneys present marked passive 
congestion, most pronounced in the cortex. The microscope reveals a greater or 
less degree of parenchymatous nephritis, with great destruction of the epithelium. 
If death takes place at a rather advanced stage of the disease, the tissues have lost 
their characteristic dryness, and the most diverse local lesions, including nephri- 
tis, may be found to have occasioned death. 

If we search for the connection between the pathological changes just de- 
scribed and the cause of the disease, or again between these lesions and the clin- 
ical symptoms, the first point to guide us is that the comma bacilli are found 
only in the lumen of the intestine, and never in the blood or in other parts of 
the body. The intestinal symptoms are satisfactorily explained by this abnor- 
mal state of the intestine, but for all the other grave symptoms we have to 
seek some special cause. The desiccation which the body undergoes as a result 
of the excessive liquid dejections can not fail to affect the tissues, but can not 
fully explain the symptoms, for the circulatory disturbances and the cardiac 
failure at least may develop before large evacuations have occurred. It has also 
been settled beyond question by means of the newer investigations that precisely 
the worst symptoms of cholera — namely, the muscular cramps, the subnormal tem- 
perature, and the changes in the blood — are occasioned by the chemical results of 
tissue metamorphosis in the comma bacilli, that is, by the so-called toxines. Some 
of these have been already isolated chemically by Brieger and others. It is an 
interesting circumstance that the amount and virulence of the toxines formed 
by the comma bacilli seem to depend on the physical characteristics of the nutrient 
material on which the culture grows. 



CHOLEKA 



91 



As to the complications which occur in the later stages of the disease and 
which are embraced under the generic name of cholera typhoid, we regard them as 
mainly secondary. The choleraic process itself does not cause them, but is merely 
the occasion for their appearance. The examination of the intestine in such 
cases shows that numerous other varieties of bacteria follow closely upon the 
comma bacillus, gaining entrance to the system by treading in its footsteps. 
Cholera nephritis is probably due to various causes. Some forms of nephritis seem 
to be caused by specific cholera toxines (in analogy with scarlatinal nephritis), 
while others are probably of a secondary septic nature. 

Diagnosis. — A positive diagnosis of cholera can be made only by finding the 
comma bacilli in the stools. When an epidemic prevails it is often neither neces- 
sary nor possible to make the search in each individual case. Sporadic cases or 
the first cases of a beginning epidemic can and must be diagnosticated only in 
this way, which gives absolute certainty. We can not give here a detailed account 
of the bacteriological diagnosis, but we may state briefly that, when cholera exists, 
the simple microscopical examination of a smear preparation sometimes makes 
the diagnosis extremely probable. For this purpose a small clump of mucus is 
taken from a stool as fresh as possible, spread on a cover-glass as thinly as possi- 
ble, fixed by passing it carefully through the flame several times, and stained with 
an aqueous solution of methylene blue or carbol-fuchsine. In actual cholera we 
then find the comma bacilli sometimes in large amount (almost a pure culture) 
or especially arranged in characteristic small groups. To render our diagnosis un- 
assailable we must employ gelatine or agar plate cultures, etc., the details of 
which are to be found in the text -books of bacteriology. 

All those affections whose symptoms are like those of cholera may be con- 
founded with true cholera, especially cholera morbus (vide infra) ; and also cer- 
tain cases of poisoning, especially acute arsenical poisoning, may give rise to 
symptoms wonderfully like cholera. 

The prognosis should always be guarded at the beginning, even if the symp- 
toms be mild, for, as already mentioned, a simple diarrhoea may prove to be 
" premonitory " of a severe attack of cholera. During the real attack the prog- 
nosis grows graver in proportion as the case presents the characteristics of as- 
phyxia and cyanosis. The mortality in many epidemics is frightful. All the 
inhabitants of a house or street may in a brief period be swept away. Accurate 
statistics are diflicult to give. If we count the typical cases alone, the mortality 
is not infrequently fifty to seventy per cent. In about two thirds of the fatal 
cases death occurs during the first days of the stage of asphyxia, and in about one 
third during the second period, known as " cholera typhoid." The influence of 
the diet and the hygienic surroundings of the patient before his illness is impor- 
tant. A greater proportion of children and old people perish than of the mid- 
dle-aged. 

Prophylaxis and Treatment. — The measures to be taken to prevent the spread 
of the disease, when it has once started in a place, can be only briefly discussed 
here. The chief things are the quickest isolation possible of the first cases that 
occur, the disinfection of the stools and all linen, objects, etc., soiled by the stools, 
and finally the determination of the source of infection (drinking-water, etc.), 
in order to prevent further infection. The evacuations (stools and vomitus) can 
be best disinfected with a five-per-cent. solution of carbolic acid or with milk of 
lime, chloride of lime, etc.; the linen and other objects should be disinfected in a 
special disinfecting apparatus. It is very important to keep a strict oversight of 
the drinking-water, milk, and all articles of food eaten in an uncooked con- 
dition. 

In regard to individual prophylaxis, we must remember especially that any 
slight gastric or intestinal catarrh increases the liability to the disease. Hence, 



92 



ACUTE GENEKAL INFECTIOUS DISEASES 



at the time of a cholera epidemic, careful dietetic restrictions are imperatively 
necessary and every disturbance of the stomach or the intestines, even the slight- 
est, needs the promptest and most careful treatment. It is best wholly to avoid 
the use of water that has not been boiled, raw vegetables, etc. 

[Various efforts have been made to render human beings immune to choleraic 
infection. The best results seem to have been attained by inoculating Haffkine's 
attenuated virus. — V.] 

In the treatment of the cholera attack itself many physicians even now use 
opium (laudanum or pure opium in powder, gr. ss.-j, grm. 0.03-0.05), while others, 
especially at the beginning of the disease, prefer large doses of calomel (gr. v-x, 
grm. 0.3-0.5, several times), and during the subsequent course they give con- 
tinued small doses of calomel (gr. ss.-j, grm. 0.03-0.05, every two hours). In 
the algid stage warmth is especially advisable. Hot baths, hot packs, sweat- 
boxes with dry or moist hot air, embrocations of hot oil, an abundant supply 
of hot drinks (coffee, tea, mulled wine, broths) are praised by all physicians, 
and they must certainly be used. The remaining treatment is symptomatic; 
morphine or ice for the vomiting and embrocations of chloroform oil or sub- 
cutaneous injections of morphine for the painful cramps in the calves. The 
weaker the heart becomes, the more energetically must we give stimulants (injec- 
tions of camphor or ether, champagne). 

Among the newer methods of treatment tried during the last epidemic we may 
mention subcutaneous infusions of warm " normal " (0.6 per cent.) salt solution 
in the infraclavicular region or under the skin of the abdomen. By uninter- 
rupted infusion by means of an irrigator or a funnel two or three quarts (litres) 
of salt solution can be infused in twenty-four hours. Intravenous injections have 
given still better results, and injections into the abdominal cavity have also been 
tried. Cantani strongly recommends intestinal injections (" enteroclysis ") with 
warm tannin solutions at a temperature of 100° to 104° F. (38°-40° C). The 
fluid contains 5 to 10 parts of tannic acid, 50 parts of gum arabic, and 2 or 3 
parts of laudanum to 2,000 parts of water. All these methods are believed to 
have shown some favorable results, but none of them has been able to attain gen- 
eral recognition and use. After many experiments most physicians have finally 
gone back to the old forms of treatment. 

[The vital importance of the serious treatment of a beginning diarrhoea dur- 
ing a cholera epidemic can not be too strongly insisted on. Kest, simple diet, and 
a little medication will, in the vast majority of instances, entirely prevent grave 
consequences. The apparently trifling character of the symptoms is apt to lead 
people into a false security. Those who can leave an infected district should do 
so without delay. 

With reference to the prevention of an epidemic, a pure water supply and 
strict cleanliness in its broad sense possess far more virtue than cordons of troops 
or measures of quarantine. It is more practicable to destroy the soil than to keep 
out the seed in these days of constant and rapid international communication. 
The systematic disinfection of all cholera discharges or articles soiled by them 
should be a matter of course.] 

Great caution must be exercised about the diet, not merely during the attack 
itself, but for a considerable time afterward. At first we can allow only thin por- 
ridge, milk, broths, and toast or rusks. It is advisable to administer dilute 
hydrochloric acid with the food. 

The treatment of cholera typhoid varies greatly, of course, according to 
the kind of attack. The separate complications should receive their customary 
treatment. 

[In the first stage, absolute rest, opium, and lumps of ice by the mouth ad libi- 
tum are the chief measures on which reliance is to be placed. It should be remem- 



MALAEIAL DISEASES 



93 



bered that the entire function of the intestinal tract is reversed ; thus, instead of 
an absorbing, it has become an excreting surface. 

In the stage of collapse the nervous system is more or less paralyzed, the blood 
is damaged by the loss of its watery constitutents, and the circulation of that fluid 
is greatly impeded. The subcutaneous or gastric absorption of drugs is conse- 
quently delayed or suspended. The utility of any active internal treatment dur- 
ing this stage is very questionable. Certainly narcotism by opium is highly un- 
desirable. Mild external stimulation and the tentative administration of ice and 
small quantities of champagne or food are, at all events, not likely to do harm. 
Nature sometimes reasserts herself when the conditions are seemingly desperate, 
and the third stage, or that of reaction, comes on. In this stage, careful nursing 
and a sensible symptomatic but in no way meddlesome treatment are most like- 
ly to be followed by good results.] 



CHAPTER XIV 

MALARIAL DISEASES 

{Intermittent Fever. Fever and Ague. Swamp Fever) 

etiology and Pathological Anatomy. — Malarial poisoning is the best exam- 
ple of a purely " miasmatic " affection. The poison which produces the disease is 
without doubt localized in certain places, in which every human being is liable to 
become its victim; but if an infected person comes to a place free from malaria 
and not naturally favorable to its development, there is no danger that he will 
cause the disease in others. The disease is never caught through contact with the 
patient. It is not at all contagious ; the malarial poison, after it has once pene- 
trated into the body, has practically no opportunity to escape again in an efficient 
form from the diseased system into the outer world; but the blood of a patient 
injected into a healthy person may transfer the disease (Gerhardt and others). 

If we except the polar zones, there are few regions where malaria is not en- 
demic in certain parts, at least from time to time, if not constantly. There is, 
however, great variation in the virulence as well as in the number of cases. While 
the common forms of intermittent fever are very frequent in Germany, in numer- 
ous places, especially on the shores of the North and Baltic Seas, and also in 
the alluvial lands of the Vistula, Oder, Elbe, etc., yet the grave forms of the dis- 
ease are very rare. Other lands are notorious for the severe malarial diseases, 
e. g., Hungary, the lands lying on the lower Danube, the Roman Campagna, the 
Pontine marshes, Sicily, and numerous districts in other parts of the world, 
chiefly tropical. Numerous observations have only served to confirm the opinion 
that the soil is the true home and cradle of the malarial poison, and that the 
virus, escaping thence into the lower strata of the atmosphere, may be taken into 
the system, probably during inspiration. Permanent dampness of the soil is essen- 
tial to the development of the malarial poison. This explains why marshy dis- 
tricts are so often malarial. The ground must not be covered by a great amount 
of water, but must during the dry season lie exposed to the atmospheric air. The 
access of air to the moist soil seems to be a second essential condition for the devel- 
opment of the malarial germs. A third influential factor is the temperature of 
the air, as proven by the great prevalence of the disease in southern countries and 
in the summer season. 

The special agent which causes malaria was first described by Laveran in 1881, 
and soon after by Marchiafava and Celli. Since then many other observers, espe- 



91 



ACUTE GENERAL INFECTIOUS DISEASES 



cially in Italy, have investigated the subject and have given us very interesting 
information about these peculiar parasites. Besides the writers named we may 
refer to the studies of Golgi, Guarnieri, Canalis, etc. The parasite belongs to 
the protozoa (whether to the sporozoa or rhizopoda is still uncertain), and is now 
generally called the Plasmodium malarias. The organisms are found in the blood 
of men sick with malaria, in unstained specimens or in specimens stained with 
methylene blue, and are at first inclosed in the red blood-corpuscles. Here they 
appear as delicate protoplasmic bodies with an indication of a nucleus; at rest they 
have a rounded form, but they may assume various shapes through their amoeboid 
movements (see Fig. 10). These movements probably have some relation to the 
nutrition of the parasite, which takes place at the expense of the red blood-corpuscle 



Fig. 10.— Different forms of the malarial Plasmodium according to Marchiafava and Celli. a, b, c, or- 
dinary Plasmodia without pigment, d, e, spore formation in Plasmodia. /, g, pigmented plasmodia 
with spore formation, h, i, oval and crescentic forms of plasmodia. k, pigmented Plasmodium 
with flagellse. 

that shelters it. The haemoglobine taken up by the plasmodium is thus changed to 
melanine, which probably contains no iron, and the black granules of this mela- 
nine can easily be seen in the body of the adult parasite. The second phase in 
the life of the plasmodium now begins and serves for its propagation and in- 
crease. The amoeboid movements cease, the pigment granules collect in a ring 
about the periphery, in radiating stripes, or in the center of the parasite, while 
the rest of the mass in a few hours breaks up into a number of rounded spores. 
Their inclosing capsule disappears, the spores are set free in the blood and pene- 
trate other red blood-corpuscles. 

Besides these chief forms of the malarial plasmodium just described, there 
are also other forms (crescentic form, flagellated form) whose relations to one 
another and to the ordinary type are still obscure. This fact alone seems to be 
certain that the different clinical forms of malaria — tertian, quartan, pernicious, 
etc. — correspond to different biological forms of the plasmodium. By inocula- 
tion of the blood into another human being we can therefore produce nothing but a 
tertian from a tertian or a quartan from a quartan. The quotidian fever is due to 
two tertians co-existing in the same person, each individual tertian owing its origin 
to a special generation of the plasmodium. The continuous and pernicious 
malarial fevers are characterized by the presence of many of the crescentic forms 
of development. 

Although no one has yet been successful in establishing this view of the plas- 




MALARIAL DISEASES 



95 



modia by means of pure cultures and inoculation of the same, yet the relation 
of the plasmodium to malaria seems evident from the fact that in every patient 
with malaria the plasmodia can be easily demonstrated in the blood, while these 
same forms are never detected in the blood except in malaria. The way in which 
the plasmodia enter the human body is not yet known. It may be by inhalation 
or by the stings of insects. 

[It has now been proved that malarial organisms can be communicated by 
certain varieties of mosquito (anopheles claviger and a. pictus) to man, and also 
by man to the mosquito. The obvious deduction is that a healthy man should 
guard himself from mosquitoes for his own sake and an already infected man for 
the sake of others. — V.] 

The investigations with regard to the plasmodium of malaria have also ex- 
plained the long-recognized fact that in chronic malaria large amounts of pig- 
ment collect in the internal viscera. These deposits are most abundant in the 
spleen, which in the chronic varieties of the disease develops into a firm, hard 
tumor; but they are also found in the bone-marrow, liver, brain, and kidneys, 
leading finally in the liver and the kidneys, in frequent instances, to processes of 
chronic degeneration and inflammation. It is especially noteworthy that in 
those patients who present the most marked cerebral disturbances (pernicious 
comatose fever, vide infra), the cerebral capillaries are found to be completely 
occluded with pigmented plasmodia. 

[Periodical fever is very widely distributed in the United States, and in the 
southern portions occurs in severe though not in the severest forms. Some regions 
which were formerly free from it are no longer so, and, vice versa, some regions 
which were greatly subject to it are now exempt; these changes are closely con- 
nected with the clearing and upturning of virgin soil largely impregnated with 
decaying vegetable matter, and with the subsequent cultivation of the same for 
considerable periods of time. The poison does not extend far above the surface of 
the ground, as is shown by the relative safety of sleeping in the upper as compared 
with the lower story of a house; during the night the poison seems to exist in 
greater intensity than during the day. Attacks are more liable to occur during 
the spring and autumn than at other seasons. 

The hopes which have been entertained in some quarters that malarial regions 
might be rendered healthy by large plantations of the Australian eucalyptus glob- 
ulus, a rapidly growing tree which absorbs immense quantities of water, do not 
seem likely to be realized in the light of Erench experience in Africa, and in that 
of the Trappist monks in Italy.] 

Klebs and Tommasi-Crudeli have made extensive investigations as to the 
nature of the malarial poison. We must regard it as organic. The authorities 
just named state that the true cause of malaria is a specific variety of bacillus. 
They found peculiar bacilli and their spores both in the earth of malarial regions 
and in the adjacent strata of the atmosphere; and, by infecting rabbits with 
these, they were able to induce attacks of fever, swelling of the spleen, and the 
characteristic formation of pigment matter (vide infra). Before this, bacilli and 
spores had been found in the blood and spleen of patients suffering from malaria. 
It can not yet be said just how much significance these discoveries have. 

[To Laveran really belongs the credit for the discovery and accurate descrip- 
tion of the plasmodium. His work in Algiers has been substantiated by observers 
in widely separated malarial regions, and, at the same time, no very important 
additions have been made to it. 

It is difficult to overrate the diagnostic and therapeutic importance of this dis- 
covery. The ordinary intermittents are usually easy of diagnosis, but the remit- 
tent forms often simulate typhoid fever, while the pernicious form may resemble 
uraemia or intracranial disease. Especially in pernicious cases life may be saved 



96 



ACUTE GENEBAL INFECTIOUS DISEASES 



by prompt and appropriate treatment, which must be based, of course, on accurate 
diagnosis. The following details may be of use to those who are not familiar with 
the method of blood examination. The finger tips should first be scrubbed with a 
nail-brush, and soap and water, and then washed in alcohol or ether, to obviate the 
danger of mistaking minute particles of dirt for the pigment-granules derived from 
the destruction of red blood-corpuscles. A portion of a drop of blood is then to be 
received on a scrupulously clean object- or cover-glass, and squeezed out between 
the two, so that a thin layer of blood with separation of the individual corpuscles 
is secured. The amceboid forms of the plasmodium retain their movements for a 
number of minutes in a warm room, much longer, of course, with a warm stage. 
The presence of pigment-granules in the red corpuscles may be the readiest indi- 
cation of the presence of the organism. The crescentic forms are found more 
especially in chronic cases which have been under treatment by quinine, as is 
stated by Osier. Many of the other forms can be found in the blood only during 
a paroxysm. The editor has seen them in abundance in a cachectic malarial 
patient from Panama, and failed to find them again after a single large dose of 
quinine, which terminated the chills. 

In dried and stained specimens it is also possible to detect the organisms, but 
amoeboid movement is, of course, lost.] 

Liability to the disease is very widespread. No race, no age, no sex, enjoys 
immunity. It is a noticeable fact that those who have had the disease once are 
all the more apt to have it again. Former patients, although they feel perfectly 
well in a non-malarious region, are very liable to fresh attacks, or at least much 
discomfort, as soon as they re-enter an infected district. The time of incubation 
does not seem to be constant. It is put at from six to twenty days, but may be 
shorter. We shall consider below chiefly the common forms of intermittent, such 
as appear in Germany, contenting ourselves with a very brief description of the 
severer forms. 

Varieties of Malarial Disease 

1. Intermittent Fever. — This is the simplest form, and has for its especial 
characteristic the relative brevity of the febrile attacks, which almost always 
exhibit a remarkably uniform type. A febrile attack of this kind is frequently 
the very first symptom of the disease. In other cases the paroxysm of fever is 
preceded by a prodromal stage lasting several days, during which the patient feels 
languid, has no real appetite, complains of headache and pain in the back of the 
neck and in the limbs, and often even thus early presents a slightly yellowish 
complexion and an enlarged spleen. 

In the typical attack of intermittent fever there are three stages. The attack 
begins with a chill. There is pronounced malaise, attended by intense chilliness 
and more or less shivering. The skin is cool and pale, the face may be somewhat 
livid. The temperature of the interior of the body is elevated, and rapidly rises 
higher. In by far the greater number of cases the attack occurs in the morning, 
or at least before noon, and but seldom later in the day. This cold stage varies 
greatly in length, usually lasting an hour or two. ' 

The chilliness is followed by the hot stage. The skin grows burning hot, the 
face flushes, the pulse, which was before small, becomes full, and the action of the 
heart is excited. At first the temperature continues to increase, and reaches in 
this stage its maximum for the attack. It is exceptional for it to remain under 
104° (40° C), and by no means rare for it to touch 106°, or even 107° (41°-41.5° 
C). This stage almost always lasts longer than the preceding, generally about 
three to five hours. The temperature may begin to fall as early as the latter part 
of the hot stage, but may persist till the beginning of the third stage. 

In this sweating stage the skin grows moist, and there is soon a profuse gen- 



MALARIAL DISEASES 



97 



eral perspiration. The patient begins to feel much better. In a few hours the 
temperature usually becomes normal, and, after lasting in all about eight to twelve 
hours, the attack is over. It may be shorter or rarely longer. Usually, however, 
the temperature keeps on sinking slowly, so as to be still subnormal even on the 
next morning, perhaps not above 97° (36° C). 

There are certain peculiarities in the temperature-curve which we have our- 
selves observed. The elevation of temperature is almost invariably more rapid 
than its decline. The rise is most abrupt during the first hours of the cold stage, 
and slower during the first portion of the hot stage. The ascent is but very sel- 
dom interrupted. During the hot stage, when the fever is highest, in the neigh- 
borhood of 106° E. (41° C), there are not infrequently two little summits to the 
fever-curve, if the temperature be taken at short intervals. But the temperature 
may for hours remain the same. The temperature generally begins to fall some 
little time before the perspiration is evident. The decline is slow. It may be per- 
fectly continuous, or it may be interrupted by fresh elevations, which are some- 




Fig. 11.— Quotidian inter- Fig. 12.— Tertian intermittent fever, 

mittent fever. 

[Chinin 2.0 = Quinine 30 grains.] 



times slight and sometimes considerable. In many cases the descent is by steps, 
the temperature remaining the same for half an hour or an hour, and then 
abruptly falling a couple of degrees and remaining for a time at this new level. 

The chief characteristic is not, however, the nature of the single attacks, but 
the peculiar manner of their repetition. If the case is not under treatment, the 
single attacks keep recurring for a time, either daily, as in the quotidian variety, 
or every second day. This latter type of tertian intermittent fever (cf. Figs. 11 
and 12) is probably the most frequent. There may exceptionally be still longer 
afebrile intervals. Thus we have quartans, quintans, etc. If there are two attacks 
in one day, a rare event among us, we have a double quotidian. If there is 
a violent attack every second day, and on the intervening days there are milder 
attacks, it is a case of double tertian. Very often the attacks do not recur at just 
the same time of day, but a few hours earlier each time. Less frequently they 
are later. This peculiarity is expressed by the term " anticipating " or " retard- 
ing," as the case may be — e. g., a retarding tertian ague. In cases of long stand- 
ing, the paroxysms may finally lose all regularity, so that the fever is described as 
a erratic." 

7 



98 



ACUTE GENEKAL INFECTIOUS DISEASES 



Next to the febrile attacks, the swelling of the spleen is the most constant and 
important symptom. It is usually considerable and capable of demonstration by 
percussion and palpation. At first the tumor increases with every fresh attack, 
and diminishes but little during the intervals. After the patient is freed from his 
attacks of fever the spleen may continue enlarged for some time. It is tender on 
pressure. [Certainly in many cases tenderness is absent. — V.] The liver may 
likewise be swollen, but this is less constant and also less important. 

Certain changes in the skin are very characteristic, chief among which is a 
peculiar yellowish-brown discoloration. This is due to an abnormal deposition of 
pigment in the skin. Herpes on the lips or nose is seen very frequently during 
the attacks. We have seen one case of herpes on the cornea. Mention has also 
been made of urticaria, purpura, and other eruptions. 

Other internal organs than those already spoken of are rarely much disturbed. 
One symptom should be mentioned, which we have ourselves seen several times, 
viz., a quite marked acute dilatation of the heart during the attack. There were 
no bad results, and the normal condition was soon re-established. We may hear 
during the attack functional cardiac murmurs of a blowing character. Thoracic 
examination, particularly if made during the attack, may afford the signs of a 
dry bronchitis. Sometimes there is considerable diarrhoea, or other evidence of 
intestinal derangement. Catarrhal jaundice is confined to the severer cases. 
Sometimes the urine has a moderate amount of albumen. Genuine nephritis is 
met with only in the graver varieties of the disease. The increased excretion of 
urea on the days of the fever results, as in any fever, from the increased destruc- 
tion of albumen. Severe pain in the cervical and upper dorsal vertebras is re- 
garded as characteristic of intermittent. 

Besides the typical attacks, rudimentary and modified ones are not rare, in 
which the separate stages are ill defined, or in part wanting. We are most apt to 
see this in cases which have been already treated with quinine. Children do not 
have a true rigor. They merely become pale or livid. They may present marked 
nervous symptoms. 

2. Pernicious Intermittent Fever. — This dangerous form occurs only in the 
true malarial districts, and is often preceded by a few attacks of a milder charac- 
ter. Then appear, in addition to the more or less perfectly marked stages of the 
febrile attack, other graver symptoms which not infrequently end in death. 
Severe nervous symptoms are most frequent. There may be unconsciousness, 
coma, delirium, or epileptiform or tetanic convulsions. None of these symptoms 
persist longer, as a rule, than does the common sort of an attack, and in a favor- 
able case vanish completely when the sweating, which is usually profuse, begins. 
The great danger comes from the recurrence of the attacks. A second form of 
pernicious intermittent fever causes violent gastro-intestinal symptoms, which 
may almost exactly imitate the algid stage of cholera, with vomiting, diarrhoea, 
and collapse; or there may be severe cardialgia, dysentery, and the like. In the 
so-called pernicious intermittent with jaundice, intense jaundice appears during 
the attack, with vomiting and diarrhoea, and sometimes the gravest nervous symp- 
toms. There are certain very peculiar forms, in which local disorders, such as 
pleurisy or pneumonia, can be demonstrated during every attack, but vanish 
wholly or in part when the temperature declines, only to appear again during the 
next attack. 

[The pernicious form occurs in isolated cases wherever the ordinary variety of 
the disease prevails, but is much more common in the Southern and Western 
States, and there varies in frequency in different years. Periodicity in the attack 
is not always observed. The pernicious character is not always manifested in the 
first attack, one or more mild paroxysms being often precedent, In this country 
the algid form of pernicious periodic fever is often called " congestive chills,"" 



MALAEIAL DISEASES 



99 



and this form is more common than the comatose or another form mentioned below 
by the author — the hemorrhagic. In the latter the blood escapes from the kid- 
neys, and less constantly from the mucous membrane. During the late civil war 
the mortality among the white soldiers of the United States army from pernicious 
malarial fever was 23.91 per cent.] 

3. Remittent and Continuous Forms of Malarial Fever. — These are generally 
severe, and are seen, like the preceding, only in the worst haunts of malaria. The 
proof that they have the same aetiology as intermittent fever lies in the fact that 
they are sometimes developed out of the milder forms ; but it is to be noticed that 
many types of disease which physicians in the tropics describe as malarial affec- 
tions have not yet been proved to our satisfaction to have an actual identity of 
origin with the common intermittent fever. A positive diagnosis can be made 
only by examining the blood for the plasmodia. The symptoms of this variety are 
likewise those of a severe constitutional infection. Gastro-intestinal symptoms 
may predominate ; or there may be such grave nervous symptoms as coma, deliri- 
um, and convulsions; or there may be jaundice, hematuria, and even a general 
hemorrhagic diathesis; or various local disorders may exist, such as pneumonia, 
nephritis, and hepatic and splenic abscesses. The fever is high, but without any 
sort of regular intermissions, maintaining for one or two weeks a remittent or a 
tolerably continuous type. Milder forms may end in recovery after eight to four- 
teen days, but often death ensues at this time, or even earlier. 

[The remittent form apparently shows a greater intensity of the poison or a 
greater susceptibility of the individual. In the United States army, from 1861 to 
1866, its mortality was twelve times as great as that from the intermittent form.] 

4. Chronic Malarial Cachexia. — This occurs in the true malarial regions, and 
affects not only persons who have had frequent attacks of pronounced intermittent 
or remittent fever, but also those who have never had acute attacks. The condi- 
tion is chronic. It may exhibit a genuine intermittent character. The patient 
usually has a decidedly yellowish, malarial complexion, and almost always the 
spleen is evidently enlarged. There are no regular febrile attacks, but merely 
symptoms of general debility, anorexia, tendency to diarrhoea, or, more rarely, 
constipation, vertigo, wakefulness, frequent perspiration, pain in the muscles and 
joints, dyspnoea, and palpitation. There may be such nervous symptoms as trem- 
bling, paralysis, and mental disturbance [or multiple neuritis, q. v.~] ; or we may 
see intestinal symptoms and jaundice. Dropsy occurs; also epistaxis, cutaneous 
ecchymoses, and other signs of a scorbutic condition. The spleen and liver gradu- 
ally become greatly hypertrophied and melanotic. At the same time there may 
be an irregular fever, approaching either an intermittent or a remittent in type. 
Finally, secondary diseases are possible — e. g., tuberculosis, amyloid, or dysentery 
— and these may prove the immediate cause of death. The milder forms may 
be cured, but seldom unless the patient abandons forever the malarial district. 

5. Masked Intermittent. — This is the designation of cases in which, although 
there is no fever, certain other disturbances arise in regular intermittent attacks. 
Chief among these is neuralgia. Its favorite seat is the supra-orbital branch of 
the trigeminus. It may occur in the other branches of the same nerve, or in the 
sciatic, the anterior crural, the nerves of the brachial plexus, and elsewhere. Car- 
dialgia and enteralgia may occur in the same way. These attacks last from thirty 
minutes to several hours, and are frequently associated with all sorts of constitu- 
tional symptoms, but, as we have said, are afebrile. There may be a splenic tumor, 
which aids diagnosis; but this sign may be wanting. 

Numerous other intermittent disorders besides neuralgia have been described 
as masked intermittent. The list includes anesthesia, convulsions, and paralysis; 
also intermittent hemorrhage, oedema, cutaneous affections, and intestinal symp- 
toms. We must add, however, that those who have described diseases of this sort, 



100 



ACUTE GENEKAL INFECTIOUS DISEASES 



some of which seem strange enough, have not always been as critical as they 
ought, and that the connection between many cases of " masked intermittent " and 
true malaria is more than doubtful. 

[6. Typho-Malarial Fever. — This is a term which was formerly in use, but it 
is not a distinct disease. It expresses a combination in the same individual 
at the same time of the effects of the special poison causative of each affection. 
Typhoid being a continued fever, its complication with malaria results in a 
pyrexia of a remittent type. The combination of the two occurs in malarial re- 
gions, especially in the Southern States, and may be seen in non-malarial regions 
in the persons of those in whom malaria, contracted elsewhere, is in a more or less 
active state. 

The characteristic symptoms of the two diseases are intermingled, those of 
typhoid, the graver disease, usually predominating. The history of the case and 
careful observation of the symptoms will generally clear up any doubts felt as 
to the diagnosis in the early stages. It would naturally be supposed that the 
combined affections must produce an illness more severe in character and more 
unfavorable as regards prognosis than belongs to simple typhoid. Such does not, 
however, seem to be the case. Woodward's statistics show that the mortality of 
uncomplicated typhoid was far greater among the white and colored troops alike 
during our late civil war than was the mortality of typho-malarial fever. 

The treatment as regards the typhoid fever differs in no way from that suitable 
for cases of the ordinary affection; the periodic element demands the manage- 
ment appropriate to simple intermittent or remittent fever.] 

Diagnosis. — It is often very difficult to diagnosticate a case of intermittent 
fever at the first visit, particularly in a place where malarial poisoning is infre- 
quent. The history of the case is by no means always enough to put one on the 
right track ; and a single examination of the patient may prove equally negative 
in its practical results, whether it is made during the febrile stage or in the inter- 
val. Continued observation, however, will almost always disclose the regularity of 
the febrile attacks, the splenic tumor, the characteristic complexion, and the 
herpes; and our diagnosis becomes evident. Still it is not very exceptional for 
an intermitting fever to be taken at first for an intermittent malarial one, while 
eventually some quite different disease is found to produce the symptom. Pyaemia 
may give rise to mistakes of this kind; also purulent phlebitis, acute ulcerative 
endocarditis, and even tuberculosis. We should be very cautious in making a 
hasty diagnosis of " irregular intermittent fever." Our own experience has taught 
us that almost invariably the case turns out to be something else. Where there is 
doubt we may, in addition to a careful consideration of all the symptoms and a 
thorough physical examination, be aided by the therapeutic action of qui- 
nine (vide infra). If a high fever of intermitting type is affected by large 
doses of quinine but temporarily if at all, then a diagnosis of malarial intermit- 
tent fever is rendered doubtful. An absolutely certain diagnosis can be made 
only by finding the plasmodia in the blood under the microscope. We have 
already said that the greatest skepticism is requisite in the diagnosis of " masked 
intermittent." 

Treatment. — Malarial poisoning is one of the few diseases upon which we can 
make a direct attack with assured success. In quinine we possess a remedy which 
probably acts upon the very cause of the disease, and its therapeutic efficacy 
is undisputed. Quinine is therefore the sovereign remedy in all forms of 
malarial poisoning, and is often the only drug employed. In the mild cases, 
which are the only kind that occur in Germany, we do not usually give the remedy 
upon the instant that the patient comes under treatment. It is best to wait for 
one or two attacks, partly to make sure of our diagnosis, and partly to learn what 
the type of the fever is, whether quotidian, tertian, anticipating, or recurring at 



MALAEIAL DISEASES 



101 



the same hour; and in most cases this delay works no harm to the patient. Dur- 
ing the attack itself there is seldom any use in special treatment. Of course, 
the patient must stay in bed and be kept warm during the cold stage, and have 
lighter coverings during the hot stage. During the afebrile interval the patient 
may be up if he feels strong enough and is careful.. Quinine (hydrochlorate or 
sulphate) is given about five or six hours before the next attack is due. It is 
best to administer one large dose of twenty to thirty grains (1.5-2 grm.), either 
in solution or in capsules of seven grains (0.50 grm.) each. If the quinine be 
given in powder or capsules, it is a good way to follow it with a few drops of 
muriatic acid, to promote its solution in the stomach. Often one large dose pre- 
vents the next attack. In other cases it does occur, but with less subjective dis- 
turbance, no chill, and more moderate fever. We must then give another large 
dose before the second attack is expected. If the attack does. not take place, then 
we may give for several days quinine to the amount of eight grains (0.5 grm.) 
per diem. After all, relapses are possible, even at the end of several weeks; but 
they yield readily to quinine. 

In the treatment of pernicious intermittent fever, of the masked forms, of the 
remittent and continued fevers, and of malarial cachexia, the chief remedy is like- 
wise quinine, given in sufficient doses. Baccelli has shown that sometimes in 
pernicious fever the direct injection of quinine into a vein may save life. In all 
cases of considerable duration it is also of the greatest importance to remove the 
patient from the malarial region, if it can possibly be done. This often proves to 
be the only way to avoid relapses and attain a perfect cure. 

In cases of longer standing, quinine sometimes loses its power. Then we resort 
to arsenic. It is frequently employed in malarial cachexia and in intermittent 
neuralgia, either alone or combined with iron. We give gtt. v to viij of Fowler's 
solution two or three times a day in water. It is still better to give pills of arseni- 
ous acid containing gr. ^ - (grm. 0.002-0.003) and gradually increasing to a 
daily dose of gr. \ - A (grm. 0.010-0.012). It may be added that arsenic is also said 
to have a prophylactic virtue : a long-continued use of it is stated to render a per- 
son proof against malarial poisoning. We will not speak of the numerous other 
remedies recommended, such as eucalyptus, piperine, pilocarpine, berberine, and 
many others, for they can be entirely dispensed with. 

The management of the severe varieties of malarial disease involves symptom- 
atic treatment as well as the administration of quinine. We can not enter into 
the particulars. In combating the grave, nervous, intestinal, pulmonary, and renal 
symptoms, the dropsy and the ansemia, the physician must conform to the general 
rules of treatment. 

[There is nothing to be gained by allowing a patient to have an unnecessary 
chill. If there is a reasonable probability that his paroxysms are due to malaria, 
a prompt effort should be made to cut them short. Four hours is the shortest 
time that it is safe to allow for quinine by the stomach with probability that the 
expected chill will be prevented. The drug acts much more promptly when 
given hypodermically. The hydrobromate is preferred by some to the sulphate 
for subcutaneous use on account of the necessity of using acid to dissolve the 
latter, and the consequent risk of abscess. Such a risk should have no weight if 
the physician has any suspicion that he has to deal with the pernicious form of 
the disease. If the stomach is irritable, the remedy can be given by enema. 
Quinine can also be given by suppository, though it may thus produce some irri- 
tability of the rectum; but the impossibility of disguising the bitter taste of the 
remedy or of making children swallow capsules renders this a valuable means of 
treatment sometimes in infants and young children. 

Warburg's tincture is an antiperiodic which does good service in cases which 
do not yield to the ordinary methods of treatment. 



102 



ACUTE GENEKAL INFECTIOUS DISEASES 



The hypodermic injection of pilocarpine is reported to abort an impending 
chill. 

Some prefer divided and smaller to the single and large dose of quinine or one 
of its substitutes, a difference of view which is of minor importance. 

In the remittent forms boldness in the use of quinine is required. Cinchonism 
should be induced as promptly as may be, and maintained to a mild degree for 
several days; the quantity of the drug can then be gradually diminished. 

The treatment of the pernicious forms of periodic fever presents itself under 
three main heads: 

1. The prevention of pernicious paroxysms. 

2. The treatment of the paroxysm when present. 

3. The prevention of a recurrence. 

1. We have seen, that very frequently the pernicious character is manifested 
after the occurrence of one or more mild attacks ; consequently, in localities and 
seasons marked by the occurrence of grave cases it is an imperative duty to treat 
every mild case promptly and energetically, a course which unquestionably saves 
many a life. 

2. The management of the paroxysm differs according to the form which it 
assumes ; in other words, is largely symptomatic. Bemiss (Pepper's " System of 
Medicine ") says : " The cure of a congestive chill is one of the most difficult prob- 
lems the physician can possibly encounter." Heat externally, opium and chloro- 
form by the mouth, and morphine and atropine subcutaneously, nutrition by the 
stomach or rectum, according to circumstances, and alcoholics if the action of the 
heart is feeble, are the measures of widest application. 

Whatever the type of the attack, a weak heart calls for alcoholic stimulation. 
Cinchonism is always to be induced as rapidly as possible. 

In the comatose form it is to be remembered that the cerebral and other nervous 
symptoms are not due to congestion, but probably to a combination of the malarial 
and secondary blood-poisons. To quote Bemiss again : " Efforts to nourish the 
patient must never be relaxed. One must see many of these cases before he can 
realize how often they recover from conditions apparently hopeless when promptly 
treated and properly nourished." 

The hsemorrhagic form, like the others, demands cinchonism and careful nutri- 
tion, but also haemostatics. Purgative doses of calomel are indicated in some cases 
of each form, but should not be given in a routine manner. 

3. Prompt cinchonism is the chief means of attaining the third aim of treat- 
ment. Bemoval to a healthy locality should be secured if possible, and the general 
condition of the patient requires careful attention. 

It remains to add that those going to a malarial region can often avoid con- 
tracting the disease by taking advice of a local physician as to hygienic precau- 
tions, and by moderate divided doses of quinine.] 



CHAPTEB XV 
DENGUE 

[This affection has never appeared in Germany, and hence, doubtless, was 
omitted by the author. The name " dengue " is supposed to be a Spanish corrup- 
tion of dandy, the term dandy fever having been applied to the disease by the 
West India negroes on account of the stiff carriage of those affected by it. An- 
other name is " break-bone fever." 



DENGUE 



103 



The disease generally appears in epidemics, and is almost exclusively confined 
to tropical and semi-tropical countries. In 1870 an epidemic supposed to be 
dengue prevailed in Philadelphia, and outbreaks have occurred repeatedly in the 
Southern States in the last hundred years. In 1880 Charleston, Savannah, New 
Orleans, and other Southern cities were visited by it.. There are those who main- 
tain that dengue and epidemic influenza are identical, a view which the facts do 
not seem to the editor to bear out. 

iEtiology. — As to the causation but little is known. Those who have had 
opportunities of studying the disease consider it both contagious and infectious, 
and the inference that it depends on a specific germ is readily suggested. It 
seems to prefer low lands along the sea-shore, and to be influenced by meteoro- 
logical conditions in that it generally prevails during the summer and disappears 
as cold weather comes on. Neither age, sex, nor condition affords any protection 
from the disease ; it was thought by Dickson that one attack generally confers im- 
munity for life. 

Pathology. — The disease is so rarely fatal that few opportunities have 
been afforded for its post-mortem study. So far as is known, it has no pecul- 
iar lesions. The prominence and the character of the muscle and joint pains 
have led some observers to think the affection related in some way to rheu- 
matism. 

Symptoms and Course. — The onset is usually sudden, but a pronounced chill is 
said never to occur. Prodromata similar to those of other infectious diseases are 
sometimes observed, but the first symptom is very often pain and stiffness in the 
muscles and joints, with frequent swelling of the latter. The large and small 
joints are equally affected, and the pain is increased by motion. With the pain 
there is a rise in temperature and in the frequency of the pulse. The pain is apt 
to increase during the first two or three days and disappear on the fifth, but irreg- 
ular remissions are liable to occur. As the thermometer falls the pain and other 
symptoms diminish, but reappear in full force with any subsequent rise. During 
the later days of the disease a skin eruption appears on the upper part of the body, 
and in severe cases becomes general in about two days. This eruption is very 
variable in character ; it may appear simply as an erythema, or simulate the erup- 
tions of scarlet fever, rubeola, lichen, or urticaria ; it is apt to be associated with 
well-marked heat and itching of the skin. In mild cases the eruption is evanes- 
cent or absent. Swelling of the lymphatic glands is not uncommon; in severe 
cases the mucous membrane of the mouth, throat, and nose is reddened, and haem- 
orrhage from the outlets of the body has been observed. Pregnant women are 
apt to miscarry. Delirium is rare in adults, but common in children ; the face is 
generally flushed, and the eyes are injected; the tongue becomes increasingly 
coated as the disease progresses, the appetite is lost, nausea is not uncommon, 
vomiting is rare. The bowels and the kidneys present no constant or distinctive 
symptoms. 

In mild cases recovery is sometimes rapid; sometimes, and especially after 
severe cases, convalescence is very tedious, the muscular and articular pain and 
stiffness passing off gradually, and the glandular swelling lasting for weeks. 
Copious skin eruptions are followed by desquamation. 

Diagnosis and Prognosis. — As to diagnosis there can seldom be any difficulty 
during the prevalence of an epidemic. The first cases are the only ones which are 
liable to be mistaken, and even their nature can not remain long in doubt. The 
prognosis is uniformly good. 

Treatment. — We are acquainted with no agent capable of aborting, or cutting 
short the disease; nor is there any known measure of prophylaxis except for an 
individual to keep away from those places in which the affection is known to 
prevail. 



104 



ACUTE GENERAL INFECTIOUS DISEASES 



The treatment of the attack is simply symptomatic; notable pain calls for 
opium in some form. Quinine has not seemed to be of service. Debility follow- 
ing- the attack demands suitable alimentation and tonics.] 



CHAPTER XVI 
YELLOW FEVER 

[This disease is not a visitant of Germany, but its consideration can not be 
omitted from a text-book on the practice of medicine for use in America. In the 
following description the aim will be to bring out the more important features of 
the disease, while for fuller details the reader is referred to larger works and 
monographs. 

iEtiology. — Yellow fever is an acute infectious disease, confined within cer- 
tain geographical limits, and occurring chiefly in epidemics of greater or less ex- 
tent. In certain localities, notably Havana and New Orleans, a season rarely 
passes without some sporadic cases. The influence of temperature is well estab- 
lished ; the disease prevails, namely, during- the summer or the warm season, and 
is abruptly arrested by one or two decided frosts; dampness is favorable to it. 
That it depends ultimately on a special cause and does not originate de novo are 
undisputed facts. [Sanarelli claims to have found the specific germ in a minute 
bacterium, occurring in pairs and with rounded ends, which he calls the bacillus 
icteroides. Other authorities do not as yet admit that this bacillus is certainly the 
cause of yellow fever. — V.] The poison appears to be more active at night than 
during the day, prefers low-lying districts, and in them hugs the ground to a cer- 
tain extent. Bad sanitary conditions are most important accessory causes of the 
disease, furnishing the soil for the multiplication of the poison. There can be 
little doubt that, under the observance of strict personal and public cleanliness, 
yellow fever visitations might be made simply a matter of history. The trans- 
mission of the poison may take place through the atmospheric air, thus finding its 
way to the blood through the lungs ; conclusive evidence is lacking- that it gains 
entrance to the system through the alimentary canal. [Recent investigations 
seem to indicate that it may be transmitted by mosquitoes. — V.] While the air 
may be the medium of transmission, the distance to which the poison can be car- 
ried by the air alone is very short ; it can, however, be transported to an indefinite 
distance by f omites, especially if inclosed in trunks, packing-cases, letters, and the 
like. Its vitality may thus be maintained for very long periods. It is a remark- 
able fact that in large cities the infection may be of great virulence, but confined 
to a limited district or districts, by carefully shunning which unprotected persons 
are comparatively safe. An infected area is apt to extend itself, but the progress 
is slow, and is interrupted by streams of water, high walls, , or simply streets. 

That the disease is not, strictly speaking, contagious is the nearly unanimous 
opinion of those competent to form one. In other words, the poison is not thrown 
off in a matured state from the body of an individual suffering from the disease ; 
but, after being so thrown off, remains in the atmosphere or lodges on solid bodies, 
and then undergoes changes which render it active for evil. One attack of the 
disease renders the system of that person insusceptible forever after ; the natives 
of a yellow-fever district are far less liable to contract the disease than are those 
who move into the district from elsewhere; until these have passed through an 
attack they can not consider themselves as acclimated. The negro race is sus- 
ceptible to the disease, though in a less degree than the whites, and in the colored 



YELLOW FEVER 



105 



the affection is far less fatal. Neither age nor sex has any special bearing on sus- 
ceptibility. That fear, anxiety, worry, or anything which tends to depress the 
nervous system increases the individual liability is highly probable. The stage 
of incubation is very variable, ranging from one day to three weeks or even 
more. 

Pathological Anatomy. — The disease involves no constant and peculiar le- 
sions. In rapidly fatal cases, congestion and often haemorrhage are found, espe- 
cially in the nervous system, liver, kidneys, and digestive tract. In fatal cases 
of longer duration more or less parenchymatous degeneration is found. A fatty 
degeneration of the liver is quite common, and imparts a yellow coloration to the 
organ, giving rise to the terms cafe au lait, or box-wood liver. Jaundice of the 
skin and tissues generally is also observable after death, and depends upon causes 
in no way connected with mechanical obstruction to the flow of bile into the intes- 
tine during life. Splenic enlargement is conspicuous by its absence. 

Course and Symptoms. — The onset of the disease is generally sudden, but it 
may be preceded for a few days by malaise and other signs of general constitu- 
tional disturbance; the initial chill is seldom severe, reaction following soon and 
the thermometer rising to 102°-105°; hyperpyrexia is rare. The pulse-rate does 
not increase proportionately with the fever. The face becomes flushed and the 
eyes injected and watery; headache and pain in the back are early and usually 
very prominent symptoms. The bowels are confined ; the tongue is apt to be clean 
if it was so before the disease came on ; the stomach is usually somewhat irritable, 
and there may be vomiting ; moderate epigastric tenderness is common ; the mind 
remains clear, as a rule, but delirium is not very uncommon, and in children a 
convulsion may usher in the attack as in other acute infectious diseases ; the con- 
dition of the urine is at first not remarkable, but albumen may soon appear. This 
hot or febrile stage may last from twelve hours to several days. The pulse gen- 
erally declines in frequency before the disease has reached its maximum. As the 
fever disappears the other symptoms vanish also, and the second, or " stage of 
calm," begins. From this point recovery may be rapid and uninterrupted, the 
whole disease consisting of but a single febrile paroxysm of greater or less inten- 
sity and of short duration. 

In grave cases, and gravity is often foreshadowed in the first stage by marked 
capillary congestion of the surface of the body irrespective of the intensity of the 
other symptoms, and after a stage of calm lasting for some hours, but rarely ex- 
ceeding twenty-four, more distinctive symptoms appear. The pulse is very com- 
pressible, the surface of the body is cool, vomiting occurs or becomes more promi- 
nent, and haemorrhage is now apt to take place. The escape of blood into the 
stomach, its retention and the changes which it there undergoes, and its subse- 
quent expulsion, explain the dreaded and characteristic symptom know as " black 
vomit." Tarry stools sometimes are observed. Haemorrhage elsewhere is also 
common, occurring from the gums, the nose, eyes, uterus, kidneys, into the skin, 
etc. Albuminuria with casts is very common. Jaundice, sometimes of a lemon- 
yellow hue, comes on, and is rarely lacking in severe cases. From this symptom 
the name of the disease is derived. 

In cases marked by more or less complete suppression of urine, coma and con- 
vulsions, probably largely uraemic, come on. Some severe cases are of the " walk- 
ing " type, the patients going about while the malady is far advanced, or even up 
to the time of death. As a rule, however, muscular prostration is marked. 

If the disease does not prove fatal in this third stage, convalescence comes on 
more or less gradually, and is followed by complete recovery; relapses, however, 
occasionally occur. 

The duration of the affection is variable, but, on the whole, short, usually 
being less than a week. 



106 ACUTE GEKEKAL INFECTIOUS DISEASES 



Diagnosis. — In mild cases the symptoms are not distinctive, and the diagnosis 
at the commencement of an epidemic is not likely to be reached except by an 
experienced observer, and even by him more or less conjectnrally. During an 
epidemic the severe lumbar pain, the headache, the suffusion of the eyes, and the 
moderate gastric irritability, are all-sufficient for diagnostic purposes. Severer 
cases are also marked by capillary congestion of the surface of the body, and the 
third stage with the black vomit, haemorrhage, jaundice, slow pulse, scanty urine, 
and prostration is characteristic. Of course, all the above symptoms are not pres- 
ent in every case. The only disease which can well give rise to confusion is remit- 
tent fever with jaundice. This affection has a different temperature-curve, is not 
confined to the yellow-fever zone, is controlled by quinine, and is not accompanied 
by black vomit. 

Prognosis. — This varies in any given locality with the character of the preva- 
lent epidemic. The death-rate is sometimes very high, sometimes moderate ; it is 
greater in hospital than in private practice. 

In the first stage of the disease the chief element in the formation of the prog- 
nosis seems to be the presence of marked and general capillary congestion of the 
skin, a symptom which foretells a severe attack. The absence of this symptom is 
rather less important than its presence. Cases may turn out to be severe in which 
it is lacking. The frequent deceptiveness of the stage of calm is to be remem- 
bered. 

Yellowness, black vomit, and suppression of urine are symptoms denoting the 
greatest gravity, but do not justify the complete abandonment of hope. 

Treatment. — There are no means in our power of aborting the disease. Pre- 
vention is to be attained by cleanliness in its large sense, and by careful quaran- 
tine against things rather than persons. Individuals from infected localities may 
safely be admitted into non-infected localities, provided that they and their cloth- 
ing and effects are thoroughly disinfected. Merchandise, the mails, and the like, 
must be excluded or disinfected. So also vessels and all other means of commu- 
nication. 

The earlier proper treatment can be instituted, the better. Absolute rest and 
good ventilation are the first requisites. Emetics and cathartics are not indicated 
by the disease itself ; the condition of the stomach and bowels should be inquired 
into, and indigestible food or an accumulation of faeces should be removed if 
present. A hot mustard foot-bath early in the attack is useful. For the lumbar 
pains, opium or morphine are indicated. Sinapisms, or other similar external 
counter-irritants, with ice internally, and hydrocyanic acid or chloroform, are 
serviceable against gastric irritability. High fever is to be combated by cold 
spongings, the wet pack, and the cold bath. For haemorrhage, styptic remedies 
may be used, though it is doubtful whether, when given internally, they are really 
of much benefit. Of course, no medication is to be resorted to which is likely to 
heighten a tendency to emesis. 

[Much work has been done with antitoxines for yellow fever, but with no 
settled results, as yet. Sternberg's formula for internal use is said to be valuable 
for quieting the stomach and promoting diuresis. It is as follows: Sod. bicarb., 
gr. cl; hydrarg. chlorid. corros., gr. ^; aquae purae, O ij. M. S. Three table- 
spoonfuls ice-cold hourly. — V.] 

Suppression of urine is to be met by dry cups to the loins, diuretic remedies 
internally if the condition of the stomach allows, or the hot-air bath. The results 
of pilocarpine are disappointing according to Bemiss, who states that he has seen 
good effects from large enemata of water, preferably cold, if there be notable fever 
in these cases. Prostration is an indication for the use of alcoholic stimulants, 
among which iced dry champagne ranks high. It will be seen that the treatment 
is entirely symptomatic. The disease is self-limited, has a short course, and the 



PLAGUE 



107 



patient will recover if he can be kept alive until the poison is exhausted. During 
the attack and until convalescence is thoroughly established the management of 
the diet is all-important. Small quantities of the most easily assimilable food 
may be given at short intervals if they are tolerated by the stomach; if not, ali- 
mentation must be by the rectum, and the lower bowel .in this disease is generally 
in a fair condition for this method of nutrition. 

Courage and hopefulness on the part of the physician may do much good, and 
the services of a skillful and experienced nurse are of the utmost importance. I 
am told that in New Orleans, and perhaps elsewhere, it is customary, for those 
who are not protected and can afford this course, to secure in advance a nurse as 
soon as an epidemic breaks out. They then take to their beds at the first sign of 
illness.] 



CHAPTER XVII 
PLAGUE 

(Bubonic Plague. Malignant Adenitis. Black Death) 

[Definition. — Plague is an acute, febrile, infectious disease, occurring endem- 
ically and epidemically, somewhat contagious, and occasioned by the bacillus 
pestis bubonicce. 

Historical Remarks. — Although it is difficult to identify diseases from the 
descriptions of ancient authors, Hirsch believes that the first historical account 
of the plague relates to an epidemic affecting Libya, Egypt, and Syria, at the 
end of the third or the beginning of the second century before Christ. Pan- 
demics occurred in the sixth century of our era ; the fourteenth, when, under the 
name of the " Black Death," it is estimated to have destroyed twenty-five million 
of the inhabitants of Europe ; and the seventeenth century. The great plague of 
London in 1665 destroyed seventy thousand out of a population of four hundred 
and sixty thousand. 

From the end of the seventeenth century the disease gradually yielded to the 
march of sanitary improvement. Like leprosy, it is now unknown in countries 
where it formerly was a terrible scourge. It remains endemic in northern Africa, 
southwestern Arabia, India, southern China, and a large district in the neigh- 
borhood of the Caspian Sea (Payne). At the present writing the disease is ex- 
tended widely over the habitable globe, but the immunity from its ravages which 
civilized races now enjoy well illustrates the prophylactic value of modern 
hygiene. 

Plague became active in south China in 1894, afflicted Hong-Kong from 1895 
to 1898, and has occurred there within a year. In three years, ending September, 
1899, there were 319,040 cases in the Bombay presidency, and of these, 250,677 
were fatal. It appeared in Egypt in 1899; also in Oporto, Algiers, and South 
Africa. In the year 1900 there were cases in the Chinese quarter of San Eran- 
cisco, Honolulu, Manila, Australia, and Glasgow. 

ZEtiology. — The plague is due to a minute organism, known as the bacillus 
pestis bubonicse. This organism is constantly found in those suffering" from 
the disease and in their bodies after death, and a pure culture of it will cause 
in animals a disease unquestionably like that seen in men. In 1898, an assistant 
in a pathological laboratory in Vienna came down with the disease, while occu- 
pied with infected animals — there being no possibility of human contagion. The 
attack was fatal and entailed the fatal illness of the attending physician. There 
are three cases on record of successful inoculation, one by a physician, "Whyte. 



108 



ACUTE GENERAL INFECTIOUS DISEASES 



upon himself in 1802, and fatal, and two upon condemned criminals, who took 
the disease but survived. These three cases, however, occurred at times when 
the disease was epidemic. 

The mode of growth of the bacillus is characteristic. It stains readily with 
the ordinary aniline dyes — e. g., Loeffler's blue or weak carbol-f uchsine. It is de- 
colorized by Gram's method. Its ends stain more deeply than the central portion, 
giving it somewhat the appearance of a diplococcus. It has no spores. Like other 
micro-organisms, its virulence varies greatly under varying circumstances of cul- 
ture and transmission through animals. When an epidemic is imminent, the 
first cases are often mild, then the intensity of the poison increases rapidly, 
abating again toward the end of the visitation. Lower animals and even insects 
are liable to infection. The list includes rats, mice, dogs, and also flies, fleas, 
lice, mosquitoes, ants, and bugs. The external circumstances which most favor 
the spread of the disease are overcrowding, poverty, and filth. Great extremes of 
temperature are unfavorable to its development; a certain degree of moisture, 
on the other hand, fosters its growth. The geological character of a place, or 
the elevation above the sea, has little influence. The immense practical impor- 
tance of proper social and hygienic conditions is illustrated by the percentage of 
deaths among the different races in Hong-Kong during the late epidemic: Chi- 
nese, 90.4; Hindoos, 77; Japanese, 60; Europeans, 18.2. These figures indicate 
very fairly the relative hygienic conditions of the classes enumerated. It is un- 
doubtedly lack of a favorable soil that has freed Europe and the civilized parts 
of America from the disease. 

The mode of infection varies. It is believed that most cases are due to the 
entrance of the germ through some trauma, or fissure of the skin — e. g., through 
the bite of insects or the scratches occasioned by the same. In support of this 
view, the fact has been emphasized that the characteristic buboes are mainly in 
the groin, and among barefooted people ; but against it is the experience of Euro- 
peans, who, with their lower extremities protected, also have a preponderance of 
inguinal adenitis. In cases with pulmonary localization the sputum is danger- 
ous, either if it is projected upon the conjunctivae, or presumably if it is inhaled 
when suspended in the air mixed with minute particles of moisture. Localities 
and houses seem to hold and transmit the infection, persons in the lowest part 
of the house, nearest the soil, being most apt to suffer. It seems very difficult to 
disinfect a dwelling by ordinary methods, the poison sometimes surviving a 
deluge of liquid disinfectants. On the other hand, soldiers wisely directed can 
engage in the purification of a dangerous locality with impunity. 

Certain articles are capable of transmitting the infection. The Sanitary 
Conference at Venice, in 1898, enumerated in this class : used body linen, cloth- 
ing, bedding, and other personal effects, rags, bagging, carpets, old embroidery, 
green hides and skins, raw silk and wool, animal and human hair. 

Animals fed upon the infected viscera acquire the disease, but it has not been 
proved that man becomes infected through the ingesta, although the bacilli are 
found in the dejections. At any rate, during an epidemic it would be wise to 
have all drinking water boiled, and to eat no raw fruit or otner uncooked food. 

Course and Symptoms. — The period of incubation is usually three to five 
days. It may be as short as thirty-six hours, or, exceptionally, extend to fourteen 
days. The Conference at Venice settled upon ten days, for quarantine purposes. 
During incubation the symptoms are uncharacteristic, if any at all appear. The 
onset of the disease is usually abrupt, with rigors or chilliness, intense headache, 
and general pains. The temperature may be 104°-105° F. (40°-41° C.) on the 
first day, but is more apt to reach such a height by the third day. The pulse is 
somewhat characteristic, being rapid, out of proportion to the general condition, 
ranging from 100 to 120 or even 140. It soon becomes feeble, dicrotic, hard to 



PLAGUE 



109 



count, and, toward death, intermittent. The heart is weak, and its first sound 
gradually becomes indistinct, and its right side dilated. The condition of the 
tongue is regarded as important for diagnosis. It has a white, moist coat at first, 
later becoming dry and brownish. Exceptionally, it may be brown from the start. 
Quite constantly the edges and tip and often the median furrow are clean. 

The throat and tonsils are red and congested. Sometimes the tonsils seem to 
be the gate of entrance for the poison, and in such cases the cervical glands are 
apt to be much enlarged. The eyes are congested and sunken, with a dark ring 
around them. 

The general appearance of the patient gives the impression of sepsis. The 
countenance may have a " fatuous, listless, unconcerned " expression, or may be 
" pain-drawn and haggard." In children the onset in this, as in other infectious 
diseases, may be marked by convulsions. Delirium is common; this may be 
quiet or, exceptionally, maniacal. The gait is early affected, becoming feeble and 
staggering, and suggesting alcoholic intoxication. The speech is thick and husky, 
due to lingual paresis, and is quite characteristic. 

Adenitis is present in sixty-five to one hundred per cent, of the cases. It is 
this circumstance which has given rise to the name bubonic plague. The change 
in the glands usually becomes apparent by the third day, but it may precede the 
constitutional symptoms or may be delayed to the sixth day. At first an enlarged 
gland is felt, varying in size from a walnut to a small orange. This is tender 
and often extremely painful; soon there is a collateral oedema, making a large 
swelling in the neighborhood. The favorite location of the adenitis is the fem- 
oral or inguinal region. It is usually unilateral. Other points of development 
are the axilla, neck, and less often the back of the knee and the elbow. The 
parotid gland also may be affected. Sometimes more than one group of glands 
are affected at the same time, and post mortem there may be found enlargement 
of every gland in the body. The buboes may remain hard until death; in other 
cases they suppurate, which is regarded as favorable. On the other hand, if they 
soften or disappear during the height of an attack, death may be expected. By 
the eighth or tenth day the skin over a bubo may slough; and if a patient sur- 
vives, convalescence may be prolonged for weeks by the adenitis with its compli- 
cations. There are apt to be subcutaneous haemorrhages in the skin over buboes, 
as well as petechias in various other parts of the surface, or more extensive haem- 
orrhagic stains. Exceptionally, there may be a rash resembling that seen in 
severe exanthematic typhus. Haemorrhage is a sign of severity; it may occur 
from the nose, mouth, stomach, lungs, intestine, kidneys, or womb. A pregnant 
woman is almost certain to miscarry. 

Boils and abscesses may occur in the disease. Certain lesions called carbun- 
cles sometimes appear. They are really areas of moist gangrene, extending hori- 
zontally instead of deeply into the tissues, and they may attain a diameter of sev- 
eral inches. 

The urine is scanty, and is often retained or actually suppressed. Apart from 
renal haemorrhage it shows merely acute congestion, as in other infectious dis- 
eases. The liver is enlarged and tender; the spleen is always very much en- 
larged, up to three or four times its usual size. There may be persistent vomit- 
ing at the onset of the disease. Constipation is present, as a rule, but there may 
be severe diarrhoea. In ordinary cases respiration is somewhat hurried. 

Fluid withdrawn from a bubo in its early stages shows the characteristic ba- 
cillus. When suppuration has occurred the organism may not be found, having 
probably been destroyed by the agents of suppuration. The circulating blood 
contains the organisms, but they are isolated from it with some difficulty. After 
death the viscera, particularly the spleen, are found to contain great numbers of 
the germs. 



110 



ACUTE GENERAL INFECTIOUS DISEASES 



In the pneumonic cases of plague the disease is septicemic in its characteris- 
tics and fatality; hence, cough is a very important symptom. The signs in the 
chest are remarkably slight. There may be a small lobule of consolidation found, 
particularly in the lower part of the back or at the apex. The signs vary from 
one day to another. The expectoration may be scanty or absent, and if present 
may seem merely bronchitic. It is more apt to be sero-mucous than muco-puru- 
lent. Often the sputum is almost a pure culture of the specific organisms. 
Pneumonic cases are almost invariably fatal before the end of the third day. 
As a rule, they are not associated with enlargement of the glands in any part of 
the body. 

A third variety of plague is the septicemic, in which death occurs by the sec- 
ond or third day. There is delirium, merging into coma; all the glands are 
enlarged but not prominent; hemorrhage is frequent and apyrexia not un- 
common. 

Pestis Minor. — At the beginning of an epidemic there may be cases of very 
little severity, but with bubonic manifestations of a mild type. This form almost 
always runs a favorable course, and lasts about two weeks. Its importance in 
the way of prophylaxis and public hygiene may be very great. 

Diagnosis. — The general picture of the disease is that of a profound sepsis, 
plus the peculiar adenitis. Sometimes the changes in the glands are attended 
with no subjective symptoms, and the physician is in danger of regarding the 
case as, for instance, typhoid or typhus fever. Typhoid fever has a more grad- 
ual onset, a relatively slower pulse, rose-spots, and eventually a Widal reaction. 
Typhus fever runs fourteen days instead of a week, is more regularly associated 
with an eruption, and has different etiological relations. The enlarged glands 
might be mistaken for tuberculosis or syphilis, and the symptomatic parotitis has 
been regarded as mumps, but due care would make mistakes of this sort infre- 
quent. Diphtheria has been suspected in a case attended by such changes in the 
cervical glands that the mouth could not readily be inspected. Cases with ingui- 
nal adenitis have been regarded as gonorrhoea, in both sexes (Hossack and 
Colvin). 

Malaria has been confounded with plague, but the temperature curve, the 
efficacy of quinine, and the discovery of plasmodia in the blood should enable 
one to recognize it. So much oedema is sometimes associated with the buboes 
as to simulate erysipelas. Cases of severe influenza and of pneumonic plague 
greatly resemble each other in everything, except prognosis and the micro-organ- 
isms of the sputum. Other diseases which have been simulated by plag'ue are 
puerperal fever, septico-pyemia, cerebro-spinal meningitis, cerebral embolism, 
epilepsy, uremic coma, diarrhea, debility, marasmus, and alcoholic poisoning 
(Hossack). 

Prognosis.- — When at its height, the disease is fatal in perhaps ninety per cent, 
of the cases. The average fatality of epidemics has been stated as from thirty-five 
to fifty per cent. Death may occur as early as the second or third day: if life is 
preserved beyond the sixth there is hope of recovery. Petechie, hemorrhages, 
and pulmonary signs are of fatal omen. 

Treatment. — "With the present ease of human intercommunication we can 
not hope, with the strictest quarantine, to exclude every infectious germ, but we 
can render the exposed locality unsuitable for its growth. This is well illustrated 
by the recent experience of Glasgow, where the disease has now ceased after a 
minimum loss of life (27 cases and 8 deaths). Major Edie. United States health- 
officer at Manila, says : * " The opinion I have formed of plague from the experi- 
ence of the past six months is that little difficulty will be found in controlling it 



* Surgeon-General's report, 1900. 



EPIDEMIC CEEEBBO-SPIXAL MENINGITIS 



111 



in any intelligent community with modern sanitary conditions." The physi- 
cians, nurses, and visitors at well-regulated plague hospitals do not catch the 
disease. 

Therapeutic measures have been, until recently, mainly symptomatic and 
apparently futile. Two forms of specific treatment have been introduced. Yersin 
has prepared an antitoxic serum from the horse, precisely analogous to the anti- 
diphtheritic serum obtained from the same animal. This preparation keeps 
well, is harmless, painless, and confers immediate immunity to the disease, last- 
ing about fourteen days. It is to a certain extent curative in cases already 
diseased, the more so the earlier it is given. HafTkine has prepared a vaccine 
fluid by subjecting a culture of the bacilli, in broth, to a temperature of 70° C. 
for one hour. This sterilized fluid contains the dead germs, and also the toxines 
developed incidentally to their growth. It confers immunity to infection, begin- 
ning the seventh day after inoculation. The injection is best repeated two or 
three times, at intervals of eight days. The local reaction from this is consider- 
able, but does not last more than two or three days, and the person treated re- 
mains immune for months. Haffkine's fluid is said to aggravate an impending 
attack, if it is given during the period of incubation, so that a person who might 
otherwise have survived the disease may lose his life. The most recent writers 
on the treatment of the plague are not in full accord as to the value of these 
injections just described. Major Edie (already quoted) says: "A thorough test 
has not been given to either the Haffkine material or the Yersin serum, but we 
have not been favorably impressed with either." The reports from India are 
more encouraging. — V.] 



CHAPTEK XVIII 

EPIDEMIC CEREBRO-SPINAL MENINGITIS 

(Spotted Fever. Cerebrospinal Fever) 

Etiology. — The epidemic form of cerebro-spinal meningitis has been known 
only since the beginning of the nineteenth century. The first epidemics were ob- 
served in southern France and in Geneva. Smaller ones occurred in Germany in 
1822 and 1853; but it was not till 1863 that the disease became at all frequent 
among us. Since that date there have been more or less extensive epidemics almost 
every year. The southern and central portions of Germany are particularly liable 
to them. Sporadic cases may occur at any time. 

Most of the epidemics appear in the winter and spring. We do not know any 
particular factors which promote the disease. It often seems to be decidedly 
endemic. Barracks, work-houses., and the like have been marked by tolerably 
extensive epidemics. Whether the disease can be carried by patients to places 
previously free from it is still uncertain. It is not directly contagious. Children 
and young adults are the most frequent victims; but now and then elderly per- 
sons are attacked. Sex can not be shown to have much influence. 

That the disease is infectious is clearly shown not only by its epidemic and en- 
demic character, but by its whole course. The peculiar pathogenic organisms 
and the manner of infection have not yet, however, been positively ascertained. 
Diplococci are usually found in the purulent exudation in the meninges, which 
are so much like Frankel's pneumonia diplococci that many authors have consid- 
ered the germs of croupous pneumonia and of epidemic meningitis as identical. 
It is confirmatory of this that many clinical facts suggest a relationship between 
the two diseases : the appearance of herpes, the comparative frequency of sec- 



112 



ACUTE GEKEKAL INFECTIOUS DISEASES 



ondary purulent meningitis in pneumonia, the occasional co-existence of epidem- 
ics of pneumonia and meningitis, etc. On the other hand, we must not overlook 
the clinical differences, especially the atypical course of epidemic meningitis, 
which almost never ends by crisis. The chief point is that, assuming that pneu- 
monia and epidemic meningitis are due to identical germs, we can not explain 
why the same germ at certain times finds its way to the lungs, and at other times 
and in other localities goes to the cerebral meninges. In the separate epidemic 
occurrence of cerebro-spinal meningitis we find a strong argument for the specific 
individuality of the disease. Weichselbaum and others have recently found in 
epidemic meningitis another peculiar diplococcus which is called the diplococcus 
intracellularis meningitidis. This diplococcus, arranged in pairs or tetrads, is 
found chiefly within the pus cells, and externally closely resembles the gonococcus. 
Further research is necessary to determine the significance and constancy of its 
presence. [Later researches seem to show that this coccus is the actual cause of 
the disease. — K.] 

With regard to the gate of entrance of infection in primary epidemic menin- 
gitis, perhaps the specific poison may enter through the nostrils and the cribriform 
plate to the otherwise so well protected envelopes of the central nervous system. 

[Sanitary conditions seem to play a less important role in this than in many 
other infectious diseases. During the epidemic which visited New England in 
1873 the writer was interne at the Massachusetts General Hospital, and there saw 
a number of cases. The disease was also prevalent among horses at the same 
time, and it is curious to note that a like association of the affection in men and 
animals was observed in Vermont in 1811, and in New York city in 1871. During 
the year 1873, 216 deaths were returned as due to this malady in the city of 
Boston.] 

Pathological Anatomy. — The autopsy discloses an acute purulent cerebro- 
spinal leptomeningitis. It is only in rapidly fatal cases that slight and incipient 
lesions have been met with. As a rule, the extent and intensity of the objective 
lesions correspond to the severity of the symptoms. In the brain the purulent 
inflammation attacks the convexity as well as the base. It is usually most marked 
along the larger blood-vessels and in the fissures of the cortex. Of the spinal 
cord the posterior surface suffers most. Frequently the lumbar portion is more 
affected than the parts above. It is, however, exceptional for the disease to be 
limited to the meninges; it is prone to extend into the underlying parenchyma. 
The microscope reveals clumps of pus-corpuscles about the blood-vessels, where 
they penetrate into the tissues, and not infrequently there are numerous centers 
of genuine encephalitis. These latter may be visible to the naked eye. Excep- 
tionally there may even be cerebral abscesses of considerable size. The vessels are 
distended with blood, clear into the central ganglia, and ecchymoses are frequent. 
The cerebral ventricles are usually enlarged, and filled with a cloudy serum, or 
even with pus. It is plain that these lesions of the cerebro-spinal parenchyma 
greatly modify the clinical picture, and that they must frequently have more to 
do with the severity of the symptoms than has the leptomeningitis itself. 

Clinical History. — Prodromata are relatively rare, and if present they are not 
severe, being confined to general malaise, with slight headache, and pain in the 
limbs. Usually the disease begins rather suddenly; there is intense headache, 
often felt mainly in the occiput, pain and stiffness in the back of the 
neck, and great general discomfort. It is not rare for vomiting to occur at first. 
Very often there are among the early symptoms such important mental disturb- 
ances as stupor or delirium. There is usually fever from the first. An initial 
rigor may occur, but it is not the rule. 

The intensity of these first symptoms is not always the same. Subsequently to 
them the course of the disease may vary greatly. First there are very acute, vio- 



EPIDEMIC CEKEBEO-SPINAL MENINGITIS 



113 



lent forms, termed " explosive " (meningitis cerebro-spinalis siderans, meningite 
foudroyante), in which the cerebral symptoms are very severe, and the patient 
survives only a few days or even hours. Again, there are abortive cases. These 
begin with equally threatening symptoms, but after a few days completely recover 
with remarkable rapidity. The majority of cases last about two to four weeks. 
In severe cases death may come as early as the first week. The disease is often 
protracted to six or eight weeks' duration, or even longer, and may end in death 
after all. Cases that last a good while sometimes exhibit a remarkably inter- 
mittent character. Finally, there are a considerable number of mild cases in which 
none of the symptoms are very pronounced, and recovery is relatively early. 

The symptoms of the disease may be divided into (1) the severe general symp- 
toms, referable to the brain and spinal cord; (2) the more localized, nervous symp- 
toms; and (3) the results of the constitutional infection, including fever and 
symptoms in other parts of the body. 

1. Among the less definite cerebral symptoms headache is important. It is 
usually terribly severe. It is chiefly occipital, but sometimes is frontal or tem- 
poral. Like most of the symptoms of meningitis, the headache undergoes very 
frequent changes in intensity during the course of the disease. For a time it may 
remit, only to recur with fresh severity. Marked vertigo and a sense of fullness 
in the head may accompany it. 

The pain in the head is re-enforced by intense pain in the nape of the neck and 
back, due to the spinal meningitis. There is almost always considerable tender- 
ness along the whole spinal column. The erector spinas is contracted, making 
the back straight and rigid, or even producing opisthotonos; and the head is 
bent backward by the reflex contraction of the neighboring muscles. 

In most of the severe cases intelligence is blunted ; we find all degrees of dis- 
turbance, from slight drowsiness to delirium on the one hand, or deep coma on the 
other. Some cases begin with marked maniacal excitement. These symptoms 
likewise may undergo frequent variation in their intensity. General convulsions 
occur in very severe cases alone, and are of evil omen. 

The vomiting is also to be regarded as of cerebral origin. It frequently is an 
early symptom, but may be deferred. 

2. Symptoms referable to the individual cerebral nerves are manifold and 
variable. The most frequent disturbances are in the nerves that supply the muscles 
of the eye. They include strabismus; nystagmus, or slow movements independ- 
ent of volition; unilateral or bilateral ptosis; slow reaction of the pupils, or 
inequality of them, or myosis or mydriasis. In the area of distribution of the 
facial there is often a noticeable contraction of the muscles, giving the face a 
peculiar, painfully distorted look. Trismus, or tetanus of the masseters, is rare, 
and usually a bad sign. 

Disturbance of the nerves of special sense is frequent. Deafness may be 
due to the stupor, but is often the result of an extension of the inflammation 
to the acoustic nerve. The purulent inflammation may be propagated as far as 
the labyrinth, or even into the middle ear. Tinnitus aurium is also frequent. 
Disturbances of vision are far less frequently observed, but optic neuritis has 
been repeatedly found by the ophthalmoscope. Severe purulent irido-choroiditis 
has been also observed. It is probably due to extension of the inflammation 
along the .sheath of the optic nerve. Conjunctivitis and keratitis sometimes 
occur; but they are probably caused by external injuries rendered possible by the 
imperfect closure of the lids, or the diminished sensitiveness of the parts. We 
have several times found the sense of smell diminished. 

Disturbances in the area of distribution of the spinal nerves are, on the whole, 
less frequent. The only one of value in diagnosis is the cutaneous hyperaasthesia. 
It is apt to be particularly severe in the extremities, and it may be so extreme that 
8 



114 ACUTE GENEKAL INFECTIOUS DISEASES 

the light touch of a finger or a needle causes great pain. Sometimes there is a 
slight twitching in the muscles of the extremities. This has, however, no special 
significance. There is often rigidity and stiffness of the muscles. Kernig has 
called attention to the frequent appearance of flexure contractions in the legs, 
and sometimes also in the arms, if the patients are caused to sit up or if the 
thigh is passively bent upon the trunk. As might be expected, there is no in- 
variable rule about the reflexes. The cutaneous reflexes are usually well marked, 
and the tendon reflexes may be ; but in some cases we have found the tendon 
reflexes markedly diminished or even abolished. Such a condition is probably 
due to some lesion of the fibers of the posterior nerve-roots. 

All of the nervous symptoms above enumerated result from one of two causes- 
— either the roots of the nerves are affected by the purulent exudation, or the 
inflammation extends inward to the central organs themselves. This extension is 
the explanation also of other symptoms sometimes observed — viz., hemiplegia, 
paraplegia, partial convulsions, and aphasia. 

3. In addition to all these nervous disturbances, we see also symptoms refer- 
able to other parts of the body. Of this class there is one cutaneous affection 
which is a very valuable aid to diagnosis. Herpes labialis or herpes facialis is apt 
to appear soon after the beginning of the meningitis. It is seen in more than half 
the cases, and as frequently in severe as in mild attacks. Other eruptions occur 
now and then — e. g., roseola, urticaria, or petechias. Sometimes they are so sym- 
metrically distributed upon the two halves of the body as to suggest the idea of a 
nervous origin. 

The digestive system seldom displays severe symptoms beyond the vomiting 
already mentioned. Anorexia and constipation are, indeed, usually present, as 
in many grave diseases. We have seen mild dysentery a few times. ISTow and 
then a slight jaundice has been noticed. The spleen is often somewhat swollen, 
but very rarely attains great size. 

Swelling of the joints has been observed quite often; it is much more frequent 
in some epidemics than in others. The enlargement may be an early or a later 
symptom. It does not usually prove serious. 

The urinary apparatus is seldom affected. The urine may contain some albu- 
men and a few casts. Polyuria is an interesting symptom, probably of nervous 
origin. It is more apt to occur in the latter part of the disease. In a number of 
cases sugar has been found in the urine. Cystitis is a secondary disorder which 
is not very rare, particularly in severe cases when the catheter has been used. 

Pulmonary and bronchial symptoms are likewise secondary. They occur very 
often in bad cases. It is evident how easily the stupor of the patient may lead to 
the inhalation of solid matter, with consequent bronchitis and lobular pneu- 
monia. 

Lesions of the circulatory system are rare. Acute endocarditis has been ob- 
served only a few times. The pulse is usually somewhat accelerated, seldom 
rendered slow. Very frequently the pulse-rate is remarkably variable, un- 
doubtedly because of variation in the supply of nervous force. Slight irregu- 
larities in the pulse are also common. In the blood we find quite a marked 
leucocytosis. 

4. The fever in epidemic meningitis conforms to no single type. It does not 
correspond at all to the severity of the other symptoms ; the worst cases may run 
their course with little or no fever. In most instances the fever has irregular re- 
missions. It seldom exceeds 104° (40° C). Sometimes the fever exhibits a decid- 
edly intermittent character. It is in these cases particularly that we find the 
variation in the intensity of all the symptoms of which mention has been made 
repeatedly. The variations in the temperature do not, however, always run par- 
allel with the changes in the other symptoms. In mild cases the fever is usually 



EPIDEMIC CEKEBKO-SPIXAL MENINGITIS 



115 



moderate and brief. The abortive attacks may present high temperatures at 
first, but these quickly abate. In case of a fatal issue there is sometimes hyper- 
pyrexia before death, reaching 108° to 109° (42°-43° C). In the severer but 
not fatal cases the fever declines slowly but irregularly. The fever may be over, 
long before the other symptoms disappear. 

It is impossible to portray all the forms, symptoms, and courses the disease 
may have. The chief varieties have been already mentioned; but in reality these 
are only types which run into one another without sharply defined border-lines. 
It is in itself a characteristic of epidemic meningitis that most of the more 
tedious cases have a variable, uncertain course. We may even meet with a com- 
plete intermission of all the symptoms, lasting for quite a while, so that the return 
of the trouble may fairly be called a relapse. 

Sequelae are not rare after severe cases. Persistent deafness is the most fre- 
quent. It results from the complications, already mentioned, which affect the 
labyrinth and the middle ear. Little children may become deaf and dumb. 
Again, vision may be deranged, because of retinitis, atrophy of the optic nerve, 
or corneal opacities, etc. It is not very rare for meningitis to leave grave nerv- 
ous disorders behind it. These are frequently the symptoms of a chronic hydro- 
cephalus. We may observe headache, sudden unconsciousness, or even convul- 
sions, mental impairment, and weakness of the extremities. Or there may be 
localized disturbances due to permanent injury of limited portions of the brain or 
spinal cord, such as hemiplegia, paraplegia, and aphasia. From many of these 
conditions there may be a gradual recovery, but others prove incurable. 

The diagnosis of cerebro-spinal meningitis is not difficult in a well-developed 
case, particularly if the prevalence of an epidemic puts us in mind of the disease. 
Diagnosis is more difficult in sporadic cases, and most difficult of all when the 
patient does not come under observation till he is very ill and when we can not 
obtain the previous history. Important factors are the abrupt onset, the speedy 
appearance of grave cerebral symptoms, the characteristic headache and pain in 
the back, the stiffness of the neck, and the herpes labialis. 

If we find evident symptoms of meningitis, we have still to decide whether the 
case is one of primary epidemic disease, or secondary, due perhaps to extension 
from some other part. Bearing this last possibility in mind, we should examine 
the ears carefully; for, as is well known, chronic otitis media may set up a puru- 
lent meningitis. Again, it may be very difficult to exclude a tubercular menin- 
gitis. Here we should consider other circumstances that might render tuberculosis 
probable, such as the general condition of the patient, heredity, previous pleurisy, 
the results of thoracic examination, or scrofulous disease of the bones or joints. 
The existence of herpes points toward epidemic meningitis, for it is exceptional 
in the other forms of the disease. It is sometimes difficult to distinguish between 
meningitis and severe cases of other acute infectious diseases — e. g., typhoid 
fever and septic diseases. Here we must weigh all the circumstances carefully. 

Lumbar puncture has greatly aided the diagnosis of meningitis. This was 
recently introduced by Quincke, and it has often been performed since. As 
Quincke first showed, we can usually reach the subarachnoid space of the cauda 
equina without difficulty between the third and fourth lumbar vertebrae with 
an aspirating needle about eight centimetres long. The patient should lie on one 
side. In this way we can obtain more or less of any meningitic exudation that 
may be present. In epidemic meningitis we often obtain a sero-purulent or 
purulent exudation which can be examined bacteriologically. [The discovery of 
the diplococcus intracellularis in the fluid withdrawn by lumbar puncture is of 
extreme importance in the diagnosis of doubtful or sporadic cases. — K.] 

This is a good opportunity to mention the secondary meningitis which is 
said to occur with relative frequency just at the time of an epidemic. The com- 



116 ACUTE GEXEKAL INFECTIOUS DISEASES 



bination of croupous pneumonia (q. v.) and purulent meningitis has been 
repeatedly observed. Still, it is not easy to determine whether the cause of this 
secondary meningitis is actually identical with that of the epidemic form (vide 
supra). In other acute diseases, such as typhoid and articular rheumatism, when 
they occur at the time of an epidemic, the " tendency to meningitis " is potent 
enough to make meningeal symptoms more frequent than usual. It has not been 
clearly demonstrated, however, that this fact is actually due to the epidemic men- 
ingitis. 

The prognosis depends chiefly upon the severity of the cerebral symptoms. 
Yet we should be guarded in our utterances, even when the case seems mild, or 
has apparently made the first steps toward convalescence. The disease sometimes 
changes for the worse at a late period. In general the mortality is about thirty 
to forty per cent. Probably this estimate does not take into account many very 
mild cases. 

Treatment is purely symptomatic. There is no specific for meningitis. A 
valuable remedy is cold applications. Ice-bags are placed upon the head, arid, if 
possible, along the spine. There are long and narrow rubber bags for the latter 
purpose. These applications are borne well by most patients and afford decided 
relief. The local abstraction of blood has also an undeniably beneficial influence, 
however difficult this may be to explain. Leeches are put behind the ears, and 
cupping-glasses on the back of the neck and along the spine. Mercurial ointment 
is often rubbed in, not only locally but also in the same way as in treating syphi- 
lis. Its efficacy is doubtful. The narcotics are of great value. The best is mor- 
phine given subcutaneously. It lessens the pain, and often affords the uneasy and 
delirious patient rest and sleep. Chloral and bromide of potash may also be em- 
ployed. Iodide of potash is often given internally, to the amount of twenty to 
thirty grains (grammes 1.5-2) in a day, especially in cases with a slow course. 
The evacuation of a part of the meningitic exudation by lumbar puncture (vide 
supra) is sometimes followed by a temporary improvement of the symptoms, but 
no actual and permanent therapeutic result has yet been obtained by lumbar punc- 
ture. 

The fever hardly ever requires special treatment. Quinine exerts no influence 
in the intermittent type. Antipyrine is better borne, and it also, like the other 
nervines, sometimes relieves the nervous symptoms. Cool baths are not to be 
recommended, but hot baths or hot packs sometimes seem to be of decided benefit. 
Later, warm baths are often beneficial. Local complications — e. g., affecting the 
eye or the ear — require special treatment. The swelling of the joints which some- 
times occurs we have thought to be somewhat relieved by salicylic acid. 



CHAPTEK XIX 

SEPTIC AND PYEMIC DISEASES 

(Spontaneous Septicopyemia) 

The septic and pysemic processes which follow serious injuries or operations 
belong to surgery ; but analogous diseases occur in persons who are apparently in 
perfect condition. They take the form of an extremely severe acute infectious 
disease, usually fatal. There can scarcely be a doubt that in almost all these 
cases there is some small break in the continuity of the external skin or the 
mucous membrane which affords an entrance for the infectious material; but, 
since the infection itself is wholly unnoticed, the general disease seems a primary 



SEPTIC AND PY.EMIC DISEASES 



117 



affection, and its correct interpretation often occasions the physician considerable 
difficulty. Even if the septic infection be correctly recognized, it is sometimes 
impossible to determine the point of origin. For such cases Leube has intro- 
duced the name of " cryptogenic " septicopyemia. We must add, however, that 
in many cases at least, a careful inquiry and examination will reveal the origin 
of the infection. In many cases, however, a complete explanation of the occur- 
rence of the infection is given only by the autopsy, and the origin of some cases 
remains obscure even after a careful autopsy. 

The causes of pyemic and septic affections are chiefly the same pus cocci 
which produce many circumscribed inflammations and suppurations, especially the 
streptococcus pyogenes, the staphylococcus pyogenes albus, and the staphylococcus 
pyogenes aureus. We can not make any definite clinical distinction in the septic 
affections according to the special cocci that produce them; but, in general, it is 
the rule that the severe, fatal pyemic and septicemic affections are most often 
due to streptococci — for example, many cases of pyemia, of puerperal sepsis, of 
severe ulcerative endocarditis, etc. The staphylococci seem on the whole to cause 
more benign forms of suppurative or septic disease. As we shall see later, it is 
not improbable that acute articular rheumatism must be regarded as such a 
staphylococcus infection. Mixed infections with streptococci and staphylococci 
also occur, and, finally, other micro-organisms (pneumonia diplococci, gonococci) 
may sometimes cause forms of disease which have many points of similarity to 
the other septic diseases. 

The essential thing in all septic infections is the general disease of the body 
caused by the entrance of the germs into the circulation and their increase 
therein. The form and severity of the disease thus caused depends probably 
in part upon the special variety and in part upon the varying specific " viru- 
lence " of the bacteria that have entered the system, but the form and severity 
also depend upon the greater or less resistance of the body, which varies in indi- 
viduals. If the micrococci enter the general circulation only, they cause a large 
number of intoxication symptoms, due to the action of different "toxines" formed 
by the chemical changes in the micrococci. The micrococci, however, may collect 
in the smaller blood-vessels ("micrococcus foci," "micrococcus emboli"), and in 
this way may cause circumscribed or extensive suppuration in the various organs. 
In prevailing parlance we call this multiple abscess formation pyemia, and the 
cases with severe (toxic) general symptoms, hemorrhage, etc. (vide infra), but 
without suppuration, we call septicemia or sepsis. Since, however, the two 
groups of symptoms may be associated with each other in many ways, we often 
speak of septicopyemia. 

It is very important for the correct understanding of all these conditions to 
bear in mind that, in different cases, different organs or parts of the body may 
become the chief seat for the localization of the micrococci. Hence severe local 
disorders may arise, which, of course, may give diverse aspects to the clinical 
picture according to the special localization. This is the reason why many of 
these affections were formerly regarded as separate diseases, although in reality 
they were only different localizations and forms of the same infectious process. 
iVmong these affections were the so-called " acute osteomyelitis " almost always 
caused by the staphylococcus pyogenes aureus, " malignant endocarditis," certain 
forms of " malignant erysipelas," etc. In their clinical aspect these differences 
are, of course, still of great importance, but the etiological connection of all 
these cases must always be emphasized, because only by putting a proper stress upon 
this point can we obtain a correct understanding of all the combinations mani- 
fested in the clinical course of the disease. 

Before we consider the details of the anatomical changes in septic affections, 
we would mention those circumstances (exciting causes), which, we know by ex- 



118 ACUTE GENEKAL INFECTIOUS DISEASES 



perience, most commonly cause or render possible the occurrence of septic infec- 
tion. In each individual case it must be our task, as we have said, either during 
the patient's life or at the autopsy, to determine if possible the point of origin of 
the infection. The following are chiefly to be considered: 1. The puerperal pro- 
cesses take the first place. Both after delivery, and still more frequently after 
abortion, the raw surface of the uterus may be the door of entrance for the septic 
poison, but a gross pathological change is not necessarily to be seen in the uterus 
itself or in its appendages. We do find, often enough, diphtheritic and gan- 
grenous inflammation at the place where the placenta was inserted, or purulent 
thrombi in the veins of the uterus and of the pelvis, etc. ; but in other cases the. 
uterus is merely a gate of entrance for the poison, remaining itself normal. 
2. The septic poison may also be absorbed through slight abrasions of the skin, 
injuries, felons, whitlows, etc. ; and these may be almost completely healed by 
the time the severe symptoms of disease are developed. Bed-sores belong in this 
category. 3. Ulcers of the mucous membranes may give rise to infection. This 
is the explanation of those cases of sepsis which, in rare instances, follow all sorts 
of intestinal ulcers (simple intestinal ulcers, typhoid, dysentery, etc.), diphthe- 
ritic processes in the pharynx, even mild tonsillar affections, etc. In the descrip- 
tion of scarlet fever and pharyngeal diphtheria we have already considered this 
important form of secondary sepsis in detail. 4. Lastly, we sometimes find no 
other source for the pysemia than a suppurating disease of the bones, joints, or 
other parts, previously existing. We must here suppose that some connection was 
formed between the original pus cavity and the blood or lymph channels, and that 
thus the micrococci entered the general circulation and were enabled rapidly 
to increase. 

The above enumeration by no means exhausts all the possibilities; still, it 
will be found to explain most cases. The more minutely we search for a place 
of entrance for the septic virus, the rarer will the " cryptogenic " cases be in 
which the starting-point of the infection remains unknown. [The editor has 
seen two clear cases, one confirmed by autopsy, of general septic infection and 
malignant endocarditis as a sequel of gonorrhoea.] 

Pathological Anatomy. — The most striking feature at the autopsy of such 
cases is that there is never found a lesion of one organ exclusively. Several, or 
it may be almost all of the organs, exhibit numerous limited foci of disease. The 
lesions sometimes consist for the most part of multiple abscesses, sometimes of 
numerous ecchymoses, and sometimes of combinations of the two. The abscesses 
are found chiefly in the lungs, kidneys, liver, spleen, muscles, heart, brain, and 
thyroid gland. Quite extensive purulent inflammation is also found. This at- 
tacks the joints or causes phlegmon of the muscles or skin by preference, but it 
also attacks the pleura, the meninges, and the eye, where it causes purulent 
choroiditis, panophthalmitis, and purulent degeneration of the vitreous. Puru- 
lent phlebitis also occurs. The ecchymoses are most frequent upon the surface 
of the body, the serous membranes (pericardium, pleura), the retina, the conjunc- 
tiva, the brain, the pelvis of the kidney, etc. Beside these multiple abscesses and 
ecchymoses, there is frequently another disorder, which seems to be the very 
focus of the disease, viz., acute ulcerative endocarditis (cf. the appropriate 
chapter). This usually attacks the mitral valve, more rarely the valves of the 
aorta, and quite exceptionally the valves of the right side of the heart. Finally 
come a number of changes common to all severe constitutional infectious diseases 
— acute splenic tumor, " cloudy swelling " of the liver and kidneys, a dryness and 
dark-red color of the muscles, etc. 

In regard to the special origin of all these symptoms we may certainly 
refer the abscesses, the purulent inflammation, and the endocarditis to the 
immediate presence of the micrococci themselves, while the parenchymatous 



SEPTIC AND PYEMIC DISEASES 



119 



degenerations of different organs, the haemorrhages, and probably the splenic en- 
largement and the diffuse acute nephritis, are to be regarded as due to toxic 
action. Microscopic examination of the internal organs gives us a very instruc- 
tive insight into the morbid process. This often reveals the presence of many 
tiny foci of disease, in the center of which we often see a little blood-vessel com- 
pletely filled with micrococci ("micrococcus embolus"). As Weigert first found, 
the primary action of a little focus of micrococci upon the surrounding tissues 
consists of a circumscribed cell necrosis, a small focus of " coagulation-necrotic " 
cells without nuclei. This may be followed later by circumscribed suppuration. 

Clinical History. — It is our intention to discuss below those cases chiefly 
which are of interest to the physician rather than the surgeon — i. e., where the 
septicopyemia is an apparently primary, acute, and grave disease. Many of the 
■essential traits of this type of disease are identical with those of the pyaemia 
which complicates the effects of serious wounds or the inflammation subsequent 
to childbirth ; but it is precisely because no cause at all presents itself that many 
cases of this form of sepsis seem so obscure, and are so often wrongly diagnosti- 
cated. Besides, the patient may be very ill indeed before the physician sees him ; 
and this adds greatly to the difficulties of a correct diagnosis. 

The beginning of the disease is usually rather abrupt. An apparently healthy 
person is attacked with febrile symptoms, headache, and " rheumatic " pains 
in the muscles, joints, and loins. There may also be gastro-intestinal symptoms 
of considerable severity, including vomiting and diarrhoea. Usually the patient 
feels ill enough to take speedily to his bed. The symptoms now increase rapidly, 
and develop into a severe illness which may resemble either a bad case of typhoid 
fever or miliary tuberculosis. Or the cerebral symptoms, such as headache, 
stupor, and delirium, may become so prominent that the attack seems like menin- 
gitis. If the trouble in the joints (vide infra) predominates and there are signs 
of endocarditis, the disease may at first be taken for a violent attack of acute 
articular rheumatism. 

Taking up the separate symptoms, we shall first name those which belong to 
•every severe acute infectious disease and have nothing characteristic about them. 
In this list belong the general prostration, the anorexia, the mental disturbance, 
the stupor and delirium, the headache, the subjective symptoms of fever, the dry- 
ness of the tongue, and finally the acute splenic tumor which can often be made 
•out. There are, however, other and more characteristic symptoms; and it is 
chiefly upon these that the diagnosis rests, provided we can make one at all. 
These are : 

1. The Course of the Fever. — In many cases it must be confessed that this 
is not at all characteristic. It may even be so like that of typhoid fever, at 
least for some time, as to lead to a wrong diagnosis. In other cases, however, the 
temperature-curve does aid us greatly, viz., when it represents an intermitting 
fever with marked elevations, reaching 106° (41° C.) and higher, and often 
accompanied by a chill, and with subsequent deep depressions. The curve may 
thus come to resemble closely that of a quotidian or even tertian intermittent 
fever. This true " pyaemic " fever, in which the rise in temperature is usually asso- 
ciated with a severe chill, occurs chiefly in the cases with multiple abscesses. 
Sometimes, again, the course of the fever is made up of similar paroxysmal eleva- 
tions, separated by periods of ordinary remitting fever. 

2. Cutaneous Symptoms. — These are very frequent, and a great aid to diag- 
nosis. The haemorrhages into the skin are of chief importance. They may be 
either punctiform petechia? or more extensive ecchymoses. Of other cutaneous 
appearances, the first in relative frequency is an erythema resembling scarlatina. 
It is not improbable, as we have already said, that many cases which have been 
described as severe scarlet fever occurring during childbed were in reality septic 



120 



ACUTE GEKEKAL INFECTIOUS DISEASES 



disease. We also sometimes see eruptions resembling erythema exsudativum 
multiforme or erythema nodosum, and also in some cases roseola, pustular erup- 
tions, and herpes. Extensive inflammations of the skin like erysipelas are espe- 
cially characteristic of certain cases. They are seen on the lateral surfaces of 
the thorax, the back, the thighs, etc., and often end in phlegmonous suppuration. 
When they occur we can usually make a very positive diagnosis of septic in- 
fection. 

3. Circulatory Disturbances. — An ability to recognize the cardiac lesions 
would be very desirable ; but often this is impossible before death. Endocardial 
murmurs are often wanting, even in cases where the autopsy discloses abundant 
exudation and ulcers upon the valves. Still, in some cases of this sort we have 
found the heart-sounds noticeably deficient in clearness. Sometimes we hear 
very loud or low, blowing sounds. The cardiac dullness is often quite normal, in 
other cases somewhat increased. In some cases fibrinous or purulent pericarditis 
develops. Functional disturbances of the heart's action are almost always pres- 
ent. The heart's action is excited and very rapid (120 to 140 or more), or in rare 
cases abnormally slow. Irregularity and inequality of the pulse are common. 
The tension of the pulse is usually low, and the frequent pallor and mild cyanosis 
of the patient point to a diminished energy in the heart's action. In the blood 
we find almost invariably a more or less pronounced leucocytosis. The presence 
of micrococci in the blood would naturally be of the greatest significance. They 
have, in fact, been repeatedly found in septic affections during life, but more 
extensive clinical bacteriological investigations are still needed in regard to this 
point. 

4. The grave cerebral symptoms are for the most part quite analogous to those 
of other severe acute infectious diseases. They may be present, and yet no 
marked objective lesions may be found after death. In other cases they have an 
anatomical basis — in purulent meningitis, hemorrhagic pachymeningitis, cere- 
bral haemorrhage, or abscess. These conditions, just enumerated, may excite 
localized cerebral symptoms, e. g., hemiplegia. 

5. Affections of the joints are comparatively frequent, and of great value in 
diagnosis. We may find serous, or more likely purulent inflammation, or even peri- 
articular abscesses. If they appear early in the attack, they may, as we have 
said, lead to an erroneous diagnosis of acute articular rheumatism. Suppurative 
processes affecting the periosteum and the marrow of the bones not infrequently 
accompany the joint affections. Only in rare cases do the bones remain wholly 
unaffected, as is evident from the frequent occurrence of pain in the long bones. 
If there is decided suppuration in the bones we speak of an acute osteomyelitis. 
This is seen especially in the lower extremities. It is almost always occasioned 
by the staphylococcus aureus. In earlier times such cases were termed bone- 
typhoid. Finally, abscesses and extensive phlegmonous suppuration in the mus- 
cles are not uncommon. 

6. Renal changes are very frequent, but abscesses and haemorrhages may be 
numerous in the kidneys, or haemorrhages in the mucous membrane of the pelvis 
of the kidney, without materially altering the character of the urine. In most 
cases, however, an acute septic nephritis is conjoined with the infarctions and 
abscesses, and then the urine exhibits all the characteristics of acute Bright's 
disease, having a small or large amount of albumen, red and white blood-corpus- 
cles, epithelium, and casts. 

7. The pulmonary symptoms are in part secondary. Bronchitis and lobular 
pneumonia develop as in all other severe constitutional diseases. The pulmonary 
abscesses of themselves give rise usually to no objective symptoms — or, at most, to 
a marked dyspnoea, out of all proportion to the scanty physical signs. Empyema 
is a not infrequent result of infection of the pleura, due to the foci of disease 



SEPTIC AXD PYEMIC DISEASES 



121 



which are situated upon the outer surface of the lungs, or perhaps sometimes to 
the condition of the blood. If the aspirating-needle shows the actual existence of 
empyema, this fact may make the diagnosis of the constitutional disease much 
easier. A fibrinous pleurisy of slight degree is often found at the autopsy, and it 
may be diagnosticated during life by the detection of a slight pleuritic friction-rub. 

8. Of the abdominal symptoms we have already mentioned the acute splenic 
tumor. It is almost impossible to diagnosticate infarctions and abscesses in the 
spleen. If the spleen is enlarged and noticeably painful, we may suspect their 
existence. There are sometimes quite severe intestinal symptoms, such as a pro- 
fuse " septic diarrhoea," in cases where the autopsy does not show any particularly 
grave lesions. Still intestinal ecchymoses and intestinal diphtheria have some- 
times been observed. We should mention that often the skin has a faint jaun- 
diced hue. This is sometimes the result of duodenal catarrh, but more frequently 
it is to be regarded as a " hepato-hsematogenous " jaundice due to a decomposition 
of the blood. 

9. Ocular Distur~ba?ices. — The purulent inflammations of the eye, which are 
probably of embolic origin and which may develop into diffuse septic panoph- 
thalmitis, have been known for some time. Lately, Litten and others have called 
attention to more minute changes in the fundus of the eye. These are revealed 
through the ophthalmoscope, and have great diagnostic value. Chief among 
them is retinal haemorrhage, which is sometimes accompanied by a white spot in 
the center, corresponding to a necrosis of the retina in that place ; but there may 
be similar white spots without haemorrhage. 

Course of the Disease and Prognosis. — In severe general septic infection 
death sometimes occurs in a few days. In other cases the disease continues 
longer, the symptoms lasting two or three weeks or even more. Improvement 
sometimes takes place, followed by a relapse. Here, too, the result is often fatal, 
although the infection may finally be completely overcome. We may also accept 
as certain that there are mild, curable forms of septic disease. In these the 
signs of general infection may predominate, such as fever with general intoxica- 
tion, cardiac weakness, pains in the joints, albuminuria or exanthemata, or, in 
other cases, the chief symptoms may be due to a special localization of the germs 
or their toxines (acute endocarditis, septic nephritis, septic inflammation of the 
serous membranes, septic enteritis, etc.). As we shall see later, acute articular 
rheumatism (polyarthritis acuta) is probably nothing but a benign septic 
infection. 

Diagnosis. — It is self-evident that a disease which combines symptoms so 
manifold and so ambiguous must be very difficult to recognize. We will re- 
capitulate the chief diseases to be excluded. A case may greatly resemble typhoid 
fever when there is persistent prostration, diarrhoea, an eruption like roseola, and 
an enlarged spleen. In discriminating, we should consider with great care the 
possible aetiology — e.g., external injuries, etc.; we should remember that most 
septic affections begin rather more rapidly; and we should look for swelling of 
the joints, cutaneous ecchymoses, nephritis, phlegmonous suppurations, an inter- 
mitting form of fever, and septic disease of the retina. We have repeatedly 
found that leucocytosis was a very valuable sign, since it is almost always absent 
in typhoid fever, but a positive result from Widal's serum reaction (vide page 
22) renders a diagnosis of typhoid very probable. It is all the more possible 
for the disease to resemble meningitis, because, as we have said, meningeal dis- 
turbance may be one of the symptoms of the sepsis and color the whole pic- 
ture. Here the characteristic symptoms of septic poisoning already mentioned 
would be of some value in diagnosis, and the physical signs of endocarditis or 
of a greatly enlarged spleen would be worth still more. There may be much 
difficulty in the differential diagnosis between acute sepsis and acute miliary 



122 



ACUTE GENERAL INFECTIOUS DISEASES 



tuberculosis. Here we should consider carefully each separate symptom, and, 
above all, the aetiology, searching for something that would explain the occur- 
rence of sepsis on the one hand, or of acute miliary tuberculosis (q. v.) on the 
other. If we found miliary tubercles in the choroid by means of the ophthal- 
moscope, or tubercle bacilli in the sputum or in the blood (which is, of course, 
not always possible), all doubt would vanish. At the beginning of a septic 
attack the rigors may arouse suspicions of intermittent fever. Usually the early 
appearance of other symptoms corrects this idea; but, if not, the powerless- 
ness of quinine will. If a severe acute nephritis has developed itself in a septic 
case, all the symptoms may be erroneously referred to uraemia; but persistent 
observation will usually lead us to the right conclusion. As to the conditions 
of great prostration resembling acute sepsis, which occur in acute (primary) 
ulcerative endocarditis and in severe articular rheumatism, see the appropriate 
chapters. 

In general the diagnosis of acute sepsis can rarely be settled during the first 
days of the disease, but on further observation and with due attention a toler- 
ably definite diagnosis can often be made. The chief elements for diagnosis are 
a careful consideration of the aetiology, attention to the whole clinical picture, 
and to any individual symptoms especially characteristic of septic infection 
(purulent inflammation, chills and fever, cutaneous and retinal haemorrhages, 
nephritis, marked leucocytosis, etc.). 

We must refer the reader to the appropriate chapters for the morbid condi- 
tions allied to acute sepsis, such as " primary acute endocarditis," " acute articu- 
lar rheumatism," " purpura hemorrhagica," etc. 

The treatment is merely symptomatic. Of course we try again and again 
to cut short the attacks of fever by large doses of quinine or antipyrine, but 
never with any but temporary success. With marked swelling of the joints we 
may try salicylic acid. Of other remedies, cardiac stimulants are most fre- 
quently employed, and narcotics if necessary. Great stress is to be laid on keep- 
ing up the physical strength by careful nourishment. Circumscribed suppura- 
tion (empyema, phlegmon, etc.), when it exists, of course requires the proper 
surgical treatment. 

CHAPTER XX 

HYDROPHOBIA 

(Rabies canina. Lyssa) 

iEtiology. Rabies in Dogs. — A peculiar infectious disease sometimes occurs 
in dogs, and more rarely in some other animals — viz., the wolf, fox, cat, etc. 
Men who are bitten by the animal may catch the disease, and thus suffer from 
very severe symptoms originating in the central nervous system. 

Two forms of madness are distinguished in dogs — the raving madness and the 
quiet madness. Bollinger describes the raving form as beginning with prodro- 
mata, the melancholy stage, lasting one to three days. The animal is low-spirited, 
timorous, and without appetite. Then comes the stage of irritation or of mania, 
in which the animal is possessed with an impulse to bite. It seems determined to 
run away and rove about, and it utters a peculiar howl. The dog will not touch 
his ordinary food, but he often swallows straw, hair, earth, bits of wood, etc. In 
the third or paralytic stage paralysis appears. The dog looks lean and wretched, 
and always dies on the tenth day at the latest. In what is called the quiet mad- 
ness there is no maniacal stage. The symptoms of paralysis, affecting chiefly the 
hind limbs and the lower jaw, occur earlier and are sooner fatal. Marked patho- 



HYDROPHOBIA 



123 



logical changes are not found. There are pulmonary and intestinal catarrh and 
passive congestion of the viscera, and the stomach often contains foreign bodies 
in place of the usual partially digested food. 

[On the Western plains hydrophobia is said not infrequently to follow skunk 
bites. The bite is inflicted during sleep on persons passing the night in the open 
air or in tents to which the animal can gain access.] 

Rabies is transferred to the human being almost invariably by the bite of some 
raving animal, and this animal is almost always a dog; much more rarely a wolf 
or cat. It is of practical importance, and it has been repeatedly confirmed, that 
the bite of such an animal, although still in the incubation period of hydrophobia, 
can convey the disease to man. The poison, which is not yet known in its pure 
form, is evidently contained in the saliva or slaver and in the blood of mad ani- 
mals, and can, by means of these substances, be successfully inoculated in other 
animals. Pasteur has discovered another way to produce the disease experi- 
mentally. He takes minute portions of the brain, medulla oblongata, or some 
other internal viscus of a mad dog, and either injects them into the veins of a 
healthy animal, or trephines, and then inserts them beneath the meninges. The 
virulence of the rabic poison when thus manipulated undergoes, under special con- 
ditions, very peculiar alterations, which will be detailed at the close of this 
chapter. 

About one half of those who are bitten by mad animals exhibit no subsequent 
symptoms. Still this can scarcely be due to inherent immunity from the dis- 
ease, and it must result chiefly from imperfect infection. Experience has shown 
that infection is especially apt to follow when a nerve has been injured by the 
bite; and infection occurs more readily the larger and the nearer the brain the 
wound is. Wounds of the head are therefore the most dangerous. The dura- 
tion of incubation until rabies finally breaks out seems to vary greatly. As a rule 
it is about three to six months, but observers have reported instances both of 
shorter and of much longer duration. 

Clinical History. — The disease begins with a general feeling of indisposition, 
anorexia, headache, and uneasiness. This last is partially explained, to be sure, 
by a dread of what is impending. If the bite was in the face, frequent convulsive 
sneezing may occur. Even now, in this prodromal stage, a marked aversion to 
liquids is a usual and early symptom. The attempt to swallow excites slight con- 
vulsive disturbances. Painful sensations may arise once more in the bitten place, 
although this has usually been cicatrized long before, and the neighboring lymph- 
glands are often found to be swollen. 

Only a day or two later the second, hydrophobic stage begins. The especial 
characteristic of this consists in the peculiar attacks of tonic convulsions. The 
pharynx suffers most, but convulsions also attack the muscles of respiration and 
those of the trunk and extremities. A terrible feeling of anxiety and oppression 
accompanies these attacks, so that one who has once witnessed the sight can never 
forget it. The convulsions always seem to be reflex, and are produced by the 
slightest causes, particularly by any attempt to swallow, or sometimes by the mere 
sight of water. They recur at gradually diminishing intervals, and last from a 
few minutes to half an hour. The excitement of the patient may reach the pitch 
of delirium or mania. The pulse is at first full and rapid, but later it is small 
and irregular. The temperature is usually only slightly elevated, but it may be 
high. There is great thirst, accompanied by burning pain in the throat. Usu- 
ally there is marked salivation. 

This condition lasts one to three days. Then death occurs, ushered in by vio- 
lent convulsions. Death may also be preceded by a brief third stage of paralysis, 
during which there are no convulsive attacks. Cases of recovery in man, if they 
ever happen, are extremely rare. 



121 



ACUTE GENERAL INFECTIOUS DISEASES 



The autopsy shows very little. The brain and medulla especially show no 
gross changes, so that we may conclude that hydrophobia is chiefly the effect of a 
toxine. The microscope has repeatedly detected very minute haemorrhages, clus- 
ters of lymph-cells around the blood-vessels, etc. There have been only a few 
investigations of the finer microscopical changes in the motor ganglion cells of 
the medulla, etc. The throat may present the signs of catarrh. The lungs are 
congested, and often oedematous. The blood is dark, with few clots. The heart, 
liver, and spleen are apparently normal. 

The diagnosis is usually easy, particularly if we know of the possibility of 
infection. We are guided by the convulsions following attempts to swallow, as 
well as by the whole group of symptoms. Hydrophobia is distinguished from 
traumatic tetanus by the absence of trismus and of the characteristic tension of 
the muscles of the back and abdomen, by the convulsions coming in separate 
attacks, and by the usually greater length of incubation. There is only one 
form of tetanus which bears very great resemblance to rabies, viz., the so-called 
hydrophobic tetanus (vide infra). It should be mentioned that the mere dread 
of hydrophobia may cause an easily excited person to have the nervous symp- 
toms of the disease (" hysterical hydrophobia "), but of course without disastrous 
results. Hysteria, also, may give rise to convulsions on swallowing somewhat 
resembling those of hydrophobia. 

However hopeless treatment seems, we must at least try to mitigate the pa- 
tient's suffering. Narcotics accomplish this best — e. g., opium or chloral, or, most 
useful of all, the inhalation of chloroform. Curare has been administered repeat- 
edly, and does seem to lessen the violence of the attacks. The attempt to find a 
serum-therapy for hydrophobia has unfortunately not been thus far successful. 

Prophylaxis is extremely important. We can not consider in detail the regu- 
lations (muzzling) which the government should make in order to prevent the 
spread of the disease. As to individual prophylaxis, every suspicious bite should 
be very thoroughly disinfected, and then cauterized either with carbolic acid, 
caustic potash, or the red-hot iron. It has also been recommended that the entire 
wound or scar should be excised, along with any swollen lymphatic glands which 
may be found in the neighborhood. Internal remedies to prevent the outbreak 
of the disease are probably quite useless. 

On the other hand, Pasteur has recently made a series of extremely remarkable 
observations which have led to a special method of prophylactic inoculation 
against rabies in human beings. If a bit of the spinal marrow taken from a mad 
dog (an emulsion of the substance of the cord rubbed up in salt solution or 
bouillon) is introduced beneath the dura mater of a rabbit by means of trephining, 
the animal exhibits the symptoms of rabies after fourteen days' incubation. If 
in the same way a second rabbit is inoculated from the first, and so on, the viru- 
lence of the inoculated material increases gradually with every inoculation, while 
the period of incubation grows shorter and shorter, till it lasts but seven days. 
Beyond this point the period of incubation does not seem to diminish. If, on the 
other hand, the same series of inoculations are made on apes, the virulence 
of the poisonous matter does not increase, but diminishes. If dogs are inocu- 
lated with material artificially attenuated in this manner, the animals remain 
in good health, and furthermore acquire an immunity against more virulent 
inoculations, so that they may be bitten by mad dogs without becoming infected. 

Pasteur has also published a still more simple and valuable method of artifi- 
cial attenuation of the virus. He removes small portions of the spinal marrow of 
rabbits which are suffering from rabies in its most violent form produced by the 
above-detailed method, and these bits of marrow he exposes to air which has 
been wholly deprived of moisture. In this way the poison contained in the spinal 
marrow gradually and progressively loses its virulence, until it finally becomes 



GLAXDEKS 



125 



inert. A portion of spinal marrow which by long drying has completely lost its 
original virulence is then rubbed up in sterilized bouillon and injected into some 
animal — for instance, a dog — and then in regular succession pieces of marrow 
which have been dried for shorter and shorter periods and so contain more and 
more of the poison, until finally the point is reached when it is possible to use for 
the injection pieces which are perfectly fresh and extremely poisonous, without 
affecting the animal's health. That is, the animal has attained immunity from 
the disease. 

This second method has now been employed by Pasteur on several thousands 
of human beings who were said to have been bitten by mad dogs. According to 
the reports, so small a number of these inoculated persons (about one per cent.) 
have actually been attacked later by hydrophobia that we can no longer doubt 
the prophylactic value of Pasteur's protective inoculations, especially as we have 
to do with observations which are by no means unique in bacteriology. The dan- 
ger that hydrophobia may perhaps be excited by such a " protective inoculation " 
can not be wholly excluded, but it will certainly grow less and less. 

Prophylactic inoculation for hydrophobia can at present be practiced only 
in special institutes. In most civilized countries, therefore, such institutions 
have already been established on the plan of the Pasteur Institute in Paris. 



CHAPTEK XXI 

GLANDERS 

{Farcy) 

. -ZEtiology. — Glanders is a disease of the horse and some animals allied to it — 
viz., the ass and mule. It can, however, be transferred to man. It is character- 
ized by peculiar new growths, either like nodes ("farcy-buds"), or more rarely 
diffuse. These are very prone to suppurate and break down. Such nodes, and 
the ulcers which they leave behind them, occur most frequently in the mucous 
membrane of the nose. In horses the purulent nasal discharge is one of the 
earliest and most important symptoms of the disease. Similar nodes are found 
in the larynx, lungs, liver, spleen, and kidneys, and often also in the skin. The 
cutaneous swellings and deep, crater-like ulcers belong to that form of the dis- 
ease which is called " farcy." The corresponding lymphatic vessels and glands 
are usually much swollen. The animal has fever, grows weaker and weaker, and 
almost invariably dies at the end of one to three weeks. 

Glanders in man is always referable to infection from a diseased animal, 
although in certain instances it is impossible to demonstrate the source. The 
disease is therefore commonest among persons who have much to do with horses 
— e.g., hostlers, coachmen, 'farmers, and cavalrymen. The virus is usually con- 
veyed by the pus and nasal secretions of the diseased animals. A little of this 
falls upon some excoriation on the hand or some crack in the skin, and is absorbed. 
Han does not seem very liable to the disease ; it is of rare occurrence. 

Loffler and Schiitz have discovered the specific disease-producing agent. These 
investigators were able to demonstrate in all the products of glanders delicate 
bacilli about the size of the bacilli of tuberculosis. These bacilli can be reared 
artificially, and, if inoculated upon horses and other animals, they give rise to a 
typical attack of glanders in every instance. The bacilli of glanders can scarcely 
ever be detected in the blood. It is also very interesting that they rapidly lose their 
virulence in purified cultures outside of the living body. This is one more proof of 



126 ACUTE GENERAL INFECTIOUS DISEASES 



the fact, which is lately coming more and more into prominence, that the external 
influences surrounding the life of bacteria modify greatly their biological pecul- 
iarities. By repeated inoculations of glanders in the horse the virulence of the 
bacilli rapidly diminishes, while, on the other hand, by repeated inoculation in 
the weasel the virulence is very considerably increased. 

Clinical History. — The period of incubation lasts about three to five days, and 
sometimes longer. The first symptoms are local, if the infection has resulted 
from a visible injury. There is considerable swelling and pain in this spot, and 
usually considerable lymphangitis in its neighborhood. In other cases, however, 
the disease begins with indefinite constitutional symptoms, such as fever, head- 
ache, and pain in the limbs, so that there may be some resemblance to beginning 
typhoid fever. The local and general disturbances increase, and the disease soon 
attacks other parts of the body. In the skin we see small macules or papules, 
singly or in groups, which soon change to pustules like those of small-pox, or to 
larger abscesses. These abscesses burst and discharge offensive pus, leaving be- 
hind them irregular, deep ulcers. Not infrequently the joints are swollen. The 
mucous membranes are also attacked; chief among these troubles are ulcers in 
the nose. The nose swells as if with erysipelas, and there is a purulent, foul- 
smelling discharge. The nose rarely escapes. The conjunctivas, throat, mucous 
membrane of the mouth, and the larynx also undergo inflammation and ulcera- 
tion. A violent, diffuse bronchitis develops. Sometimes there is considerable 
disturbance of the stomach and intestines, giving rise to vomiting and diarrhoea. 
At the same time the constitutional symptoms become more and more severe. 
The patient grows stupid or delirious. In some few cases the severe cerebral 
symptoms are due to a purulent meningitis, perhaps through extension of the 
inflammation by contiguity from the nose. The fever is high, and sometimes it is 
quite continuous. More rarely there are chills and great elevations of tempera- 
ture, as in the fever of pyaemia. The pulse is rapid and small. The spleen is 
seldom much enlarged. The urine may contain a trace of albumen. 

In these severe acute cases the termination is almost always fatal. Death 
occurs at the end of two to four weeks. There are cases with a more chronic 
course, with tedious persistence of the troubles in the skin and mucous mem- 
branes, and milder febrile and constitutional symptoms. Such attacks appear at 
first tolerably favorable, but they may end fatally with persistent fever and 
increasing physical weakness, or they may run on for months, and at last end 
in complete recovery. 

The autopsy reveals a condition greatly resembling that in pyaemia. We find 
abscesses in many parts, particularly the muscles and the lungs, and, next in fre- 
quency to them, the spleen, brain, and other viscera. In the mucous membrane of 
the nasal cavities, the pharynx, and the larynx, are found nodes and ulcers, such 
as occur in the horse. As in septicaemia, there are often numerous haemorrhages 
into the serous and mucous membranes. It has already been mentioned that the 
specific bacilli of glanders are present in the abnormal secretions. 

Diagnosis. — Without the aid of aetiological factors the diagnosis of glanders 
is often very difficult. Indeed, until recently there have' been instances where 
even the autopsy did not suffice to exclude pyaemia; but now that the specific 
bacilli have been discovered we can clear up all doubts. We can not, however, 
enter into a particular description of the distinguishing characteristics of these 
bacilli. Their demonstration requires pure cultures. At the bedside also aeti- 
ology is all-important in diagnosis — e. g., exposure to infection, or occupation. 
Experience with a limited number of cases renders it probable that in the future 
we shall be able to demonstrate the bacilli, during the life of the patient, in 
the nasal secretions or the contents of the abscesses. The most characteristic 
symptoms are the nasal and cutaneous. In a case that takes a chronic course 



MALIGNANT PUSTULE 



127 



there is a possibility of mistaking the cutaneous ulcers for syphilitic or tubercu- 
lar sores. 

Kalning has discovered a very interesting fact, which, so far as we know, has 
not been applied to man. A substance can be obtained from cultures of glanders 
bacilli, the so-called malleine. If this be injected in small amounts in horses sick 
with glanders it causes high fever, while the injection has no effect in any other 
animal. Malleine, therefore, has the same significance in the diagnosis of glan- 
ders as tuberculine has in the diagnosis of tuberculosis. 

We have already implied that the treatment of acute cases is almost hopeless. 
We must do all we can in the way of cleanliness and disinfection to improve the 
local condition of the skin, the nose, and the throat. All abscesses and nodules 
must be opened as soon as possible and curetted and disinfected. Appropriate 
agents are. carbolic and salicylic acids. Further treatment should be in accord- 
ance with the general rules for the care of severe acute infectious diseases. An 
inunction treatment with unguentum cinereum (gr. xxx-xlv., grm. 2-3, daily) 
has a very favorable effect. Iodide of potassium, arsenic, etc., have also been 
recommended. [Malleine has been employed subcutaneously in chronic glanders, 
with " marked improvement." — V.] 



CHAPTEE XXII 



{Anthrax. 



MALIGNANT PUSTULE 

C harbor). Splenic Fever. Mycosis intestinalis. 



Carbunculus contagiosvs) 



etiology. — The cause of malignant pustule is the infection of the body with a 
specific kind of bacilli, the bacillus anthracis. This organism was discovered by 
Pollender in 1849, and a few years later, independently, by Brauell. 

These bacilli are very minute cylinders, about as long as the diameter of a 
red blood-corpuscle. They are found in enormous numbers in the blood and 
organs of animals which die of anthrax. Aniline-staining makes them more 
easily visible. By means of blood containing the bacilli, Davaine (1863) and 
others have inoculated many 
animals with the disease, in- 
cluding mice, rats, guinea- 
pigs, cows, sheep, goats, and 
birds. The bacilli can also 
be isolated and cultivated, 
and then produce infection. 
This is proof positive that 
they are the actual carriers 
of contagion. The rapid in- 
crease of the anthrax bacilli 
in the blood goes on by sub- 
division. In the artificial 
cultivations, however, the 
bacilli grow, as Koch has 
shown, into quite long 

threads, in which shortly appear minute, brilliant egg-shaped bodies (cf. Figs. 
13 and 14). The threads become disintegrated, setting free the little shining 
ovoids, the spores of anthrax, to grow into bacilli. The bacilli can live only a 
relatively brief time; but the spores have unusual tenacity of existence. They 




Fig. 13 



/Ynthrax bacilli. (From Koch.) 650 diameters. A, from 
the blood of a guinea-pig. B. from the spleen of a mouse 
after three hours 1 culture in the aqueous humor. 



128 



ACUTE GENEKAL INFECTIOUS DISEASES 



may remain dried up for years, and then be brought to further development if 
placed in favorable conditions of heat and moisture. If the spores are trans- 
ferred to animals, they develop into bacilli, and there is scarcely room to doubt 
that men and animals are quite as often infected by spores as by full-grown 
bacilli. There are facts which render it not improbable that the anthrax bacilli 
exist in other places than the bodies of men or animals, and may there complete 
their circle of development. Such places are marshes, the banks of streams, and 
the like. If it is possible for them to be carried by high water to the pasture lands, 
we have an explanation of those sudden endemic appearances of anthrax which 
sometimes occur in places previously free from the disease. 

Anthrax in animals is of great practical importance, because its favorite 
victims are the herbivorous domestic animals — viz., the cow, sheep, and horse. 
Among these it is terribly destructive. It is remarkable that the carnivora enjoy 
almost complete immunity. The disease usually runs a very acute course in ani- 
mals. Indeed, it often seems like apoplexy; the apparently healthy animal sud- 
denly falls, suffers for a few minutes from convulsions and dyspnoea, and dies. 



Fig. 14.— Anthrax bacilli ; spore formation and spore germination. (From Koch.) A, from the spleen 
of a mouse after twenty-four hours' 1 culture in the aqueous humor, spores arranged like strings of 
beads in the filaments. 650 diameters. B, germination of the spores. 650 diameters. C, the same, 
with a higher power. 1650 diameters. 

Other cases have a somewhat longer and more intermittent course, but in these 
also recovery is very rare. 

Human beings are probably infected in most cases by direct inoculation. 
Shepherds, farmers, butchers, and others who come in contact with animals suffer- 
ing from anthrax, are liable to infection through any little wound or scratch 
upon the hands. Very often the disease is caught from hides, hair, or other parts 
of dead animals. In workshops and factories where wool and hides have been 
used which came from diseased animals, anthrax has repeatedly occurred. Cur- 
riers, rope-makers, paper-makers, hatters, furriers, brush-workers, and those who 
handle horse-hair and wool, are all exposed. Anthrax has also acquired the name 
of " rag-pickers' disease." Another way of infection, supposed to happen among 
animals as well as men, is through the sting of insects — e. g., flies — bringing the 
poison from diseased animals. It is not likely that the virus can be absorbed 
through the unbroken skin. It is certain, however, that the intestine may some- 
times afford ingress to the infectious matter. Koch has proved this by putting 
spores in the food of sheep. Intestinal mycosis in man (vide infra) may very 
possibly be due to a similar mode of infection. Many cases of poisoning from eat- 
ing meat have been referred to the ingestion of the flesh of animals who died from 
anthrax. Some observations on pulmonary anthrax seem to favor the idea that 
the poison may be inhaled with dust and develop primarily in the lungs. 




MALIGNANT PUSTULE 



129 



Clinical History. — Anthrax in man has two distinct forms. These may ap- 
pear in combination. The first begins with a local disorder of the skin at the 
point of infection — viz., the malignant pustule, or anthrax carbuncle. The sec- 
ond and rarer form presents the symptoms of a severe acute constitutional infec- 
tion. An accompanying cutaneous disorder or other local disease is sometimes 
observed. 

1. The malignant pustule usually comes on the hand, the arm,, or the throat, 
and appears from three to seven days after infection. A vesicle forms at the 
infected spot, grows rapidly, becomes excoriated, and usually takes on a charac- 
teristic appearance, being of a dark-bluish or black color. The surrounding 
parts become diffusely swollen and red. Secondary vesicles may surround the 
original one. The swelling becomes more and more extensive. Inflamed lymph- 
vessels or veins radiate in red lines from the pustule, and the neighboring glands 
are also affected. These appearances are accompanied by fever, and more or less 
prostration. In a favorable case the swelling subsides, the scab falls off, and 
there is at last complete recovery. But in other cases the constitutional infection 
becomes more and more prominent, and eclipses the local disorder. The fever and 
prostration increase. Severe intestinal symptoms appear, or else stupor, delirium, 
and other nervous disturbances ; and death may ensue after a few days' illness. 

The so-called anthrax oedema (malignant oedema, oedeme charhonneux, charhon 
blanc) is a form of primary anthrax of the skin differing from malignant pus- 
tule. It is seen chiefly in the eyelids, lips, and mucous membrane of the mouth 
and tongue, and also in other parts of the skin. In this form we see a circum- 
scribed, doughy, cedematous swelling, in which small bullae with sero-sanguineous 
contents often develop. These bullae may become gangrenous. On the neck and 
back the anthrax oedema may sometimes be of considerable extent. The other 
symptoms are similar to those of malignant pustule. We can not make an abso- 
lute separation of the two forms. 

2. Intestinal Anthrax ("Intestinal Mycosis"). — A quite different picture is 
presented by this second form, which is called intestinal anthrax (formerly intes- 
tinal mycosis) from the marked intestinal lesions. In this the cutaneous dis- 
order, if it exists at all, is insignificant compared with the severe constitutional 
disturbance. It is only within a few years that the labors of Buhl, Waldeyer, E. 
Wagner, Leube, and others have shown that attacks of this kind have any connec- 
tion with anthrax. 

In cases of this sort the attack is usually rather sudden, beginning with chilli- 
ness, vomiting, headache, and languor. The diagnosis is usually very obscure at 
first, unless the calling of the patient suggests the possibility of anthrax. On 
careful examination, we may find some places where the skin is broken, or pos- 
sibly a small characteristic pustule. In a case which came under our own obser- 
vation a pustule had existed on the back of the right hand for some weeks before 
severe symptoms appeared, but had not attracted the attention of the patient at 
all. In this case, therefore, the constitutional infection seems to have come from 
the local disease. But in other cases cutaneous troubles, in the form of small car- 
buncles, may occur secondarily in the course of the disease. Haemorrhages into 
the skin and mucous membranes (especially on the gums) also occur. 

Of other symptoms, the gastro-intestinal deserve to be mentioned first. Vom- 
iting occurs frequently, and also a moderate, painless, and sometimes bloody diar- 
rhoea. There is usually severe dyspnoea, and a marked sense of oppression in the 
thorax, but without objective pulmonary signs. Very soon there is collapse; the 
nose and extremities grow cool ; the pulse is rapid, but small ; and there is livid- 
ity. In a few instances tetanic or epileptiform convulsions have been observed. 
(Edematous swelling of the eyelids is sometimes seen. The temperature is sel- 
dom much elevated. It may be subnormal. In a few days the prostration be- 
9 



130 



ACUTE GENERAL INFECTIOUS DISEASES 



comes complete, and death ensues. Sometimes these severe general symptoms are 
associated with the signs of a circumscribed pneumonia (vide infra). 

Milder forms apparently occur, but here the diagnosis may not be absolutely 
certain. We have seen a few such cases originating in a rope-walk where Russian 
hair was used. The constitutional symptoms were only moderately severe, the 
fever was mild, and recovery occurred after two or three weeks. 

3. Pulmonary Anthrax. — Pulmonary anthrax probably arises, as we have said, 
from the inhalation of dust containing anthrax spores. The disease runs its 
course as a broncho-pneumonia, usually bilateral and associated with high fever, 
pleurisy, severe dyspnoea, cardiac weakness, and great general prostration. The 
anthrax bacilli can be found in the sputum and the pleuritic exudation, and 
sometimes in the blood. Most cases of this type terminate fatally in a few days. 

Pathology. — In the fatal cases of anthrax the intestinal lesions are the most 
characteristic. Besides the signs of catarrhal inflammation, we find peculiar 
lesions in the mucous membrane of the small intestine, and sometimes in the 
upper portion of the colon. These consist of dark, infiltrated spots, with haem- 
orrhages, the spots being somewhat larger than a silver dime. The microscope 
reveals numerous collections of anthrax bacilli, situated chiefly in the lumen of 
the blood-vessels. The spleen is usually only moderately enlarged, but dark and 
congested. There may be ecchymoses in the kidneys, the brain, and the serous 
membranes. Often there is swelling of the lymph-glands. In one case which we 
saw, with slight intestinal lesions, the mesenteric glands were considerably en- 
larged, and the bronchial lymph-glands were perfectly enormous. The bacilli 
are found in all the organs mentioned. 

The diagnosis of malignant pustule is seldom difficult, particularly if atten- 
tion be directed to the astrology. All doubt is over if we find the bacilli. The 
cases of intestinal and pulmonary anthrax may be more obscure. The chief 
point is that the attention be directed to the possibility of anthrax by the patient's 
occupation, the severe general symptoms, and any pustule on the skin. For a 
positive diagnosis we need, of course, to find the bacilli in any pustule on the 
skin or in the blood. 

Treatment. — 1. Prophylactic inoculation. Toussaint and Pasteur were the 
first to show that the virulence of anthrax bacteria can be artificially diminished 
by certain external influences. If the bacilli are kept under cultivation for sev- 
eral weeks at an unchanging temperature of 106° to 107.5° (42°-43° C), they 
preserve their external appearance completely, as well as their ability to grow, 
but gradually lose their power of infection. Inoculations made with this " vac- 
cine virus " produce at most an insignificant disturbance. But what is especially 
remarkable is that the animals thus vaccinated are protected thereafter from in- 
fection with actual anthrax. Pasteur was the first to make this assertion; and 
he proposed that the prophylactic inoculation of sheep and other animals liable 
to anthrax should be undertaken on a large scale, promising the farmers that very 
great benefit would result. So far as experience has thus far gone, the mortality 
of anthrax in sheep and cattle seems actually to have been considerably dimin- 
ished by the many protective inoculations which have beeii performed in France 
and Hungary. 

French investigators have lately made known new methods of producing an 
artificial diminution of the growth and virulence of anthrax bacilli, and also of 
other varieties of bacteria. Chauveau has found that cultures of anthrax bacilli 
exposed for several days to an atmospheric pressure of three to twelve atmos- 
pheres, or to compressed oxygen, lose a portion of their virulence ; and that ani- 
mals inoculated with bacilli thus attenuated gain an immunity to inoculations 
with the original anthrax poison. The statements of Arloing are very remark- 
able. He says that the direct play of sunlight, or even of a concentrated artificial 



TKICHIXOSIS 



131 



light, upon the cultures exercises a restraining influence upon the growth and 
poisonous properties of the bacilli, and that inoculation material weakened in this 
way may be employed to render animals immune. 

2. The treatment of malignant pustule is surgical. Cauterization is often 
tried with such agents as caustic potash, nitric acid, or carbolic acid; but it 
should always be borne in mind that such manipulations may easily contribute to 
a local extension of the anthrax poison. For the same reason one should hesitate 
to incise or to excise the pustules. We are therefore usually obliged to confine 
ourselves to the prescription of a suitable position for the affected member, and 
the application of an ice-bag over the diseased spot. 

The treatment of intestinal and pulmonary anthrax must be purely symp- 
tomatic. In intestinal anthrax the use of calomel (gr. ij-iij, grm. 0.1-0.2, several 
times a clay) is most to be recommended. Quinine (gr. vij, grm. 0.5, four times a 
day) and carbolic acid (gr. xv, grm. 1.0, a day in pills or subcutaneously) seem also 
to have a favorable influence on the general infection. 



m 



CHAPTER XXIII 



TRICHINOSIS 

(Trichinatous Disease) 



The Natural History of Trichinae. — The trichina 
spiralis, one of the class of round worms or nematoda, 
has long been known to occur occasionally in the mus- 
cles of men and certain animals; but it was not 
until 1860 that Zenker showed that trichinae are capa- 
ble of exciting in man a dangerous and sometimes fatal 
disease. Since then numerous individual cases and 
quite extensive epidemics have been reported ; and the 
labors of Virchow, Leuckart, and others have taught 
us the anatomy and mode of development of this pecul- 
iar parasite. 

The trichina appears in two shapes — as intestinal 
trichina and as muscular trichina. The intestinal 
form is a small white worm, visible to the naked eye. 
The female is 3-4 mm. long, the male only 1-1.5 mm. 
They have well-developed digestive and sexual organs. 
The male is distinguished by two little processes at 
the tail. The muscular trichina (vide Fig. 15) is a 
small worm 0.7-1 mm. long. It is found coiled up 
among the muscular fibers, inside a connective-tissue 
capsule, which is often calcified. 

The events in the life of the trichina are remark- 
able. If living muscular trichinae reach the human 
stomach through the eating of trichinatous pork, the 
capsules are dissolved, and the trichinae, thus set free, 
grow in two or three days into sexually perfect intes- 
tinal trichinae. In the uterus of the impregnated 

female the eggs develop into embryos, which are born already hatched. The 
birth of embryos begins seven days after the ingestion of the muscular trichinae, 
and seems to continue for some time. A single female is said to produce more 



Fig. 15.— (From Heller.) An 
isolated primitive bundle 
with two free trichina? in 
the sheath of the sarco- 
lemma. Much enlarged. 



132 ACUTE GENEKAL INFECTIOUS DISEASES 



than one thousand embryos. These latter begin their travels soon after birth, 
and reach the voluntary muscles. As to the routes they choose we are still 
somewhat in doubt. Some authorities state that the trichinae penetrate through 
the walls of the intestine and the abdominal cavity into the connective tis- 
sue. Others affirm that they enter the lymphatic vessels, or exceptionally the 
blood-vessels. They penetrate into the primitive fibers of the muscles, and cause 
them to disintegrate. Finally, they coil themselves up, attain the size of mus- 
cular trichinae in about fourteen days, and become encapsulated. Each capsule 
usually contains but one, although it may inclose as many as four. The capsule 
is formed partly by an excretion from the trichina, and partly from the reflex 
hyperplasia of the surrounding connective tissue. The process of development is 
now complete. The muscular trichinae seem, unlike the intestinal form, to have 
a very long lease of life, and usually endure till the death of their host. They 
are often found accidentally at autopsies. They are most abundant in the dia- 
phragm, the intercostal muscles, the muscles of the larynx and throat, and the 
biceps. 

etiology of Trichinosis. — The only cause yet known for trichinatous disease 
in man is the ingestion of trichinatous raw or underdone pork — e. g., smoked ham. 
Swine are pre-eminently subject to trichinae. They probably become infected in 
various ways, e. g., from the faeces of human beings and swine suffering from 
trichinosis, or through the ingestion of the trichinatous flesh of other swine. The 
waste of slaughter-houses is often fed out to swine, and the disease thus dissemi- 
nated. Many affirm that swine are also infected by eating rats infested with 
trichinae, but the contrary condition, whereby rats become trichinatous from eat- 
ing the flesh of diseased hogs, seems more in accordance with the facts. 

Clinical History. — The symptoms in man correspond in general to the devel- 
opmental and vital processes of* the trichinae, as above depicted. In individual 
cases, however, the separate stages are quite often obscured, probably because 
all the parasites do not develop simultaneously, or because there are relapses. The 
first symptoms are gastro-intestinal. At the commencement there is a feeling of 
pressure in the epigastrium, with nausea and vomiting. Later, diarrhoea is prom- 
inent, becoming in some cases so violent as to remind one of cholera. It is not 
impossible, although rare, to find intestinal trichinae in the stools. Sometimes 
there is constipation instead of diarrhoea. In some cases the initial gastro-intes- 
tinal symptoms are but slight. Frequently, even in the beginning of the disease, 
there is complaint of pain and stiffness in the muscles, too early for it to be due 
to the migrations of the trichinae. 

The genuine severe muscular symptoms, due to the myositis produced by the 
trichinae in the muscles, do not begin till the second week, or even later. In many 
cases, where the invading parasites seem to be relatively few in number, the 
muscular symptoms are slig*ht, or wholly absent. In the more severe cases, how- 
ever, they may be extremely violent and distressing. The muscles become 
swollen, firm and hard, very tender on pressure, and very painful. The patient 
avoids all movements and contraction of the muscles as much as possible, lying 
motionless in bed, with flexed arms and with legs either extended or likewise flexed. 
The patellar reflex almost always disappears, and on testing the electrical re- 
actions there is found a considerable diminution of muscular excitability to 
both the galvanic and faradic currents, sometimes associated with delayed con- 
tractions, and abnormally long duration of the same after the stimulus ceases 
(Eisenlohr). The masseters and the pharyngeal and laryngeal muscles are at- 
tacked, so that there is difficulty in mastication and deglutition, and hoarseness. 
The involvement of the ocular muscles causes pain in the eyes. The condition 
of the diaphragm, intercostals, and abdominal muscles causes serious difficulty 
in respiration. There is distressing dyspnoea, and expectoration is so hampered 



TKICHINOSIS 



133 



that secretions accumulate in the air-passages. In some- fatal cases of trichinosis 
death is due principally to this impairment of respiration. The condition may- 
be aggravated by diffuse bronchitis or lobular pneumonia. 

Third in the list of important symptoms comes oedema. It appears toward the 
end of the first week in the eyelids. Somewhat later it involves the upper and 
lower extremities. What produces it is not quite clear. It has been regarded as 
in part inflammatory and in part the result of occlusion and thrombosis of the 
smaller lymphatics. Cutaneous eruptions also develop — e. g., vesicles, wheals, 
petechia, and pustules. Frequently there is profuse perspiration, consequent 
upon which abundant crops of miliaria or sudamina may appear. 

In well-marked cases there may be quite high fever and other severe constitu- 
tional symptoms in addition to the local disturbances already discussed. The 
temperature may for a time reach 104° to 106° (40°-41° C.) ; but the fever is 
seldom continuous for any length of time, being usually interrupted by fre- 
quent and considerable intermissions. There are also a rapid pulse, headache, 
stupor, and other symptoms suggesting typhus or typhoid fever. In fact, the first 
case in which trichinosis was recognized at the autopsy (by Zenker of Dresden) 
had been regarded before death as typhoid. The urine may be albuminous; and, 
in rare instances, nephritis is seen. 

[The blood shows a leucocytosis, with a great relative and absolute increase in 
polymorphonuclear eosinophilic cells. — V.] 

The duration of the disease varies widely. There are mild cases often unrec- 
ognized, which get well after slight symptoms have lasted two or three weeks. 
More pronounced cases occupy six to eight weeks, or even a much longer time. Of 
the more severe cases about one third prove fatal, usually from the fourth to the 
sixth week. Sometimes death is caused by the severity of the constitutional dis- 
turbance, but usually from disabled respiration. Even if the case ends favorably, 
recovery is often very tedious. 

Pathology. — The autopsy reveals little that is characteristic excepting the 
changes in the muscles. There are sometimes the signs of hemorrhagic catarrhal 
inflammation of the small intestine. The spleen is not enlarged. Very often 
the liver is decidedly fatty. What should cause this in trichinosis has not yet 
been determined. The lungs often present islets of lobular pneumonia, or some- 
times even of gangrene. The trichinae are found in the muscles, beginning with 
the fifth week. They can be recognized by the naked eye as little whitish lines. 
We have already named the muscles chiefly infested. Under the microscope we 
see the fibers in which the trichinae lie transformed into a fine granular mass. 
The nuclei of the muscular fibrillse are greatly increased in number in the 
neighborhood of the coiled-up parasite. Finally, the sarcolemma collapses, and 
becomes greatly thickened upon its external surface by a hyperplasia of con- 
nective tissue. The muscles also present many other degenerative changes, such 
as a flaky disintegration, waxy degeneration, and the formation of vacuoles. 
There is furthermore a marked increase of nuclei in the interstitial tissue of the 
muscles. Within the intestines are sometimes to be found, even after several 
weeks' illness, numerous living intestinal trichinae — a fact of importance from a 
therapeutic point of view. 

Diagnosis. — The diagnosis of trichinosis is generally not difficult, since the 
peculiar symptoms of the disease, especially the extensive, painful inflammation 
of the muscles and the oedema, occur in this way in only one other rare disease, 
primary acute polymyositis (q. v.). Trichinosis is distinguished from this partly 
by the peculiar aetiology (affecting several people, the use of raw pork, etc.), and 
partly by the initial gastro-intestinal symptoms. Trichinosis may also be con- 
founded with multiple neuritis and perhaps with acute articular rheumatism, but 
careful observation of the patient will usually make the diagnosis clear. An abso- 



134: 



ACUTE GENERAL INFECTIOUS DISEASES 



lutely certain diagnosis may be arrived at by finding intestinal trichinae in the 
dejections, but, as we have said, this is not an easy matter. 

Treatment. — The trichina may still be alive in pork that has been smoked 
or salted or half -cooked — e. g., many sausages are unsafe. The only possible 
prophylaxis, therefore, as far as the individual is concerned, is to avoid all such 
food. A real protection for the public against the disease is also afforded by 
governmental microscopic inspection of meat, as already established in many 
places. 

When an individual has become infected with trichinae, if it is possible that 
intestinal trichinae still are present, the treatment must always begin with the 
exhibition of purgatives, such as compound infusion of senna, calomel, or castor- 
oil. Since trichinae may be found in the intestines as long as eight weeks after 
the beginning of the first symptoms, we should not neglect local action on the 
intestinal contents even in the later stages of the disease. Of the remedies which 
are calculated to destroy the intestinal trichinae, glycerine, which was first recom- 
mended by Fiedler, seems to be the most efficient. It must be given in rather 
large doses, say a tablespoonful every hour. Other drugs are much less reliable, 
but we will name among them benzine in the total daily dose of one to two 
drachms (grm. 4 to 8) in capsules, and picric acid in pills — the daily dose being 
five to eight grains (grm. 0.3-0.5). 

Treatment is unfortunately almost wholly powerless against the myositic 
symptoms of trichinosis and their sequelae. The muscular pains can be alleviated 
by narcotics, particularly morphine subcutaneously, poultices, and chloroform-oil 
as an embrocation.* Protracted warm baths are excellent. Antipyrine and 
salicylic acid are also said to do good in many cases. 



* Generally one part of chloroform to ten of olive-oil. It is not officinal in Germany, but is weaker 
than the linimentum chloroformi (II. S. P.). — Trans. 



DISEASES OF THE RESPIRATORY ORGANS 



SECTIOX I 

Diseases of the Nose* 

CHAPTEE I 

CORYZA 

{Snuffles. BJrinitis. Cold in the Head) 

etiology. — The well-known symptoms of eoryza depend upon a catarrhal 
inflammation of the nasal mucous membrane. Although this catarrh mar often 
be due to infectious influences, still we can not deny that it is one of those dis- 
eases which may be caused by taking cold. Daily experience teaches us how often 
eoryza follows an evident exposure to cold, such as wetting the feet, but it is of 
course possible that exposure to cold may merely favor infection. TTe may men- 
tion its contagiousness as an argument in favor of its infectious character, and 
this may be illustrated by the fact that i + may be conveyed by handkerchiefs, 
kissing, etc., but an experimental transmission of common eoryza has not yet been 
successful. 

Coryza may also arise from the action of chemical irritants or mechanical 
irritants, such as dust, on the nasal mucous membrane. The iodine coryza, which 
occurs from the internal use of iodine, is especially noteworthy. In this form 
iodine can easily be detected in the nasal secretion. The idiosyncrasy of many 
people to ipecacuanha is also well known, the very smell of it setting up a coryza. 
A severe coryza is the chief symptom, too, in hay fever. f which is probably due 



* Special treatises on the pathology and therapeutics of nasal diseases are to be found in the follow- 
ing works : Michel, " Krankheiten der Nasenhohle." Fraenkel, " Diseases of the Is ose," in " Ziems- 
■sen's Cyclopedia." Stork. " Klinik der Krankheiten des Kehlkopfes, der Nase, und des Eachens." 
Schech, " Krankheiten der Mundhohle, des Eachens, und der Nase." Moldenhauer, " Krankheiten der 
Nasenhohlen." C. Eosenthal. "Die Erkrankungen der Nase und des Kehlkopfes." W. Kiesselbach 
in Penzoldt and Stintzing's " Handbueh der Tkerapie," vol. iii. etc. [Bosworth, " Diseases of the Nose 
and Throat." Burnett, "Diseases of the Ear, Nose, and Throat." Ingals. "Diseases of the Chest, 
Throat, and Nasal Cavities."] 

t The disease called hay fever (catarrJius cestivus) is of frequent occurrence in England and North 
America, although rare with us in Germany. It usually affects men in middle life, less often women. 
Some individuals are peculiarly liable to the disease. For them an attack may be produced merely 
by walking across a meadow or near a grain-field at that season when the grasses are in bloom, i. e.. 
about May to July. As already intimated, it is supposed that the grains of pollen excite the disease, 
being diffused in the air and thus drawn into the nostrils. At any rate, they have repeatedly been 
found in the nasal secretion and also in the tears of affected persons. The symptoms consist in a very 
severe coryza, with burning of the nose and violent sneezing. The erectile tissue of the nose is prob- 
ably acutely swollen. Usually these symptoms are accompanied by a well-marked conjunctivitis with 
oedema of the eyelids. In severer cases there is furthermore a catarrh of the larynx and bronchi. 
There is frequently a tendency to violent attacks of asthma ("hay-asthma"), especially at night (see 
the chapter on bronchial asthma). The treatment consists first in avoiding the cause by change of 

135 



136 DISEASES OF THE RESPIRATORY ORGANS 



to the action of the pollen of certain grasses on the respiratory mucous mem- 
brane. Finally, we must bear in mind that coryza may often be only a symptom 
of some other disease such as measles, syphilis, or glanders, and that severe purulent 
inflammation of the nasal mucous membrane may be excited by the presence of 
the secretion from a gonorrhoeal or blennorrhoeal conjunctivitis. 

The symptoms of coryza are in most of the milder cases of a local nature only. 
The secretion is troublesome ; at first it is scanty and mucous, but later it becomes 
more abundant and watery; and sometimes it is purulent. The nasal passages 
are not infrequently closed from the swelling of the mucous membrane. The 
patient necessarily has to breathe through the mouth, which explains the well- 
known nasal speech. This closure of the nares may give rise to dangerous attacks 
of dyspnoea in children, especially in infants, who have to breathe through the 
nose when sucking at the breast. The sense of smell is always diminished. The 
local sensations of pain and burning are due chiefly to a mild inflammation of the 
skin of the nostrils and upper lip set up by the irritation of the secretion. The 
irritated condition of the inflamed mucous membrane occasions a feeling of 
tickling and itching in the nose, and frequently by a reflex action violent sneez- 
ing. The symptoms are more severe if the cavities adjacent to the nose are 
attacked by catarrh, and if in them accumulations of secretion occur. Marked 
pain in the forehead occurs in catarrh of the frontal sinuses. The sinuses of the 
ethmoid and sphenoid bones, and the antrum of Highmore, may also be impli- 
cated. Much more frequently a severe coryza sets up inflammation in adjacent 
mucous membranes. Thus we find, following coryza, conjunctivitis, affection of 
the ear, sore throat, or laryngitis. In persistent coryza eczema is not infrequently 
excited on the skin of the upper lip, and mention has already been made of the 
fact that coryza may sometimes act as the exciting cause of erysipelas. 

In severe coryza we may sometimes have quite a marked general disturbance, 
and often slight elevations of temperature. The " feverish cold " of children, for 
instance, is well known. 

Treatment. — Special treatment is usually unnecessary, for most cases recover 
of themselves in a few days. It seems doubtful whether the internal use of 
quinine in fresh coryza is of service, as is claimed. With abundant secretion, 
especially in fresh cases, Hager's " coryza remedy " (as an inhalation) is worthy of 
trial; this consists of ten parts each of alcohol and carbolic acid, and five parts 
of ammonia-water. Painting the nasal mucous membrane with a solution of 
cocaine (two to five per cent.) is also greatly praised [but it may lead to the 
formation of the cocaine habit. — K.] When the secretion forms abundant dry 
scabs, an attempt should be made to wash them out by injections of warm fluids, 
such as warm milk. The upper lip and the nostrils should be smeared with 
vaseline or simple ointment to protect the skin from the action of the secre- 
tion. Only in the rare cases of a severe purulent catarrh can energetic local 
treatment of the nasal mucous membrane be necessary. Here we may use douches 
or sprays of astringents like tannin or alum, or let the patient snuff them up, or 
we may apply caustics like nitrate of silver. In children who can not blow the 
nose, it is advisable to cleanse the nose frequently with a small sponge and a one- 
per-cent. solution of boracic acid. 



residence, as by going to the sea-shore. For the nasal catarrh douches are most to "be recommended, 
such as a solution of 1 part of quinine to 500-1,000 parts of water, or a solution of carbolic acid. The 
administration of iodide of potassium might be tried, particularly where there is asthma. 



CHRONIC RHINITIS 



137 



CHAPTER II 

CHRONIC RHINITIS 

{Rhinitis chronica hypertrophica et atrophica. Ozcena) 

1. Chronic Hypertrophic Rhinitis. — It is in many cases impossible to deter- 
mine the causes of hypertrophic rhinitis. Sometimes the condition seems to 
develop as a sequel to frequently repeated nasal catarrh, although in this case the 
relation is often reversed — it being the chronic rhinitis which occasions a pre- 
disposition to the frequent acute exacerbations of the catarrh. Certain diatheses 
(anasmia, scrofula) appear to influence the development of the disease. This is 
also true of occupations which expose the individual to dust or smoke, and some- 
times true of malformation of the nose (for instance, deviation of the septum) 
and perhaps also of hereditary predisposition. 

The anatomical changes consist of a slow but progressive swelling and hyper- 
trophy of the mucous membrane. This seems spongy, and of a red or reddish- 
gray color. The greatest change is almost always found over the inferior turbi- 
nated bone, and next to that over the middle turbinated. In advanced cases the 
mucous membrane presents rough, uneven swellings, and even polypi. These 
changes are often visible upon inspection of the nostrils anteriorly, but they may 
escape discovery until a rhinoscopic examination of the posterior choanag is made. 

The disturbance occasioned by chronic hypertrophic rhinitis may be very con- 
siderable. Respiration through the nose is obstructed, the voice becomes nasal, 
the senses of smell and taste are impaired. The nasal secretion is for the most 
part increased, but it may be diminished. Often there is a tendency to nose-bleed. 
Many patients complain also of headache. 

The frequent involvement of neighboring organs is important. This applies 
particularly to the ear. Deafness is caused both by the obstruction of the open- 
ings of the Eustachian tubes, and not infrequently also by extension of the catarrh 
to the lining membrane of the tubes and the middle ear. Very frequently the 
disease is associated with chronic naso-pharyngitis or pharyngitis. The visible 
portion of the nose is not infrequently affected, as shown by redness and swelling 
of its tip. 

A fact of especial interest is that such a diseased state of the nasal mucous 
membrane may give rise to reflex neuroses (Voltolini, Hack, and others). Al- 
though, in our opinion, many of the specialists on the nose go too far in this 
direction, there is no room for doubt that attacks of migraine, vertigo, certain 
varieties of headache, and, above all, many forms of bronchial asthma, may bear 
a close relation to diseases of the nose. We shall revert to this point later on. (See 
especially the chapter on bronchial asthma.) 

The treatment of chronic hypertrophic rhinitis, in order to be successful, de- 
mands complete destruction and removal of the hypertrophic portions by means 
of the galvano-cautery. For particulars, we must refer to the directions of spe- 
cialists. In milder cases, however, benefit may follow the insufflation of a powder 
composed of one part of nitrate of silver to ten or twenty of common starch, or 
applications of lunar caustic may be made. 

2. Simple Chronic Atrophic and Fetid Atrophic Rhinitis. Ozaena Simplex. — 
The disease consists in a slow, progressive atrophy not only of the mucous mem- 
brane with its vessels and glands, but finally also of the bones, and this atrophy 
is not preceded by hypertrophy. Thus the nasal cavities become abnormally 
large. The turbinated bones grow smaller and smaller, so that finally they are 
represented merely by narrow ridges. Furthermore, the scanty purulent secretion 
has a tendency to dry up and form adherent greenish-yellow scabs and crusts, 
which undergo a peculiar putrefactive decomposition and give rise to an unbear- 



13S 



DISEASES OE THE RESPIRATORY ORGAXS 



able stench. We do not yet know what special form of bacterium causes this 
putrefactive decomposition of the secretion. When this very characteristic and 
extremely repulsive stench occurs in the nose, we usually give the affection the 
brief name of ozsena (o£eiv, to stink), but in the other and practically less 
important cases we speak of a simple atrophic rhinitis. The latter may sometimes 
become ozsena. 

Ozsena generally develops in childhood. It usually begins insidiously, but 
in other cases apparently is a sequel of some acute disease, such as measles, etc. 
Anaemia and scrofula deservedly rank as important predisposing causes. Stork 
thinks that ozsena is usually connected with syphilis in the parents. It is also 
worthy of note that patients with ozsena often have from birth a nose with a flat, 
broad bridge, which is perhaps a family trait, favoring the development of the 
disease. 

The subjective symptoms are often not marked. This is partly explained by 
the fact that the patient has usually completely lost his sense of smell, but for 
that very reason the discomfort of his friends may be the greater. The feeling 
of dryness in the nose may prove annoying, and there are often complaints of 
headache and of pressure in the eyes. Inasmuch as the naso-pharynx and the 
posterior pharyngeal wall are almost always implicated in the process, the patient 
often suffers from hacking and a tendency to cough and vomit. Such portions 
of the secretion as are swallowed sometimes give rise to a considerable chronic 
disturbance of the stomach. Upon physical examination we are first struck by 
the unusual breadth of the nostrils. With the rhinoscope the extent of the 
atrophy is still better seen. The mucous membrane is pale or slightly red, and 
covered with dry scabs. Sometimes superficial ulcers are formed. Usually, as we 
have said, the superior portion of the pharyngeal mucous membrane shares in the 
disease. The posterior wall of the pharynx is seen to be atrophied, smooth as if it 
were varnished, and often covered with crusts. The process may involve the soft 
palate, and even the larynx, and not infrequently the disease is associated with 
inflammation of the middle ear. 

It should be added that the true ozsena must not be confounded with other 
processes which likewise give rise to a foul smell from the nose. Tuberculous 
disease of the nasal mucous membrane and nasal bones is not rare, particularly in 
" scrofulous " children (Demme) ; nor should we forget the syphilitic affections of 
the nose, tertiary and hereditary syphilis. 

Treatment. — An alleviation of ozsena can be accomplished only by the aid of 
local applications as prescribed by specialists. Even then the treatment is a 
prolonged one, and demands much patience on the part of both patient and 
physician. A complete cure of atrophic rhinitis is impossible. Besides local 
applications, we must also bear in mind the necessity of constitutional treatment. 

The object of local treatment is to remove the secretion in order to get rid of 
the bad odor. ^NTasal douches, with disinfectant solutions such as permanganate of 
potassium (1-3,000) or carbolic or corrosive sublimate, are here most useful. The 
solution is carefully injected into the nose, or the fluid is allowed to run gently 
into one nostril from an irrigator while the patient keeps his head bent forward ; 
it then runs through the naso-pharynx and out through the other nostril. The 
patient soon learns to retain the fluid in the pharynx and eject it from the mouth. 
All nasal douches must at first be used with care and under the eye of the physi- 
cian. The fluid should be injected at the lowest pressure possible, so that none of 
it may enter the adjacent cavities or the Eustachian tube. Furthermore, all solu- 
tions used as a douche must be lukewarm — 90° to 95° (25°-28° R.). Besides 
the regular use of douches, painting and the insufflation of powders, such as 
boracic acid, aceto-tartrate of aluminum, etc., are sometimes employed. The in- 
sertion of tampons of dry absorbent cotton is to be recommended; under their use 



NOSE-BLEED 



139 



the secretion dries less easily and the odor is diminished.- These tampons should be 
changed daily. It is advantageous to medicate the tampons with a one-per-cent. 
solution of creoline or with Peruvian balsam or some similar drug. Tincture of 
iodine is also recommended. Of late many attempts have been made to treat 
chronic nasal catarrh by the galvano-cautery. With regard to the details of this 
as well as of other methods, we must refer to special treatises on the subject. 



CHAPTEE III 

NOSE-BLEED 

{Epistaxis) 

Although in many cases nose-bleed is only a symptom, still we are justified 
in a short description of it, partly because frequently repeated nose-bleeds often 
first call our attention to some other existing disease, and partly because the 
treatment is of practical importance. 

Many persons are subject to habitual nose-bleed, which comes on either from 
slight causes, from violently blowing the nose, from physical exertion, from over- 
heating, or even without any special cause. This habitual nose-bleed is sometimes, 
but by no means always, the sign of a general hemorrhagic diathesis, which is 
hereditary in many families. (See the chapter on haemophilia.) In other cases 
the nose-bleed is the result of some chronic disease. It occurs especially in leu- 
kaemia, in disease of the heart, in contracted kidney, and as a symptom of the 
so-called hemorrhagic diseases, such as scurvy, purpura hemorrhagica, etc. Final- 
ly, diseases of the nose itself may give rise to haemorrhage. The periodic occur- 
rence of nose-bleed in young girls as a form of so-called " vicarious menstrua- 
tion" has often been described, but we must always be very guarded in admit- 
ting it as a fact. Nose-bleed sometimes occurs at the beginning of many infec- 
tious diseases, especially typhoid and scarlet fevers, etc. We may add that the 
point of haemorrhage is very frequently at the anterior lower end of the cartilag- 
inous septum (Kiesselbach). 

In many cases nose-bleed is a very transitory symptom, wholly without danger, 
and in one sense it may even be advantageous. When there is headache, or a 
feeling of fullness in the head, there is often relief after an epistaxis. Nose- 
bleed is dangerous, however, when it takes place in those who are already weak 
and anaemic, or when it is so persistent and abundant as to cause a marked gen- 
eral anaemia. The latter is recognized by the pallor of the face, by the appearance 
of general weakness, by vertigo, tinnitus, and a weakened pulse. In such cases the 
physician's interference is always necessary. In every case of nose-bleed it is 
important to examine the posterior wall of the pharynx in order to see whether 
the blood is not flowing backward from the posterior nares. The haemorrhage is 
often thought to stop when no more blood comes from the nostrils, and yet the 
blood keeps flowing posteriorly. 

In every severe nose-bleed rest is the chief thing to be enjoined, and the patient 
must be told to avoid unnecessarily blowing, wiping, or drying the nose. By 
quietly and persistently closing the nostrils with a handkerchief a thrombus is 
often formed without any further medication, and the bleeding stops. The appli- 
cation of cold water (iced water), in which a little vinegar may be put, is a good 
thing. If the bleeding does not stop, we may next try a tampon of common 
absorbent cotton or styptic cotton in the nostril from which the blood comes. If 
this does not succeed, the posterior nares must be plugged by means of a " Bel- 



140 DISEASES OF THE BESPIRATORY ORGANS 

locq's canula." In case of emergency we may use an elastic catheter, which is 
passed through the inferior meatus into the pharynx and out by the mouth. The 
tampon is fastened to the catheter and brought up into the posterior nares by 
drawing the catheter back through the nose. Internal remedies to check the 
flow of blood are very uncertain in their action. 



SECTION II 
Diseases of the Larynx 

CHAPTER I 

ACUTE LARYNGEAL CATARRH 

(Acute Laryngitis) 

-ZEtiology. — Taking cold plays a prominent part in the popular cetiology of 
acute laryngeal catarrh. Its influence can not be wholly denied, although the 
more intimate relation between taking cold and the origin of a catarrh is still 
unknown. The disposition to laryngitis differs very much in different people, 
so that some take a catarrh much more easily and more frequently than others. 
Besides cold, direct irritants which attack the laryngeal mucous membrane often 
set up a laryngitis; among these are in particular the inhalation of smoke and 
of noxious gases and vapors. Many laryngeal catarrhs, too, arise from excessive 
speaking, shouting, or singing, particularly if other injurious influences act on the 
larynx at the same time. Finally, laryngitis may appear as a complication or as 
a secondary affection, in other diseases, especially in measles, less frequently in 
typhoid, scarlet fever, and erysipelas. Catarrh of the larynx is very often com- 
bined with catarrh of the nose, the pharynx, and the larger bronchi. 

Symptomatology. — Although the symptoms of laryngitis usually make the 
diagnosis easy and certain, yet an accurate understanding of the extent and 
intensity of the catarrh can be obtained only by a laryngoscopic examination,* 
which therefore should be employed in every severe case. The laryngeal mirror 
shows a decided reddening and swelling of the mucous membrane, varying with 
the intensity of the catarrh, and most marked on the true and false vocal cords 
and between the arytenoid cartilages. We often see small collections of mucus 
here and there on the membrane. In individual cases different parts of the 
larynx are especially affected. In intense inflammations superficial erosions are 
often met with, especially on the vocal cords. In other cases the mucous mem- 
brane shows a grayish-white coloring in some places, due to a thickening of the 
epithelium. Small hsemorrhages in the mucous membrane are also occasionally 
seen. Very often we see on phonation an incomplete closure of the glottis, so 



* More extensive observations on laryngoscopy and on many details of the pathology of laryngeal 
diseases, which have been carefully investigated by specialists and which can not be mentioned here, 
are to be found in the following works : Turck, " Klinik der Krankheiten des Kehlkopfes," 1866. 
Semeleder, " Laryngoskopie," 1863. Tobold, " Laryngoskopie," 1874. Stork, "Klinik der Krank- 
heiten des Kehlkopfes, der Nase, u. des Kachens," 1880. Mackenzie, " Diseases of the Throat and 
Nose," 1880. B. Fraenkel and v. Ziemssen, " Diseases of the Larynx," in Ziemssen's " Cyclopaedia." 
Gottstein, "Krankheiten des Kehlkopfes," third edition, 1890. Schrotter, " Vorlesungen uber die 
Krankheiten des Kehlkopfes." [See also the treatises of Bosworth, Burnett, and Ingals referred to 
on page 131.] 



ACUTE LARYNGEAL CATARRH 



141 



that a little oval space is left between the vocal cords. This slight " catarrhal 
paresis of the vocal cords " is probably of muscular origin, and depends chiefly 
upon an affection of the thyro-arytsenoid muscles. 

Of the other symptoms of laryngeal catarrh, hoarseness is particularly to be 
mentioned, for in many cases the diagnosis of laryngitis may be made from this 
alone. It is either due directly to the anatomical changes of the cords, or to the 
paresis just mentioned. The degree of hoarseness is of course very different ii, 
different cases, and varies from a simple "roughening" or "deadening" of the 
voice to a complete loss of voice (aphonia). 

The cough in laryngitis may be very severe, and is often recognizable by its 
harsh, hoarse ring as a " laryngeal cough." It is usually dry at first, and later on 
it is associated with a scanty muco-purulent expectoration, which is sometimes 
tinged with blood. 

Pain in the larynx is generally only moderate. The subjective symptoms con- 
sist chiefly of a disagreeable feeling of itching, burning, and dryness in the throat. 
After prolonged speaking, however, the pain in the larynx may sometimes be quite 
severe. External pressure on the larynx is often somewhat painful. Difficulty 
in swallowing, when it occurs, is due usually to an accompanying pharyngitis, 
but it may also be dependent upon an affection of the epiglottis and the arytenoid 
cartilages. 

The general health is affected in very different degrees. Many patients feel 
quite well except for the hoarseness, while others are affected with considerable 
debility, mild headache, and even at times slight febrile disturbances. Of late 
years we have frequently seen cases of primary acute laryngitis, with great 
hoarseness and marked catarrhal inflammation of the upper part of the larynx, 
especially of the vocal cords. These cases begin with high fever (over 104° 
[40° C.]) and quite severe general symptoms, and make a complete recovery in 
a week or two. They apparently have an infectious origin, and are perhaps con : 
nected with influenza. 

Dyspnoea is not present in the common laryngitis of adults, even if there is 
decided swelling of the false vocal cords or of the ary-epiglottic folds. There 
is, however, a severe form of acute laryngitis, the so-called laryngitis hypoglot- 
tica acuta gravis (chorditis vocalis inferior), affecting not only children, but 
adults, in which well-marked symptoms of suffocation may be present. In this 
form there is an acute, very well-marked swelling of the mucous membrane in the 
inferior, sub-chordal, laryngeal space, which leads to a stenosis. The rare 
cases of phlegmonous inflammation of the larynx may also cause considerable 
stenosis and dyspnoea. 

In children, however, on account of the greater narrowness of the child's 
larynx, symptoms of stenosis are not rare even in the milder forms of laryngitis, 
and therefore they have led to the establishment of a special disease, the so-called 
false croup. 

The false croup (laryngitis stridula) of children usually follows a slight 
coryza. A harsh, hollow, ringing cough comes on, almost always suddenly and 
usually at night, by which the child is awakened out of sleep. The paroxysms of 
coughing are broken by long-drawn, noisy inspirations. The child is anxious and 
restless, the respiration is labored. The accessory muscles of respiration are 
brought into action, but the deep inspiratory retraction of the lower intercostal 
spaces and the epigastrium shows how imperfectly the air enters the lungs. The 
pulse is small and rapid. The attack lasts several hours, when the cough gradually 
becomes looser and the breathing easier. Finally the child falls asleep and usually 
wakes the next morning quite lively and playful, a slight cough being the only 
relic of the terrifying events of the night before. The next night the same severe 
attack may be repeated, and perhaps for two or three nights more. After that 



142 



DISEASES OF THE EESPIEATOEY OEGANS 



there remains, as a rule, nothing but a slight catarrh, which completely disappears 
in a week or two. The anatomical cause of false croup is acute laryngitis with 
marked swelling of the mucous membrane on and below the vocal cords. In the 
narrow space of the child's larynx this speedily causes marked stenosis, and the 
individual attacks are probably excited by the accumulation and drying of the 
secretion during the night. There is never any true croupous-diphtheritic change 
to be seen either in the pharynx or the larynx. It is remarkable that many chil- 
dren, and sometimes several children of the same family, have a specially marked 
predisposition to false croup. The statement, therefore, that a child has had the 
croup several times almost always means that it has had this form of false croup 
just described. 

Acute laryngitis lasts only a few days in mild cases, and a week or more in 
severe cases. With improper care and unreasonable conduct on the patient's part 
an acute catarrh may run into the chronic form. We hardly ever see a fatal re- 
sult in adults, even in the severe form, and in children false croup very rarely has 
an unfavorable termination unless the child is extremely weak or rachitic. 

The treatment of acute laryngitis requires that especial attention be paid to 
the removal of all injurious influences. In every severe laryngitis the patient 
should stay in his room, and children are better off in bed. The patient should 
talk as little as possible. In all severe cases smoking, too, is to be forbidden. It 
is a good plan to furnish plenty of warm drink. Hot milk, mixed with Seltzer 
or Ems water, is readily taken by most patients. If there is a steam atomizer at 
our disposal, we may let the patient inhale simple steam, or a one- or two-per-cent. 
solution of common salt. Inhalations of astringents are usually unnecessary. 
The patient may also breathe steam without any special apparatus. When there 
is marked irritation from coughing we may give a little morphine. With more 
marked local symptoms, especially if there is much pain on swallowing, from 
swelling of the epiglottis and the mucous membrane over the arytenoid cartilages, 
the patient may suck pieces of ice slowly. In severe cases of acute laryngitis, with 
evident symptoms of stenosis, ice must be energetically used as an internal and an 
external application. Sometimes, too, a few leeches applied in the region of the 
larynx afford distinct relief. Among external applications a mustard plaster over 
the front of the neck is to be recommended when there are marked local symp- 
toms. Cold, wet compresses about the neck are also of advantage in all cases. 

In the false croup of children we should "use, as a rule, the same treatment as 
has just been described. The child should take plenty of warm drink, inhale 
warm steam or salt solution, and a mustard paste or hot poultices should be applied 
to the neck. An ice-bag on the neck is sometimes useful. We should be rather 
cautious with regard to the favorite treatment with emetics, such as ipecac and 
sulphate of copper, although it can not be denied that they sometimes work very 
well in severe dyspnoea. 

These means are entirely sufficient for the treatment of acute laryngitis. It is 
only exceptionally that we find ourselves led to employ in acute laryngeal catarrh 
an energetic local treatment of the laryngeal mucous membrane, like painting 
with a 1-15 solution of nitrate of silver. 

We must bear in mind that a rational hardening process is of distinct prophy- 
lactic value in persons, especially in children, with a recognized tendency to 
laryngitis, sore throat, etc. The best method is to bathe the neck and chest with 
cold water regularly morning and night. 

[A mild emetic can do no possible harm in false croup, and very often cuts the 
attack short. The application of a sponge, moistened with water as hot as the 
child will bear, to the region of the larynx deserves mention.] 



CHRONIC LARYNGITIS 



CHAPTER II 

CHRONIC LARYNGITIS 

( Chronic Laryngeal Catarrh) 

iEtiology. — Chronic laryngitis develops from an acute catarrh, or comes on 
gradually from the action of injurious influences on the larynx (see the preceding 
chapter). Chronic laryngitis, therefore, is in many cases due to the occupation, 
and is seen especially in singers, public speakers, criers, inn-keepers, workmen ex- 
posed to dust, etc. It is very frequent in drunkards, and in such cases it is 
almost always associated with a chronic pharyngitis. It is not probably true 
that, as frequently stated, too long a uvula may set up laryngitis by irritation of 
the entrance to the larynx. 

Symptomatology. — A laryngoscopic examination is very desirable in acute 
laryngeal catarrh, but it is the physician's absolute duty to make one in 
chronic laryngitis, for only too frequently a persistent hoarseness is referred 
to a " simple " catarrh when the laryngoscope gives quite another cause for it, 
such as paralysis of the vocal cords or new growths. Furthermore, we must al- 
ways remember that a chronic laryngitis may be a complication of tuberculosis, 
syphilis, or chronic nephritis. We should never omit a careful examination of 
the rest of the body as well as the larynx. 

The laryngoscopic appearance in chronic catarrh may be so like that in an 
acute catarrh that we can not distinguish between them without the history 
obtained from the patient. The redness of the mucous membrane, however, is 
usually less intense, and the vocal cords have more of a dirty grayish-red appear- 
ance. In most cases there is also considerable swelling of the mucous membrane 
as well as redness. Much more rarely we find atrophic conditions, resembling 
those of ozsena and sometimes associated with it. Quite frequently in persistent 
catarrhs a thickening of particular parts of the mucous membrane is developed, 
especially of the folds between the arytenoid cartilages. This swelling is of 
practical importance, because it furnishes a mechanical hindrance to the closure 
of the arytsenoid cartilages, and in that way contributes to the development of the 
hoarseness. We also find marked thickening of the false vocal cords (especially in 
public speakers and preachers) and of the true vocal cords. Virchow described, 
under the name of 'pachydermia laryngis, a condition of the larynx seen espe- 
cially in drinkers and characterized by a thickening of the epithelium over the 
whole laryngeal mucous membrane. Tiirck has described a peculiar form of 
chronic laryngitis, in which rough prominences are formed in the middle of the 
true vocal cords, under the name of chorditis tuberosa. We not infrequently find 
in chronic catarrh superficial erosions, especially on the vocal cords. We never 
see actual ulceration in simple laryngitis. We also very often see a disturbance 
of motion of one or both vocal cords, especially incomplete closure, due some- 
times to muscular paresis and sometimes to mechanical conditions. 

The other symptoms of chronic laryngitis are hoarseness, cough, and abnormal 
sensations in the larynx. The hoarseness is of every degree, from mere rough- 
ness, frequent " cracking " of the voice, to almost complete aphonia. The cough 
is ringing, hoarse, deep, and rough. The expectoration is scanty, usually simply 
mucous, but sometimes a little bloody. The subjective sensations in the larynx 
are a feeling of burning and itching, and of dryness and tickling. They usually 
increase after any protracted use of the voice. 

We must also mention as a peculiar and very rare but practically important- 
form of chronic laryngitis the ehorditis vocalis inferior hypertrophica (Ger- 
hardt), or laryngitis hypoglottica chronica hypertrophica (Ziemssen). In this 
form there is a very gradual hypertrophy, and finally a contraction of the mucous 



144 



DISEASES OF THE RESPIRATORY ORGANS 



and especially the submucous connective tissue in the inferior laryngeal space. 
More rarely the same changes are seen in the upper part of the larynx. The spe- 
cial symptom of the disease, besides a chronic hoarseness, is the appearance of a 
gradually increasing stenosis of the larynx. The respiration is always labored, 
the inspiration noisy and protracted. In many cases there are at times such 
attacks of suffocation that life can be prolonged only by tracheotomy. The diag- 
nosis can be made only by the aid of the laryngoscope. We see beneath the 
glottis a little fissure surrounded by the thick and swollen mucous membrane of 
the laryngeal walls. 

The nature of this affection is not yet fully explained. It often seems to be 
a simple chronic hypertrophic inflammation, but in other case Schrotter considers 
it the same bacillary disease of the mucous membranes which is known as rhino- 
scleroma when it occurs in the nose. 

The treatment of chronic laryngeal catarrh is always a tedious and laborious 
task, the success of which depends in great measure upon the good will and 
energy of the patient. In the first place, then, we should endeavor to remove as 
far as possible those injurious influences which have excited and kept up the 
catarrh. It is often easier to give good advice here than to follow it. Neverthe- 
less, it is the duty of the physician to impress upon the patient the urgent neces- 
sity of taking care of the larynx, and to forbid as far as possible all protracted 
speaking, singing, staying in smoke or dust, smoking, and the use of alcohol. 

Local treatment takes the second place. Among the most useful means to 
employ are sprays of astringent solutions, such as a one-per-cent. solution of 
either tannin or alum. If there is much secretion of mucus, turpentine inhala- 
tions are advisable. When there is great irritability of the larynx, the patient 
may also inhale vaporized narcotics, a mixture of fifty parts of cherry-laurel water 
with a thousand parts of water, or a four-per-cent. solution of bromide of potas- 
sium. The inhalations should be used two or three times a day, and last about five 
minutes each time. Direct applications to the larynx are much more effective than 
inhalations, but these can be employed only by the aid of a laryngeal mirror. 
Of these we use, first of all, nitrate of silver, at first in a weak solution (one to 
fifty) ; later in a more concentrated form (one to ten, or even one to five). These 
applications are made every two or three days. Besides nitrate of silver, the 
larynx may also be painted with pure tincture of iodine, or with iodine and 
glycerine (iodine, 4 parts, iodide of potassium, 6 parts, and glycerine, 500 parts), 
or with concentrated solutions of alum or tannin. 

Water-cures are also often prescribed in chronic catarrh of the larynx. These 
are of advantage from the greater care which the patient takes, and from the 
good air, the catarrh improves. Empirically, we prescribe, especially for " full- 
blooded " patients, the cold sulphur springs, such as Nenndorf, Eilsen, or Weil- 
bach, or the sulphate of sodium waters, such as Carlsbad and Marienbad, while 
we send those of delicate constitutions to Ems, Salzbrunn, Salzungen, Reichen- 
hall, etc. 

The treatment of laryngitis hypertrophica, when it leads to stenosis, must be 
mechanical. Schrotter, in particular, has devised several methods of dilating 
the stenosis gradually by the introduction of bougies and harder dilators. The 
details of this treatment are to be found in the later special works referred to 
above. 



LARYNGEAL PERICHONDRITIS 



U5 



CHAPTER III 
LARYNGEAL PERICHONDRITIS 

^Etiology and Pathological Anatomy. — The inflammation of the perichon- 
drium of the laryngeal cartilages is in very rare cases apparently a primary 
disease. It is much more frequently secondary to other laryngeal affections, 
especially tuberculosis and syphilis of the larynx. Furthermore, it develops 
secondarily in severe acute diseases, most frequently in typhoid fever, more 
rarely in small-pox, diphtheria, etc. Superficial ulcerative processes in the mu- 
cous membrane often precede the perichondritis in these cases, and the participa- 
tion of the perichondrium in the inflammation arises from their gradual deep- 
ening. Anatomically, we have to do as a rule with a purulent inflammation, 
which usually leads to the formation of circumscribed abscesses. Most laryn- 
geal abscesses have their origin in the perichondrium.* The perichondrium is 
in part destroyed by the abscess and in part elevated from the cartilage. The 
cartilage then becomes necrotic, breaks in pieces, and is expelled in small particles 
or in masses. 

Perichondritis occurs most frequently in the cricoid and arytenoid cartilages, 
much more rarely on the internal or external surface of the thyroid cartilage. 
Hence we distinguish an internal and an external perichondritis. A perichon- 
dritis of the epiglottis has also been repeatedly observed. 

Symptomatology. — In the rare cases of primary perichondritis, marked laryn- 
geal symptoms are speedily developed in a person previously healthy. These 
symptoms are pain and tenderness on pressure over the larynx, hoarseness, and 
cough; and to them are usually soon added the signs of a dangerous stenosis of 
the larynx. In secondary cases, which occur almost always in patients who are 
already seriously ill, the symptoms of stenosis are often the first to point to a 
severe disease of the larynx. On laryngoscopic examination, besides the general 
redness and swelling in particular places, we can sometimes recognize a circum- 
scribed prominence of the mucous membrane caused by the abscess. If the abscess 
be already broken we can see the abscess cavity and sometimes the cartilage lying 
free within it. In most cases we find a considerable collateral oedema of the sur- 
rounding mucous membrane, which oedema frequently has a greater share in the 
production of stenosis than has the primary affection itself. The dreaded oedema 
of the glottis (oedema of the ary-epiglottic ligament) in typhoid, tuberculosis of 
the larynx, etc., is usually due to perichondritis of the cricoid or arytsenoid car- 
tilages. Finally, we can see with the laryngoscope, especially in perichondritis 
arytaenoidea, a considerable disturbance of motion of the affected arytsenoid 
cartilage, and also of the vocal cords. 

Laryngeal perichondritis terminates fatally in a great number of cases from 
the development of stenosis. In thyroid perichondritis the pus may sometimes 
gravitate, causing a severe purulent inflammation of the mediastinum. In other 
cases the most threatening symptoms may be averted for a time, but the primary 
disease, such as tuberculosis, finally comes to an unfavorable termination. In the 
rare cases in which recovery occurs after primary perichondritis or after the 
termination of the primary disease, such as typhoid, this recovery is often incom- 
plete, since a chronic stenosis of the larynx remains from the ensuing cicatricial 
contractions. 

The diagnosis is usually obscure during the first period of severe symptoms of 
stenosis, since it is difficult to make a laryngoscopic examination, and it is also 
not always easy to determine the condition. We are usually justified, however, 



* True submucous abscesses, the so-called phlegmonous laryngitis, occur only in very rare cases. 
10 



146 DISEASES OF THE RESPIRATORY ORGANS 



in making the diagnosis, if in those diseases which we have mentioned, in which 
we know by experience that a perichondritis quite frequently occurs, the danger 
of suffocation arises in addition to the other laryngeal symptoms. It is of prac- 
tical importance to recognize stenosis of the larynx with certainty, for it demands 
speedy therapeutic interference. 

Treatment. — In the beginning of the affection we may try to reduce the in- 
flammation by the internal and external application of ice or by leeches. The 
pain may be alleviated by injections of morphine or painting with cocaine. If 
stenosis of the larynx occurs, surgical interference is usually necessary, for only in 
very rare cases do we see the abscess open of itself with a subsidence of the dan- 
gerous symptoms. In the majority of cases the patient can be saved from 
suffocation only by the timely performance of tracheotomy or laryngotomy. The 
laryngeal abscess has been repeatedly opened internally by laryngologists with 
favorable results. If a chronic stenosis of the larynx remains after a favorable 
termination of the disease, either the patient must wear a tracheal canula all his 
life, or the attempt may be made to dilate the stenosis gradually by the methods 
referred to in the preceding chapter. 



CHAPTER IV 
(EDEMA OF THE GLOTTIS 

The practical importance of the subject demands a brief special description of 
loedema of the glottis, by which we mean oedema of the entrance of the lar- 
ynx, especially of the ary-epiglottic ligaments. We have already learned to 
recognize laryngeal perichondritis as one of its most frequent causes. In less 
deeply seated inflammations in the larynx and its neighborhood, however, oedema 
of the glottis may sometimes develop as a dangerous complication, especially in 
cases of laryngitis occurring in the course of severe acute diseases, such as typhoid, 
small-pox, or erysipelas, or in inflammations of the larynx arising from severe 
mechanical or chemical irritation, as from hot steam or corrosive substances, or 
from wounds of the larynx, or, finally, from foreign bodies in the larynx. The col- 
lateral oedema in angina Ludovici, in intense inflammations of the parotid gland, 
or the tonsils, etc., may in rare cases extend to the ary-epiglottic ligaments. 
Finally, oedema of the glottis occurs in rare cases as a complication of general 
oedema of the body, as a result of Bright's disease, disease of the heart, emphysema 
of the lungs, etc. (Edema of the glottis, without extensive oedema elsewhere, 
has been repeatedly observed to come on quite suddenly, especially in acute and 
chronic nephritis. 

The chief symptom of oedema of the glottis is dyspnoea, which comes on as 
a result of the stenosis of the entrance of the larynx, ancj is sometimes extreme. 
At first this is chiefly on inspiration, but it soon comes on with, expiration also. 
Respiration, especially inspiration, is accompanied by a loud laryngeal stridor. 
As a result of the incomplete entrance of the air, the efforts at inspiration cause 
depression of the root of the neck, the epigastrium, and the sides of the thorax. 
We see with the laryngoscope, if the examination be successful, an ©edematous 
swelling of the ary-epiglottic ligaments, and often a swelling of the epiglottis and 
the false vocal cords. Sometimes we succeed in feeling the swollen parts with the 
finger. 

If the dyspnoea reaches a degree which threatens life, an operation is the only 
thing which can afford relief. Laryngologists attempt to reduce the swelling 



TUBEKCULOSIS OF THE LAKYNX 



147 



by long incisions in the (edematous parts. If this does not succeed, tracheotomy 
must be performed. If the immediate danger to life is thus averted, further 
treatment should be directed to the disease which has given rise to the oedema. 



CHAPTEE V 

TUBERCULOSIS OF THE LARYNX 

{Laryngeal Phthisis. Consumption of the Larynx) 

iEtiology. — Since tuberculosis of the larynx is in most cases combined with 
tuberculosis of other organs, especially of the lungs, we must refer to the descrip- 
tion of tuberculosis of the lungs for the general setiology and pathology of the 
disease. A particular description of the special appearances in laryngeal tuber- 
culosis is, however, justifiable, because tuberculosis may at times begin in the 
larynx and may remain isolated there, at least for a time ; and, furthermore, in 
many cases of laryngeal tuberculosis, which are evidently combined with pulmo- 
nary tuberculosis, the laryngeal symptoms are predominant in the clinical picture 
of the disease. Many physicians have, wrongly as we think, disputed the fact 
that tuberculosis can begin in the larynx. Clinical experience not infrequently 
teaches us that men, who have been apparently in good health, are attacked 
with hoarseness, the disease being at first thought to be a common laryngitis, 
but at last, by its course, proving to be tuberculosis. In spite of the most 
careful examination, there are not to be found at first the slightest physical 
signs of disease in the lungs, and not till later do the manifest signs of a pul- 
monary tuberculosis succeed the symptoms of a laryngeal affection. In such cases 
it seems to us an affectation to claim that there is a primary pulmonary tubercu- 
losis which could not be made out at first. Everything is much more in favor of 
the opinion that the tubercular poison, the tubercle bacilli, may sometimes, if not 
frequently, first fix upon the larynx, excite the first symptoms of tuberculosis 
there, and then attack the lungs. 

In the great majority of cases of laryngeal tuberculosis the symptoms are de- 
veloped, of course, secondarily in the course of chronic pulmonary phthisis. We 
shall see that in most cases the disease of the larynx is to be considered as the 
result of an infection of the mucous membrane of the larynx by the tuberculous 
sputum which passes over it. More rarely the infectious material seems to reach 
the larynx by way of the lymph- or blood-vessels. In favor of this theory we may 
mention that men of great experience (Schrotter and others) have stated that, 
where the laryngeal trouble was particularly marked on one side, that side was 
very often affected which corresponded to the affected lung. In about one fourth 
of all cases of pulmonary tuberculosis this complication occurs, if we include all 
the mild laryngeal cases. Marked and extensive tuberculosis of the larynx is 
much rarer, however. 

Pathological Anatomy. — Tuberculosis of the laryngeal mucous membrane be- 
gins, like tuberculosis of other mucous membranes, with the formation of small 
subepithelial nodules, which soon become cheesy, break down, and form small 
ulcers. In the further course of the disease there is very often a more extensive 
tubercular infiltration, which gives rise on the one hand to irregular thickening 
of the mucous membrane, and on the other to deep ulceration. The tubercular 
infiltration is most frequently situated in the interarytsenoid space, on the false or 
true cords (at first on one side), and on the epiglottis. The tuberculous ulceration 
usually develops later in one of these places. The ulceration may extend from 



148 DISEASES OF THE RESPIRATORY ORGANS 



the epiglottis to the neighboring parts of the tongue. In severe cases we often 
find a marked collateral oedema in the surrounding parts accompanying the in- 
flammation, and sometimes the tubercular perichondritis which has already been 
described. 

The rest of the laryngeal mucous membrane (especially the vocal cords) not 
involved in the specific tubercular process is usually the seat of a simple catarrh. 

Clinical Symptoms. — In the beginning of tuberculosis of the larynx the laryn- 
goscope usually shows nothing but the appearances of a simple catarrh, since the 
primary miliary nodules of tuberculosis are usually hard to make out. If the 
catarrhal symptoms be only on one side, we should always suspect tuberculosis. 
In the later stages, however, most of the special details of the destructive tuber- 
cular process, described above (ulcers, infiltration, etc.), can be very satisfacto- 
rily made out with the laryngoscope. The infiltration and ulcers are either chiefly 
on one or on both vocal cords or on the posterior wall of the larynx, or mainly in 
the neighborhood of one arytenoid cartilage, or the whole epiglottis is irregularly 
ulcerated on its edge. Single tubercular nodules are often plainly to be seen. 
In severe cases almost the whole upper portion of the larynx appears like an ulcer- 
ated surface covered with mucus. In laryngeal tuberculosis, however, the soft 
palate usually looks very pale and ansemic. The redness and swelling of the 
affected parts are more distinct in the living subject than in the cadaver; but 
the autopsy often shows a far greater extension of the tubercular disease than we 
can determine by the laryngoscope. 

The other clinical symptoms of tuberculosis of the larynx vary very much with 
the extent and intensity of the process. Sometimes they consist merely in mod- 
erate roughness and hoarseness of the voice, but in other cases they increase to the 
most painful condition which is ever seen in any variety of tuberculosis. This 
is especially apt to be the case if the ulceration involves the epiglottis and the 
arytenoid cartilages. Swallowing is then extremely painful, so that the nutri- 
tion is very often impaired, and painful attacks of coughing frequently occur. A 
practiced ear can often distinguish at once the hoarse sound of a " laryngeal 
cough" from the ordinary pulmonary cough. If severe ulcerations attack the 
vocal cords, and their free mobility is affected to a marked degree, the hoarseness 
increases, and finally reaches a complete aphonia. Death finally occurs from 
general inanition, or, exceptionally, from oedema of the glottis. 

The diagnosis of tuberculosis of the larynx is not difficult if pulmonary 
phthisis is already known to be present. When attention has been called to it 
from the onset of hoarseness or from some disturbance in swallowing, we recog- 
nize the character and seat of the changes by the aid of the laryngoscope. The 
diagnosis, however, may present much difficulty in cases where we are not sure 
that an affection of the lungs co-exists. As has been said, the symptoms at first 
are not unlike those of a simple catarrh, and the suspicion of the existence of 
tuberculosis is first aroused from the stubbornness of the disease, the condition 
of the patient, the knowledge of some inherited taint, the onset of fever, and the 
remarkable anaemia and emaciation. With the changes in the larynx which have 
been described, without evidence of pulmonary tuberculosis, the distinction be- 
tween tuberculosis and syphilis may be very difficult. In syphilis of the larynx, 
however, we find that co-existing changes in the pharynx are much commoner 
than in tuberculosis, and the cicatricial formation which is usually visible fur- 
nishes, besides, a very characteristic evidence of syphilis. The diagnosis of tuber- 
culosis of the larynx, however, is made perfectly certain in all doubtful cases by 
the discovery of tubercle bacilli in the patient's expectoration or in the secretion 
from the ulcer, which often can be easily obtained by the aid of a fine laryngeal 
brush. In regard to the laryngoscopic appearances, we may also say that a thick- 
ening and infiltration of the epiglottis with a partial ulceration of the same is an 



TUBERCULOSIS OF THE LARYNX 



149 



appearance which is almost exclusively confined to tuberculosis. The same is true 
with regard to a marked projecting infiltration of the inter-arytsenoid region. 
In doubtful cases it may aid the diagnosis to inject tuberculine (see the chapter 
on pulmonary tuberculosis). 

Treatment. — Eor the constitutional treatment of tuberculosis of the larynx the 
reader is referred to the description of pulmonary tuberculosis. We shall here 
discuss merely the local treatment. This is in the milder forms the same as for 
simple laryngeal catarrh. There is no doubt that even genuine tuberculous ulcer- 
ation of the larynx may be healed. Nevertheless permanent cures of this sort 
are exceptional. Of course very much depends upon the co-existing state of the 
lungs. Eor local treatment insufflations of iodoform and iodol were for a time 
strongly recommended, but they are now for the most part abandoned. Cauter- 
izing the tuberculous ulcers with nitrate of silver does more harm than good. 
We sometimes see better results from blowing powdered boracic acid on the ulcers 
or from a twenty-per-cent. solution of menthol in oil. At present lactic acid 
is most recommended — cauterizing the ulcers with a solution of increasing 
strength (twenty to eighty per cent.), at first daily, and later, after the ulcers 
have been cleaned off, less frequently. 

If we were to give a general estimate of the local treatment of laryngeal tuber- 
culosis we should have to admit that its success has not been great. We do not 
deny that skill and perseverance may be of much service, but only too often 
do we become discouraged by the failure of the most careful local treatment, 
and in many cases cauterization of the larynx is only a useless distress to the 
patient. 

With incipient disease there may be considerable improvement and even 
recovery without any local treatment if the larynx be spared any exertion and 
given complete rest and if, at the same time, careful general treatment be insti- 
tuted. The most we need to use is the atomizer or nebulizer with simple salt solu- 
tion, alkaline waters, etc. We have also found inhalations of a weak carbolic solu- 
tion, and especially of vapor of Peruvian balsam, of service. In advanced cases, 
vhere pronounced pulmonary tuberculosis co-exists, we must content ourselves 
with a purely palliative treatment. The constant use of cracked ice, and especially 
a lavish employment of narcotics, are of most service in relieving the pain and the 
difficulty in swallowing. Subcutaneous injections of morphine a quarter of an 
hour before a meal often afford great relief. We have seen very good results 
from cocaine. If we paint the ulcerated mucous membrane at the entrance of 
the larynx with a ten- or twenty-per-cent. solution of cocaine, in a few minutes 
such an anaesthesia of the affected parts ensues that swallowing may take place 
without any pain. The following formula may be used : 

3^ Cocaime muriatis gr. xv-xxx, gramme 1.0-2.0; 

Alcohol 3ss " 2.0; 

AquaB destillatse 3ij " 8.0. M. 

Unfortunately the action of cocaine is very transitory, so that the painting 
must be frequently repeated. With a severe laryngeal cough and irritation relief 
may also be obtained by inhalations of a two- to three-per-cent. solution of 
bromide of potassium or a three- to ten-per-cent. solution of bitter-almond water. 

If a pronounced stenosis of the larynx develop, tracheotomy is indicated. 
Many recent observations seem to show that tracheotomy may also be of service 
in marked laryngeal tuberculosis. When the laryngeal respiration is shut off 
the tubercular lesions seem to improve faster. 

In cases of pronounced but comparatively limited laryngeal tuberculosis, with- 
out much implication of the lungs, the attempt has been made, after a preliminary 
laryngotomy, to remove the diseased parts as completely as possible by surgical 



150 



DISEASES OE THE RESPIRATORY ORGANS 



means. We still lack extended practical experience in this matter, but further 
trials of the operation seem very desirable. 



CHAPTER VI 
PARALYSES OF THE LARYNGEAL MUSCLES 

1. Paralyses in the Distribution of the Superior Laryngeal Nerve. — The su- 
perior laryngeal nerve, arising from the vagus, is the sensory nerve for the mucous 
membrane of the upper portion of the larynx down to the glottis, and also for 
the mucous membrane of the epiglottis and its neighborhood. Besides this, it 
also supplies motor fibers to the crico-thyroid muscle, probably from the accessory 
nerve. Clinical experience renders it probable that the superior laryngeal nerve 
also supplies the depressors of the epiglottis, the thyro-epiglottideus, and the 
arytasno-epiglottidei muscles, and perhaps also the arytsenoideus muscle. The 
last three muscles mentioned, however, perhaps derive some motor fibers from the 
recurrent nerve also (the inferior laryngeal nerve). 

Paralysis of the crico-thyroid muscles and of the depressors of the epiglottis is 
seen most frequently after recovery from diphtheria. It is usually a part of a 
more extensive paralysis, and, in addition, is sometimes associated with anaesthe- 
sia of those portions of the mucous membrane which, as we have seen, derive their 
sensory fibers from the superior laryngeal nerve (von Ziemssen). Choking is 
therefore easy and there is danger of inhalation pneumonia. 

Paralysis of the thyro-epiglottideus and the arytseno-epiglottidei muscles is 
recognized by the immobility and the erect position of the epiglottis, which is 
directed toward the back of the tongue. 

Paralysis of the crico-thyroid muscles makes the voice rough, and especially 
renders the production of high tones impossible, since for this purpose we need 
the action of this muscle as a tensor of the vocal cords by approximating the 
cricoid and thyroid cartilages. The detection of this paralysis by the laryngo- 
scope is extremely difficult. Its chief signs are a concavity of the edges of the 
vocal cords, a lack of visible vibration in them, and perhaps, in unilateral paraly- 
sis, a higher position of the vocal cord on the sound side. 

For paralysis of the arytsenoideus muscle, vide infra. 

2. Paralyses in the Distribution of the Inferior Laryngeal or Recurrent 
Nerve. — The recurrent nerve supplies with sensory fibers the mucous membrane 
of the inferior cavity of the larynx below the glottis, and it is the motor nerve for 
all the laryngeal muscles except the crico-thyroid, and except possibly the de- 
pressors of the epiglottis (vide supra). The muscles innervated by it are ar- 
ranged according to their function in the three following groups : 

a. The openers of the glottis — the posterior crico-arytsenoid muscles. 

b. The closers of the glottis — the lateral crico-arytsenoids and the arytamoi- 
deus (transverse and oblique). 

c. The tensors of the vocal cords — the thyro-arytsenoids, which act usually 
as closers of the glottis, but which very often produce the fine differences in ten- 
sion in the vocal cords which are necessary in singing and in modulations of 
speech. They accordingly have the same task as the coarser-working crico-thy- 
roid muscles, which are innervated by the superior laryngeal nerve. 

The motor fibers for all these muscles have their special origin in the accessory 
nerve, from which they pass into the trunk of the vagus, and from this into the 
laryngeal nerves. 



PAEALYSIS OF THE LAEYFGEAL MUSCLES 151 

Most of the paralyses of the recurrent nerve are of peripheral origin. Except 
in the pure muscular pareses (vide supra), which arise not infrequently in the 
course of other laryngeal affections, peripheral paralyses of the vocal cords occur 
with the greatest relative frequency from an abnormal pressure on the trunk of 
the recurrent nerve, especially in aneurism of the arch of the aorta, which may 
cause a left-sided paralysis. Tumors of the bronchial glands, cancer of the 
oesophagus, thyroid or mediastinal tumors, and, in rare cases, even large pericar- 
dial effusions, may also cause a paralysis of the recurrent on one side. Paralyses 
on the right side are seen quite frequently in contractions at the apex of the right 
lung and in the rare cases of aneurism of the subclavian artery. The paralyses 
of the laryngeal muscles, which are sometimes met with after recovery from diph- 
theria (q. v.), also belong to the peripheral paralyses of the recurrent nerve, 
and their cause is to be found in a degeneration of the branches of the affected 
nerves. In other cases the paralysis of the recurrent nerve is due to an affection 
of its fibers in the vagus or even in the accessorius. Excluding certain injuries 
from operations, these affections are usually clue to new growths which cause a 
paralysis of conduction. Paralyses of the recurrent nerve also arise from affec- 
tions of the nucleus of the accessory nerve in diseases of the medulla, in the 
different forms of acute bulbar paralysis, in chronic bulbar paralysis, in multiple 
sclerosis, etc. The frequent hysterical paralyses affecting the closers of the glottis 
and the tensors of the vocal cords are to be regarded as central disturbances of 
innervation (see the chapter on hysteria). 

1. Complete Paralysis of the Recurrent Nerve.— Paralysis of all the laryngeal 
muscles supplied by the recurrent nerve occurs quite frequently in the pressure 
paralysis of the trunk of the recurrent, or of its 

fibers in the vagus. With the laryngoscope (see 
Eig. 16) we find the vocal cord on the paralyzed 
side in a middle position, often falsely called a 
" cadaveric position," and completely motionless 
on respiration, and also on phonation. The 
arytenoid cartilage on the paralyzed side is often 
turned inward. On phonating as strongly as pos- 
sible, the vocal cord on the sound side passes beyond FlG i6.-(From Ziemssen.) Position 
the median line, the arytenoid cartilage also crosses on inspiration in paralysis of the 

' 17 , , , . . . left vocal cord, or paralysis of 

the line, and consequently the glottis IS put m conduction in the recurrent nerve. 

an oblique position. The other symptoms are 

sometimes so slight that without a laryngoscopic examination we do not even 
think of a paralysis. The voice, however, is usually not pure; it often breaks 
into a falsetto, and the patient is easily tired by speaking. With complete 
bilateral paralysis of the recurrent nerve, which is very rare, we find both vocal 
cords motionless in a middle position. Complete aphonia exists, and it is impos- 
sible to cough, since in coughing we have to make at first a complete closure 
of the glottis. There is no dyspnoea, however, if the patient keeps quiet. 

It is an interesting fact, first reported by Eosenbach, that in incomplete re- 
current paralysis almost invariably the abductors of the vocal cords (the 
openers of the glottis) are alone paralyzed, whence the cords remain in ad- 
duction. Only with the further advance of the disease does complete recurrent 
paralysis occur; then the adductors also become paralyzed, and the vocal cords 
become completely motionless, and assume the middle, so-called cadaveric 
position. 

2. Paralysis of the Dilators of the Glottis, the Posterior Crico-arytasnoid 
Muscles. — Bilateral paralysis of these muscles is quite a rare phenomenon, but 
clinically it is of the utmost importance, since it results in a condition of most 
marked inspiratory dyspnoea. ISTeuritic changes, central diseases (tabes, multi- 




152 DISEASES OE THE EE S PIE AT OK Y OEGAXS 



pie sclerosis, etc.), cancer of the oesophagus, etc., may lead to paralysis of the 
posterior muscles. In many cases the cause is obscure. The sequela? of the 
paralysis usually develop slowly and gradually. The affection may last for years. 
The greatest impairment of breathing probably occurs when the vocal cords are 
fixed in adduction by the contracture of the antagonistic closers of the glottis. 
The dyspnoea may increase, especially from external causes, to severe attacks of 
suffocation, and tracheotomy is frequently necessary. The respiration is affected 
in such a way that inspiration only is difficult, protracted, and noisy, while expira- 
tion is free and unhindered. This depends on a valve-like action of the vocal cords. 
They are drawn together by the dilatation of the thorax on inspiration, while the 
current of air in expiration easily pushes them aside. Phonation is usually 
entirely undisturbed. With the laryngoscope (see Fig. 17) we find the glottis 

changed to a small slit, which grows narrower in- 
stead of wider on inspiration. The prognosis is 
usually unfavorable. Only in the hysterical can 
these apparently severe conditions appear and dis- 
appear again in a short time. 

In unilateral paralysis of the posterior crico- 
arytaenoid muscle there is, as a rule, no marked 
dyspnoea. The voice is somewhat hoarse, and with 
the laryngoscope we can see that the paralyzed 
vocal cord does not deviate outward on inspi- 
ration. 




Fig. 17. — (From Ziemssex. ) Complete 
bilateral paralysis of the posticus 
at the moment of inspiration. 



3. Paralysis of the Thyro-arytaenoid Muscles. 

— The paralysis or paresis of these muscles, which run into the vocal cords, and 
which are their chief tensors, is one of the most frequent of the paralyses of the 
laryngeal muscles. It occurs especially in acute and chronic catarrh of the 
laryngeal mucous membrane, and is often the chief cause of the accompanying 
hoarseness. It also frequently develops as the result of an habitual strain of the 
voice in singers and public speakers, and it is one of the commonest causes of 
hysterical aphonia. 

Paralysis of the thyro-arytaBnoid muscles may be bilateral or unilateral. It is 
frequently associated with a paresis of the other closers of the glottis, the arytag- 
noidei and the crico-thyroid muscles. With the laryngoscope (see Eig. 18), in the 
ordinary bilateral paresis of the thyro-arytaBnoid mus- 
cles, we see that on phonation the glottis does not close 
completely, but that an oval space is left between the 
vocal cords/ 

In unilateral paralysis the affected cord shows a 
concavity of its edge. The voice is always more or 
less hoarse and low and the speech is strained. 

In many cases, after a cure of the original catarrh, 
a complete recovery from the paralysis may follow by 
taking good care of the voice. Hysterical paralyses are 
diagnosticated by their sudden disappearance and reap- 
pearance, usually after some psychical disturbance. They are quite common in 
children of the age of ten to fourteen years, especially in girls. (See chapter on 
hysteria.) 

4. Paralysis of the arytgenoideus muscle is rarely an isolated phenomenon. It 
is sometimes seen in laryngeal catarrh or in hysterical aphonia. The voice is 
quite hoarse, and with the laryngoscope (see Eig. 19) we find on phonation that 
the whole anterior part of the vocal cords closes well, but that the cartilaginous 
glottis remains open as a triangular gap on account of the imperfect motion of the 
arytsenoid cartilages toward each other. When the thyro-arytasnoids are para- 




Fig. 18.— (From Ziemssex.) Pa- 
ralysis of both internal thy- 
ro-arytaenoid muscles in the 
course of an acute laryngitis. 



SPASM OF THE GLOTTIS 



153 



lyzed with the arytsenoideus, the glottis shows on phonation a narrow hour-glass 
opening (see Fig. 20). Both the anterior and the posterior portions of the glottis 
fail to close, while the vocal processes take their usual median position on phona- 
tion from the normal turning of the arytenoid cartilages inward by the action 
of the lateral crico-arytaanoid muscles. 

5. Paralysis of the lateral crico-arytaenoid muscles, as an uncomplicated con- 
dition, has never been observed with certainty. Some cases of a complete and 
simultaneous paralysis of all the closers of the glottis have been described, how- 
ever, in which the vocal cords are immovable laterally and the glottis remains 
abnormally wide open. 

We may expect success from the treatment of paralysis of the vocal cords only 
when the primary disease is capable of cure. If catarrhal or other diseases of the 
larynx co-exist, we must first treat these by the methods already mentioned. 




Fig. 19.— (From Ziemsse.n-.~i Paral- Fig. 20.— (From Ziemssen.) Bilateral 

ysis of the arytsenoideus in paralysis of the thyro-arytaenoids 

acute laryngitis. combined with paresis of the ary- 

tsenoideus. 



Paralysis from the compression of tumors, etc., max be relieved in rare cases by 
extirpation, or by partial resolution of the tumors when of strumous origin. In 
catarrhal, diphtheritic, and the so-called " rheumatic " pareses — that is, those 
which occur without any assignable cause — and also in all hysterical aphonias, 
electricity often works very well. Yon Ziemssen has made electrodes for the 
endolaryngeal stimulation of single muscles, but external galvanization is usually 
sufficient in practice. In hysterical aphonia the chief task is to accustom the 
patient again to the necessary and proper voluntary innervation. We usually 
accomplish our purpose most rapidly by commanding the patient to cough and 
then say " Ah," while we f aradize or galvanize the neck. It is often of advantage 
to reverse the current. If the patient succeeds in saying " Ah " once, the voice 
usually returns very quickly. Internally we may try subcutaneous injections of 
strychnine in doses of gr. ^ to gr. | daily (grm. 0.003 to 0.01). 



CHAPTEE YII 

SPASM OF THE GLOTTIS 

(Laryngismus Stridulus. Millars Asthma. Thymic Asthma?) 

Etiology.— Spasm of the glottis is a disease which occurs almost exclusively 
in children under three years of age, and consists of attacks of spasmodic clos- 
ure of the glottis, and consequently of most severe dyspnoea. Boys are more 
frequently attacked by this disease than girls, but the cause of this is wholly 
unknown. The old name of thymic asthma arose from the idea that the at- 
tacks were due to an increase in the size of the thymus gland, but this opinion 
is wholly unfounded. The relation between spasm of the glottis and rachitis is 



154 



DISEASES OF THE RESPIEATOKY OEGAXS 



remarkable, but it is unexplained. Nearly two thirds of all the children who 
suffer from spasm of the glottis are rachitic, but the opinion which was once held 
that spasm of the glottis has a special relation to the rachitic craniotabes is not 
clearly proved. The fact that it is often combined with eclampsia, in that the 
attacks of spasm of the glottis are aggravated by eclamptic attacks, and that the 
two alternate with each other, is an argument in favor of a central origin for 
the disease. In the cases which come on. as they often do, at the time of denti- 
tion, we think it possible to assume a reflex origin for the spasm, just as we may 
in those cases which seem to follow a laryngitis due to taking cold. 

Symptomatology. — The single attacks usually come on suddenly by day or by 
night, either without any cause or from some external influence, such as crying, 
swallowing fluid, or some psychical disturbance. They usually begin with a deep 
inspiration, followed by complete cessation of respiration. The child becomes 
pale, cyanotic, looks anxiously about, rolls his eyes, and makes strained and 
labored efforts at respiration. In severe cases there is a temporary loss of con- 
sciousness, and tonic and clonic spasms in the muscles of the extremities and 
the trunk, as has been mentioned. The attack lasts from some seconds up to two 
minutes. In very severe cases the attack may be immediately fatal. As a rule, 
however, the spasm passes off, deep, noisy inspirations follow, and in a short time 
the child is completely well. The severity of the attacks varies, moreover, in 
different cases, and it varies very markedly, too, in the same child. Sometimes 
we have only one attack or a small number of them, while in other children they 
may come on ten or twenty times a day, and even oftener. and may last with 
varying intensity for months. If the child reaches his third year the disease 
almost always disappears, but quite a large number of the children who suffer 
from spasm of the glottis die before that age. either in the attack itself or from 
other affections. 

Genuine spasm of the glottis hardly ever occurs in adults, but similar attacks, 
which, of course, have quite a different significance, are sometimes observed in 
hysteria. 

The treatment must be especially directed to the child's general condition. 
The child is usually pale and emaciated, and if we succeed in improving its nutri- 
tion with iron and cod-liver oil, the attacks become less frequent, and milder, and 
finally may wholly disappear. If rachitis exists, we should first of all try phos- 
phorus (1 part in 10,000 of cod-liver oil). The child should also be kept in mod- 
erately warm air and guarded from any exposure to cold. Internal remedies to 
prevent the recurrence of the attacks are very uncertain in their action. "We may 
employ one or two grains (gramme 0.05-0.10) of chloral hydrate in solution every 
hour or two ; bromide of potassium, ten to thirty grains daily (grammes 0.5-2.0) ; 
extract of belladonna, etc. 

In the attack itself the child must be raised up. The face should be sprinkled 
with water, or, if the attack be of long duration, a cool shower-bath should be 
given. Friction should be applied to the skin, aided by mustard, or a mustard 
plaster applied to the chest and calves. If the attacks are very frequent and in- 
tense, we must use narcotics, either inhalations of chloroform or subcutaneous in- 
jections of morphine, with care, in doses for a child of -gV to T V of a grain (gramme 
0.001 to 0.005). 



NEW GROWTHS IN THE LARYNX 



155 



CHAPTER VIII 
NEW GROWTHS IN THE LARYNX 

Since new growths in the larynx are of interest mainly to specialists and sur- 
geons, we will here only glance briefly at them. We must remember especially, 
however, that they can be recognized only by the aid of the laryngoscope. It 
unfortunately often happens that a patient is treated for a long time without 
success for a " chronic laryngeal catarrh,"' when the laryngoscope finally shows 
that a new growth is the cause of the hoarseness. It is of especial importance, 
however, to make a diagnosis as early as possible, particularly in carcinoma, 
since the earlier the operation is done the better is the chance for success (vide 
infra). 

A. Benignant Growths in the Larynx 

1. Papilloma is one of the commonest new growths in the larynx. It forms 
glandular, cauliflower-like excrescences, which are usually situated on the ante- 
rior part of the vocal cords, rarely on the false cords. The base of the swelling is 
broad or pediculated. The growths are often multiple. We do not know the spe- 
cial cause of their origin. It is worthy of note that papilloma, like other benignant 
growths in the larynx, is seen much more frequently in men than in women. 

2. Fibroma in the larynx is comparatively common. The pediculated tumors 
known as " laryngeal polypi " are usually fibromata. They are generally situated 
on the vocal cords and form whitish or reddish-brown swellings, from the size of 
2, pea to that of a cherry, vascular and dense or soft (see Eigs. 21 and 22). There 




Figs. 21 and 22 — (From Ziemssen.) Pediculated fibromata. 



is no evidence that persons who use their voices very much are especially liable to 
the formation of fibromata. 

3. Cysts and " mucous polypi " rarely occur. They are probably due to the 
retention of the secretion in a mucous gland from the stoppage of its orifice. 
We find them in the ventricles of Morgagni, on the epiglottis, etc. In a very few 
cases we also see in the larynx lipomata, myxomata, separated portions of thyroid 
gland tissue which have begun to grow, enchondromata, etc. 

The symptoms which are excited by benignant tumors in the larynx depend 
partly upon the situation and partly upon the size of the new growth. Small 
polypi may exist wholly without symptoms, and they are found only by chance on 
laryngoscopic investigation. Usually, however, the presence of disturbances of 
phonation (hoarseness, a marked change in pitch, secondary tones), persistent 
cough, or respiratory disturbances when the tumor is a large one. are the symp- 
toms which give occasion for an examination. Abnormal sensations in the larynx 
are by no means the rule, and pain is wholly absent. 

B. Malignant Growths. Carcinoma of the Larynx 
Sarcomata, arising from the true or false vocal cords, are very rare. The only 
malignant new growth of the larynx of great practical importance is carcinoma. 



156 



DISEASES OF THE EESPIEATOEY OEGANS 



Carcinomata develop usually in old people, either primarily in the larynx or 
secondarily from affection of the neighboring organs. In the first case the vocal 
cords or the ventricles of Morgagni are the points most frequently attacked. An 
extension of the disease to the larynx is seen especially in cancer of the tongue or 
pharynx, rarely in cancer of the oesophagus. 

The symptoms of cancer of the larynx develop slowly. Hoarseness, dysphagia, 
pains in the larynx often shooting up into one ear or the temporal region, the 
appearance of respiratory symptoms, and finally, but only in the later stages as a 
rule, the signs of general weakness and emaciation which are seen in almost all 
forms of carcinoma, form the picture of the disease. Enlargement of the cer- 
vical lymph-glands is sometimes an early symptom, but it may be wholly lack- 
ing. The diagnosis is possible only by the aid of the laryngoscope. Besides 
this, a digital examination may at times be of diagnostic value by the detection 
of the characteristic hardness about the entrance or in the neighborhood of 
the larynx. A general description of the laryngoscopic appearances can not 
be given on account of the diverse character of the cases. We see the uneven, 
injected new growth, covered with mucus and often ulcerated, and besides this 
at times the secondary appearances of catarrh, a developing perichondritis, etc. 
In many instances the diagnosis is quite easy, but in other cases protracted ob- 
servation is required. It may be difficult, however, at times, to distinguish it from 
tuberculosis or from syphilis. We may be aided in such cases by a search for 
tubercle bacilli, by tuberculine injections, or by the results of anti-syphilitic treat- 
ment. All the other organs of the patient therefore must always be carefully 
examined. In doubful cases it is proper to remove a bit of the endolaryngeal 
growth and examine it histologically. 

Surgical treatment is the only one for all laryngeal new growths. We must 
refer to the special works for the details. Laryngologists have devised numer- 
ous instruments for the removal of benignant polypi, by which, under the guid- 
ance of the laryngoscope, the new growth is cut, snared, crushed, or torn off. 
The performance of the operation is made much easier by inducing local anaes- 
thesia of the laryngeal mucous membrane by painting with cocaine. Never- 
theless we firmly believe that in all severe cases the " endolaryngeal " operations 
should be superseded by laryngotomy. — Carcinoma of the larynx can be cured only 
through removal of the tumor by laryngotomy (splitting of the larynx) or by 
total extirpation of the larynx. Laryngotomy is comparatively free from danger, 
while total extirpation has met with permanent success as yet in but few instances. 
If surgical interference is no longer practicable, we can endeavor merely to miti- 
gate the suffering of the patient by means of morphine, cocaine, and other nar- 
cotics. 



SECTION III 
Diseases of the Trachea and the Bronchi 
CHAPTEE I 

ACUTE CATARRH OF THE TRACHEA AND THE BRONCHI 

(Tracheitis and Acute Catarrhal Bronchitis) 

^Etiology. — Acute catarrh of the larger air-passages, of the trachea, and 
larger bronchi, is a frequent disease, and it may often arise from taking cold. It 
is conceivable that the inhalation of cold, damp air sometimes directly affects the 
mucous membrane of the upper air-passages. Bronchial catarrh is very often asso- 



ACUTE CATAEKH OF THE TEACHEA AND THE BEONCHI 157 



ciated with a coincident catarrh of the larynx, and more rarely of the pharynx. 
In the ordinary mild forms the catarrh is usually confined to the trachea and the 
first large branches of the bronchi, while the finer bronchi remain healthy. 

More intense inflammation of the bronchial mucous membrane is the result of 
active mechanical or chemical irritation. A severe bronchitis develops after 
the inhalation of noxious gases, nitrous and sulphurous oxides, chlorine, bromine, 
etc., as is often observed in operatives. The inhalation of smoke and dust, espe- 
cially vegetable dust, works in the same injurious fashion, and the followers of 
many trades and employments, such as millers, wool-workers, colliers, etc., are 
especially subject to disease from this cause. In this form of bronchitis the 
catarrh often extends to the finer bronchi. 

The bronchitis which develops in the course of other acute and chronic dis- 
eases is still commoner than the primary forms already mentioned. It is often 
due to infectious causes, such as certain infectious diseases, especially measles, 
whooping-cough, and influenza. In these diseases bronchitis is one of the most 
constant local affections, and is probably dependent immediately upon the primary 
infection. Bronchitis, however, develops secondarily in most of the other acute 
infectious diseases, and is due largely to the inhalation of noxious substances from 
the upper part of the air-passages. This is the explanation of the bronchitis in 
diphtheritic processes in the pharynx and larynx, in so far as it does not depend 
upon a direct extension of the disease, and also of the bronchitis in small-pox, 
etc. Bronchitis may also be met with in all other forms of severe disease, because 
retention of secretion, putrefactive processes, inflammation, thrush, etc., occur 
in the cavity of the mouth and pharynx, and from them chemical or organic irri- 
tants may easily be inhaled into the bronchi. The imperfect expectoration in all 
severe diseases is a still more harmful factor than this inhalation. The secre- 
tion remains in the bronchi, processes of decomposition arise in the stagnating 
mucus, bacteria collect and lead to a bronchitis, and finally to the lobular pneu- 
monia which is so often found (vide infra). The lessened power of resisting 
injurious influences, produced in the mucous membrane by severe bodily disease, 
also facilitates the development of catarrhal inflammation. In all diseases in which 
deglutition is affected (as in paralysis of the epiglottis or of the pharyngeal 
muscles), and in all diseases attended by frequent vomiting or choking (cancer of 
the oesophagus, etc.), secondary bronchitis with its sequelae may ensue from the 
inhalation of small particles of easily decomposable food. 

We do not know how far we may claim that infectious agents act as a cause of 
primary bronchitis, yet it is not improbable that many cases have such an aeti- 
ology. It is especially likely that many cases of bronchitis due to " catching cold " 
really have something infectious about them, and that the -preceding exposure to 
cold has merely lowered the natural powers of resistance, and thus permitted, or 
at any rate promoted, infection. This infection is probably not due to any special 
specific bacteria but to the ordinary germs of inflammation (staphylococci, etc.). 

Finally, we must mention that acute bronchitis is sometimes merely an ex- 
acerbation of a previous chronic bronchitis. We will return later to this impor- 
tant and not uncommon process. 

The predisposition to acute bronchitis varies in different persons. We do not 
know definitely on what ground such an increased predisposition to bronchial dis- 
ease rests, nor why we meet with it sometimes in the weak and anaemic, and at 
other times in so-called "full-blooded" persons. Bronchitis is more frequent 
in children and old people than in those in middle life. Most of the cases occur 
in the spring and autumn. 

Symptoms. — Pain in the chest may be present in some cases of simple catarrhal 
bronchitis, but usually only in a moderate degree. In severe tracheitis patients 
often have a painful feeling of soreness in the neck and behind the upper part of 



158 



DISEASES OF THE RESPIRATORY ORGANS 



tlie sternum, and this is increased on coughing. The mucous membrane of the 
bronchi, apparently, has no nerve-fibers which are sensitive to pain, and the pains 
in the chest which are often present in bronchitis are, as a rule, muscular pains 
in the intercostal muscles, or the insertion of the diaphragm, due to the severe 
paroxysms of coughing. 

Cough is one of the most constant symptoms of bronchitis, and by it usually 
the attention of the patient or of the physician is first called to the existing 
thoracic affection. The cough may of course be due to a laryngitis, if that is also 
present. There is no doubt, however, that a cough may be excited in a reflex 
manner from the mucous membrane of the trachea and of the larger as well as of 
the finer bronchi. Experiments have shown that the point of bifurcation of the 
trachea is especially irritable, and many severe paroxysms of coughing may be 
due to an irritation of this very spot from the accumulation of secretion. The 
intensity of the cough, moreover, is very different in individual cases, which is 
due in part to the degree and extent of the bronchitis and in part to the individual 
irritability of the person affected. 

The expectoration consists of the secretion and exudation from the inflamed 
mucous membrane. Its abundance and consistency vary considerably in the dif- 
ferent cases. We distinguish a catarrh with an abundant secretion from the so- 
called " dry catarrh." In the latter only a little viscid sputum is expectorated, but 
in the former the expectoration is more abundant and muco-purulent, or sero- 
mucous, a thin fluid separating into layers on standing (vide infra). Very often in 
the beginning of the disease the expectoration is scanty and viscid — the sputum 
crudum of the old physicians; and later it becomes more abundant, more fluid, 
and more purulent — the sputum coctum. In catarrh of the finer bronchi the ex- 
pectoration may contain little tough mucous or muco-purulent casts of the 
bronchi. It may be stated in general that the characteristic of simple bronchitic 
sputum is the mucous admixture in contrast to the purulent or sero-purulent 
sputum from phthisical cavities, etc. We may readily recognize the mucous con- 
tents of the sputum by the tenacity with which it clings to the bottom of the 
sputum-cup when the cup is tipped. A simple catarrhal expectoration shows noth- 
ing peculiar under the microscope. The pus-corpuscles are often swollen, and 
show more or less marked fatty degeneration. A slight admixture of blood may 
occasionally be present in severe bronchitis, but it usually has no special signifi- 
cance, being at times merely the result of severe fits of coughing. A more 
marked and persistent admixture of blood is seen in the catarrhal sputum of some 
cases of intense bronchitis in drunkards, so that we may even speak of a " hsemor- 
rhagic bronchitis." 

Dyspnoea is usually entirely absent in simple mild bronchitis, but marked short- 
ness of breath may be noticed in extensive catarrh of the finer bronchi. 

Physical Examination. — We may obtain direct evidence of the condition of 
the tracheal mucous membrane, with due practice, by the laryngoscope. We 
see a reddening of the membrane, and sometimes an abnormal abundance of 
secretion on it, if there is a tracheitis. Other methods of physical examination 
are at our service for judging of the changes in the bronchi. 

Inspection of the thorax shows nothing abnormal in the milder forms of bron- 
chitis. The respiration is somewhat accelerated and the expiration prolonged in 
severe bronchitis, especially if the finer bronchi are affected. Percussion in 
uncomplicated bronchitis shows nothing abnormal in the pulmonary resonance. 
In extensive catarrh of the finer bronchi an acute dilatation of the lung is apt to 
occur, with a descent of the lower margin of the lung. Auscultation, too, shows 
nothing unusual in many cases of mild catarrh limited to the trachea and 
large bronchi, but in the cases in which the smaller bronchi are the seat of the 
catarrh and there is a marked accumulation of secretion in them, we hear, besides 



ACUTE CATAEEH OF THE TEACHEA AND THE BEONCHI 159 



the vesicular respiration, the so-called rhonchi which almost wholly hide it. In 
dry bronchitis we speak of humming or buzzing sounds (sonorous rhonchi) or 
shrill, whistling sounds (sibilant rhonchi) according to their pitch. These sounds 
are probably due to stenosis, and are caused by the passage of the air through 
narrow portions of the bronchi. The narrowing occurs in part from the swelling 
of the mucous membrane, in part from the accumulation of secretion. The masses 
of secretion themselves, if they are set in vibration at the same time, may pos- 
sibly take part in the production of the humming noises. If the amount of secre- 
tion collected in the bronchi is more abundant and of a more fluid consistency, 
it gives rise to " moist rales " on the passage of the air. These are distinguished 
as " coarse," " medium," or " fine moist rales," according as they occur in the 
larger or smaller bronchi. 

Other symptoms of disease are often present besides those already mentioned 
as being due directly to the bronchitis. The general health is usually disturbed 
in a severe bronchial catarrh. The patient does not feel well, and has less appe- 
tite than usual. A moderate amount of fever is often present, especially toward 
evening. An increase of temperature above 102° or 103° (39° C.) is rarely seen 
except in children. The patient sometimes complains of headache, which is in- 
creased by severe coughing. There can be a question of complications only when 
the inflammation extends to other parts of the respiratory mucous membrane. 
Mild bronchitis is often associated with coryza and laryngitis, while severe bron- 
chitis may lead to catarrhal pneumonia (vide infra). 

The separate forms of bronchitis are distinguished chiefly by the degree of 
extension of the catarrh. 

1. The Milder Forms of Acute Bronchitis. — In most cases of simple primary 
bronchitis, as well as in many milder attacks of secondary bronchitis, the catarrh 
is limited to the mucous membrane of the larger bronchi. Exposure to cold and 
other injurious influences are frequent causes of the primary form. The symp- 
toms are moderate. The cough, however, may be quite troublesome. Often fever 
is absent or but slight. Upon auscultation, particularly over the lower lobes, but 
sometimes over the entire lungs, are heard numerous rather coarse wheezing or 
rattling sounds, usually with some symmetry of distribution ; but in many cases, 
as we have said, there may be nothing abnormal heard, so that the diagnosis will 
have to rest merely upon the subjective discomfort in the chest, the cough, and 
the expectoration. "With proper care, simple primary bronchitis runs its course in 
a few days, or at the most in a few weeks, and ends in complete recovery. If the 
patient exposes himself recklessly, or the astiological factors continue to be active, 
the disease may, however, grow worse, prove to be very tedious, and finally develop 
into chronic bronchitis. 

2. The Severer Febrile Forms of Acute Bronchitis. — Sometimes acute bron- 
chitis assumes a severer form, whether because the influences which give rise to 
it are unusually violent, or because it is due to some special and perhaps infectious 
cause. In such cases the symptoms are more marked, the bronchial rales more 
abundant, the general condition of the patient worse. ]STot infrequently there is 
fever for several days, or even for one or two weeks, the type being irregularly 
remittent, but the temperature is usually 102° or 103° (39° to 39.5° C), although 
it may go higher. The expectoration is usually muco-purulent, but it often con- 
tains much pus; in other cases it may be sero-muco-purulent. The amount is 
then greater, and it forms distinct layers on standing in a beaker glass. The 
author has not infrequently noticed that there is more liability in the severer 
forms of acute bronchitis to have the disease mainly limited to one lobe, or at 
least to one lung, but we may have a severe acute diffuse bronchitis on both sides. 

The aetiology of acute febrile bronchitis has been but little studied. Bacterio- 
logical examination of the sputum usually gives no definite results, since we always 



160 



DISEASES OF THE RESPIRATORY ORGANS 



find many micro-organisms. Many acute cases may be caused by the ordinary pus 
cocci. At the time of a pneumonia epidemic we have repeatedly seen cases of 
acute bronchitis with high fever and herpes, but without any signs of pneumonic 
infiltration. These were probably due to pneumococcus infection. In other cases 
there is perhaps an influenza infection. 

We would add in particular that many acute febrile cases of bronchitis prove 
on closer investigation (more careful questioning) to be acute exacerbations of a 
mild chronic bronchitis — " acute recurrent bronchitis." The chronic disease of 
the bronchial mucous membrane apparently affords a favorable opportunity for 
new infection. In other instances it is merely an acute exacerbation of the same 
chronic process. Such an acute bronchitis may of course occur repeatedly in the 
same patient. 

3. Catarrh of the Finer Bronchi — Capillary Bronchitis. — A simple primary 
bronchial catarrh rarely extends to the finest bronchi in adults. The secondary 
bronchitis, however, which develops in other severe diseases (vide supra) often 
extends into the ultimate divisions of the bronchi, and finally leads to the forma- 
tion of nodules of lobular pneumonia — " catarrhal pneumonia " (vide infra). We 
recognize the implication of the finer bronchi by hearing the high, shrill, whis- 
tling rhonchi (sibilant rhonchi), or the abundant fine, moist rales. Respiratory 
symptoms may be quite marked in extensive catarrh of the finer bronchi. Res- 
piration is evidently accelerated, the inspiration is of the costal type and re- 
quires the aid of the accessory respiratory muscles of the neck (the sterno- 
mastoids and scaleni), and expiration is usually prolonged. There is often quite 
a severe cough. The expectoration is muco-purulent and usually not very 
abundant. 

Capillary bronchitis in children is of great practical importance. Bronchitis 
in young children always has, as experience tells us, a tendency to attack the 
smaller bronchi. Extensive bronchitis is seen especially in weak children who 
are rachitic or predisposed to tuberculosis. Children have a great tendency to 
be attacked with bronchitis at the time of the first dentition. 

The parents' attention is usually called to the disease by the appearance of a 
cough, which is excited especially by the child's crying. Small children never 
expectorate, for they swallow the secretion which is coughed up into the pharynx. 
The rapidity of respiration is very striking, it being increased to sixty or eighty, 
or even more, in a minute. The respiration is also labored, but it is usually super- 
ficial, and in severe cases irregular. There is generally a distinct respiratory play 
of the alae nasi. We often see a retraction of the lower lateral portions of the 
thorax on inspiration as a result of the imperfect entrance of air into the 
smaller bronchi. The expiration is frequently noisy and groaning in children. 
We hear extensive fine, moist rales over the lungs. In severe cases the child 
becomes restless, anxious, perhaps markedly pale and cyanotic, and finally apa- 
thetic and stupid. In such cases, however, we have no longer to deal with simple 
bronchitis, but catarrhal pneumonia has already developed. The disease almost 
always runs its course with fever, the temperature rising to 104° (40° C.) and 
over. The pulse is increased to 120 or 140 or more per minute. The duration of 
the disease is seldom less than two or three weeks, and it may last much longer. 
Death may ensue, especially in ill-nourished children, partly as a result of general 
weakness, and also directly from the imperfect respiration. In such cases we find 
at the autopsy not only diffuse bronchitis, but also almost always lobular pneu- 
monia. In many cases a gradual recovery finally takes place in spite of the most 
severe symptoms. 

The secondary bronchitis in children complicating measles, whooping-cough, 
diphtheria, etc., has the same tendency to involve the finer bronchi and to lead to 
lobular pneumonia. 



ACUTE CATARRH OF THE TRACHEA AND THE BRONCHI 161 



In conclusion, we must mention that acute bronchitis, in old persons is also apt 
to attack the finer bronchi, and it may be dangerous partly from the general ex- 
haustion, partly from the occurrence of respiratory symptoms and cardiac weak- 
ness, as in lobular pneumonia. 

Diagnosis. — The diagnosis of bronchitis presents no special difficulty. It is 
obtained directly by the discovery of rhonchi on auscultation. If these fail, we 
conclude that there is a mild catarrh of the larger bronchi from the presence of 
cough and expectoration, if no cause for the cough is to be found in an affection 
of the larynx. The question is more difficult, but it must always be considered, 
whether a given bronchitis is a common primary catarrh or secondary to some 
other affection. This question naturally can be decided only by a very careful 
examination of the body. We must always remember, furthermore, that severe 
pulmonary affections may be at first quite latent and show objectively merely the 
signs of simple bronchitis, while later pneumonia, a tubercular affection, or some- 
thing similar, develops. A bronchitis which is unilateral, or in which the signs 
are to be found in circumscribed localities, must therefore be regarded as sus- 
picious. It has long been known that bronchitis in the apices of the lungs, the 
" apex-catarrh," is often the first objective change to be met with in pulmonary 
phthisis. We can only conjecture, and not pronounce with certainty on objective 
evidence, whether nodules of lobular pneumonia are present or not in diffuse 
bronchitis affecting the finer bronchi. 

From what has been said, it is clear that we should be cautious in our prog- 
nosis regarding cases of severe bronchitis, especially in children and old people. 
The prognosis in the milder forms of bronchitis is of course always very favor- 
able. 

Treatment. — The prophylaxis of primary bronchial catarrh consists in the 
removal of all the injurious influences mentioned which, as experience shows, 
may give rise to bronchitis. Careful hardening of the skin to the effects of a 
change in temperature is of service in persons, particularly children, who have a 
special tendency to bronchitis, as we have already said in regard to the prophy- 
laxis of laryngitis. It is very important to remember, in this connection, that we 
can also be successful in our prophylactic measures against secondary bronchitis. 
Keeping the mouth and pharynx clean, urging deep inspirations, and aiding 
expectoration by the timely use of tepid baths and shower-baths, may often pre- 
vent bronchitis or keep it within bounds, when it would surely develop if the 
patient were neglected. 

Simple hygienic measures suffice in the treatment of mild cases of acute bron- 
chitis. The patient should be kept warm, should remain in his room, or, if there 
be any fever, in bed. Diaphoretic remedies have long been praised as especially 
potent in the treatment of acute bronchial catarrh. The patient, therefore, should 
drink hot tea, pectoral tea* (Brustthee), or elder tea, etc., or hot milk mixed 
with Seltzer, a remedy whose efficacy is frequently praised by the patient. The 
tougher the sputum and the more difficult expectoration, the more abundantly 
should we give warm drinks (Ems water, pectoral tea, etc.). Local' treatment of 
the mucous membrane by inhalations is usually illusory, for only the smallest part 
of the inhaled fluid reaches the bronchi. We may, however, prescribe inhala- 
tions of warm steam, or a one- or two-per-cent. solution of common salt, especially 
with a dry cough and a secretion which is hard to loosen. 

Otherwise we must employ symptomatic treatment. A mustard plaster or a 
cold, wet compress about the chest does good service with severe subjective tho- 



* A favorite German household remedy, consisting of an infusion of eight parts of al tinea, three 
parts of licorice, one part of orris-root, four parts of coltfs-foot, and two parts each of mullein and anise- 
seed. — Trans. 

11 



162 



DISEASES OF THE EESPIEATOEY OEGANS 



racic symptoms. In severe cases a few dry cups may be very useful in adults, but 
local abstractions of blood are never necessary in simple bronchitis. If there is 
troublesome irritation on coughing, so as to disturb the rest at night, we may pre- 
scribe small doses of morphine, five to ten grains of Dover's powder (gramme 
0.3-0.5), fifteen to twenty drops of cherry-laurel water, codeine, etc. When ex- 
pectoration is difficult, we may use the so-called expectorants — ipecac, chloride of 
ammonium, apomorphine, senega, etc. 

We have already repeatedly mentioned the use of tepid baths and shower- 
baths, indicated in severe diffuse bronchitis developing secondarily in the course 
of other acute diseases. 

Tepid baths with shower-baths, two or three times a day, are also to be used as 
a most powerful remedy in severe cases of capillary bronchitis in children. The 
baths assist expectoration and guard against the possibility of the development of 
lobular pneumonia. Wet packs applied to the thorax or over the whole body are 
serviceable. The child should be wrapped to the neck in a sheet which has been pre- 
viously dipped in water at a temperature varying with the degree of the fever 
from 68° to 77° (16° to 20° E.) and well wrung out, It is best to leave the arms 
free. A dry woolen blanket may be wrapped around the moist sheet. This pro- 
cedure must be repeated three or four times a day. As to other remedies, we use 
the same as in adults. With weak children our care must be to keep up the 
strength by giving the most nourishing food possible and small amounts of wine. 
An emetic is sometimes indicated in cases with an abundant accumulation of 
mucus in the bronchi, and is of good service. As experience has shown, we should 
use opiates for small children only with the greatest caution. Senega and ben- 
zoin may be employed as expectorants. 

In the bronchitis of old people our chief aim should be to keep up and improve 
the patient's strength. We prescribe liquor ammonii anisatus, infusion of senega, 
etc., to aid expectoration, which is usually difficult, since the cough is feeble. We 
must keep close watch on the condition of the heart (digitalis). Tepid baths 
may be of advantage, but they must be used with care. 



CHAPTEE II 

CHRONIC BRONCHITIS 

{Chronic Bronchial Catarrh) 

etiology. — Chronic bronchial catarrh may develop gradually from external 
causes, or in rare cases it may follow acute bronchitis. The same noxious influ- 
ences which excite acute bronchitis may, by the frequent repetition of their 
action, result in chronic bronchitis. The constant inhalation of dust is one of 
the commonest causes of primary chronic bronchitis (see the chapter on diseases 
from the inhalation of dust). In many cases it is therefore a definite occupation 
disease, and is seen in millers, bakers, wool- workers, stone-cutters, colliers, etc. 

In a large number of cases severe chronic bronchial catarrh is not an inde- 
pendent disease, but occurs as a complication or a result of other diseased condi- 
tions. The combination of chronic bronchitis with emphysema of the lungs {vide 
infra) is the most common. A large number of cases also are the result of some 
form of heart disease, such as valvular disease or myocarditis, or of disease of the 
vessels, leading to stasis in the pulmonary circulation, and finally to a chronic 
catarrh of the bronchi. Chronic bronchial catarrh in renal diseases also depends 
in part upon circulatory disturbances, and in part on the toxic action of urinary 



CHROOTC BRONCHITIS 



163 



constituents which have not been normally excreted. Finally, we find a more or 
less extensive chronic catarrh of the bronchi in other chronic affections of the 
lungs and pleura, as in tuberculosis or pleurisy. 

Chronic bronchitis is seen especially in adults and old people, and more fre- 
quently in men, on account of their exposure in the various trades, than in women, 
but children may also have pronounced cases of chronic diffuse bronchitis. Such 
cases may often be referred to a previous acute disease of the respiratory organs, 
especially whooping-cough, less often measles, etc. Such cases in childhood often 
continue into later life, and on careful inquiry we may trace many of the severe 
cases of chronic bronchitis in adults back to childhood. 

Pathological Anatomy. — Chronic bronchitis is characterized anatomically by 
a persistent and chiefly venous hypersemia and swelling of the bronchial mucous 
membrane with increased secretion of mucus and morbid exudation of serum and 
pus-corpuscles. There is often a hyperplasia of the mucous membrane with puffi- 
ness of the surface. In old cases, however, we finally meet with an atrophy of 
all the layers of the mucous membrane. One of the most frequent results of 
chronic bronchitis is a cylindrical dilatation of the middle and lesser bronchi — . 
bronchiectasis — especially in the lower lobes. This arises gradually from the loss 
of elasticity of the diseased bronchial walls, and their diminished resistant pow- 
ers, as well as from the pressure of the stagnating secretions. 

Symptoms and Course of the Disease. — The symptoms which are due to 
chronic bronchitis are dyspnoea, cough, and expectoration. To these should be 
added the results of a physical examination, in making a diagnosis. 

The cough is of very different severity in different cases. Usually it is worse 
early in the morning, in the evening, and at night, than in the daytime. The 
amount of expectoration is also subject to great variations. In many cases there 
is a dry cough (catarrhe sec, vide infra), in which only small amounts of tough, 
viscid sputum are expectorated. In other cases the expectoration is more abun- 
dant and muco-purulent, sometimes rather sero-purulent, and occasionally thin 
and separating into layers on standing. In catarrh of the finer bronchi the muco- 
purulent sputum at times indicates its origin by partly formed casts. We may 
also note the formation of so-called spirals (vide infra, bronchial asthma). Mi- 
croscopically, the expectoration has no special characteristic appearances, but 
contains only the usual elements of sputum — pus-corpuscles mixed with pavement 
epithelium, ciliated epithelium, often many bacteria, sometimes needles of fat 
acids, and rarely a few pointed octahedral crystals, the so-called asthma crystals 
(vide infra). Small amounts of blood may be seen in severe chronic bronchitis, 
especially in the catarrh of passive congestion, bronchitis with very severe at- 
tacks of coughing, etc., but they do not have any bad significance. 

Dyspnoea of moderate or even severe degree may be due solely to an extensive 
catarrh of the finer bronchi with narrowing of their lumen. In many cases in 
which there is bronchitis the dyspnoea is due chiefly to some co-existing abnormal 
condition of the heart or lungs. 

Physical Examination. — The percussion in bronchitis shows no special 
change. At most the resonance may be somewhat tympanitic from the relaxa- 
tion of the lung-tissue, especially in the lower and posterior portions of the lungs, 
or, with an abundant retention of secretion in the bronchi, it may be a little 
diminished. The inspiratory descent of the lower edge of the lung is lessened 
when the entrance of air is much impeded by the contracted or plugged bronchi. 
Auscultation may give either rhonchi, whistling, hissing, humming, etc., or moist 
rales, according to the extent of the catarrh and the amount and consistency of 
the secretion. The sounds are usually to be heard over the whole lung, or espe- 
cially over the lower lobes, because here the catarrh is usually most marked, and 
retention of secretion is most apt to occur. The respiratory murmur in some 



164 



DISEASES OF THE RESPIRATORY ORGANS 



places may be quite obscured by the rales. Otherwise it is vesicular, sometimes 
exaggerated, sometimes rough and indefinite. Expiration is usually prolonged, 
because the exit of air from the alveoli is much hindered by the narrowed bron- 
chioles. The respiratory murmur may be much diminished, or even entirely sup- 
pressed in places where the bronchi are stopped by secretion, which happens most 
frequently in the lower lobes. 

Except in mild cases, we usually distinguish several different forms of chronic 
bronchial catarrh, which may run into one another. 

1. The dry chronic catarrh (catarrhe sec of Laennec) is the form in which the 
mucous membrane has only a slight secretion. The cough is usually very trou- 
blesome and labored, but the patient raises merely a little tough sputum, or none 
at all. On auscultation we hear sibilant rhonchi, but no moist rales. This form 
of catarrh is usually associated with pulmonary emphysema, and asthmatic at- 
tacks are also frequent. The disease is stubborn, and usually lasts for years. 

2. The so-called bronchial blennorrhcea is that form of chronic bronchitis in 
which we find a very copious sero-purulent exudation on the surface of the mucous 
membrane. The cough is therefore associated with a very abundant and quite 
thin expectoration, the amount of which in the twenty-four hours may exceed a 
pint (half a litre). The expectoration runs together in the sputa-cup and usually 
separates on standing, the more purulent portion sinking to the bottom, and the 
sero-mucous portion, which is usually frothy on the surface, remaining at the top. 
Numerous moist rales are heard in the lungs, especially in the lower portions. 
These diminish if large amounts of sputum are coughed up. Anatomically, the 
bronchi are almost always found dilated in this form of chronic bronchitis. 

3. The so-called serous bronchorrhcea (" catarrhe pituiteux " of Laennec) is 
quite rare but very interesting. It is characterized by the expectoration of a very- 
large amount of frothy, almost purely serous, or sero-mucous, thin sputum con- 
taining only a slight admixture of pus. The cough usually comes on in very vio- 
lent paroxysms which last from half an hour to an hour or more. The respiratory 
symptoms are quite severe, especially during these attacks, and have given rise 
to the old and useful term " asthma humidum." The expectoration collected in 
twenty-four hours may amount to one or two quarts (litres). Examination of 
the lungs usually reveals very abundant and extensive moist rales. The reso- 
nance on percussion is normal or a little diminished, from the accumulation of 
secretion. 

The special cause of this peculiar disease is quite obscure. There are mild 
afebrile and also very severe forms of this type of chronic bronchitis. We have 
seen several chronic cases, which were attended with persistent fever, and which 
led to great emaciation and weakness. In one case which came to autopsy there 
was found a marked tuberculosis of the retro-bronchial lymph-glands, while the 
lungs themselves showed hardly any striking changes. One vagus nerve was 
wholly imbedded in the tubercular mass of the glands, and it is not impossible that 
the peculiar attacks of serous expectoration were due to irritation of this nerve. 
At any rate, we should consider the possibility of such conditions in the future. 
It is worthy of note that attacks of " humid asthma," with expectoration of large 
amounts of serous sputum, have also been observed in chronic nephritis, espe- 
cially in contracted kidney (q. v.). 

Course of the Disease. — The course of most chronic bronchial catarrhs is very 
protracted. The disease usually has frequent remissions and fresh exacerbations. 
The patient is tolerably well in the pleasanter time of the year if he takes good 
care of himself, but in autumn and winter, or after exposure to various noxious 
influences, the catarrh grows worse and the patient's symptoms increase. If the 
disease has lasted for years, we usually find symptoms in the lungs, such as emphy- 
sema or chronic tuberculosis, or in the heart, such as secondary dilatation and 



CHRONIC BRONCHITIS 



165 



hypertrophy of the right ventricle, which symptoms gradually become more se- 
vere. The details of these conditions are to be found in the appropriate sections. 

Diagnosis. — The diagnosis of chronic bronchitis is not difficult in itself, and 
may easily be made by considering the patient's symptoms and by judging of the 
result of the physical examination. We must always consider, however, whether 
the bronchitis is actually a primary disease or a result or a complication of some 
other chronic disease. Therefore, in every case of chronic bronchitis, the heart 
and the kidneys (urine) must be carefully examined, as well as the lungs. 

Prognosis. — Chronic bronchitis is in most cases a very stubborn affection, 
which frequently, as we have said, shows improvement, but from which complete 
recovery is rare. The prognosis also depends greatly upon the patient's circum- 
stances, and upon the possibility of his taking care of himself and avoiding all 
harmful exposure. In secondary bronchitis the question whether the bronchitis 
is capable of material improvement or not of course depends mainly upon the 
prognosis of the primary disease. 

The danger in primary chronic bronchitis comes from the final development 
of its sequelse, especially from the gradual appearance of pulmonary emphysema, 
dilatation of the heart, secondary tuberculosis, etc. 

Treatment. — The only hope of success in severe cases in any method of treat- 
ing chronic bronchitis lies in removing the patient completely, at least for a time, 
from the action of injurious influences. The favorable result of the baths and 
health resorts that are employed depends largely upon this, that patients enjoy in 
them complete bodily rest, and are far better protected from dust and the changes 
in the weather than at home. We must make the patient comprehend the neces- 
sity of this condition as the basis of any treatment. If he can not go to a suit- 
able climate during the cold season, he must keep his room in all unpleasant 
weather, but at other times he may be permitted to stay in the open air. Further- 
more, the patient must be warned to avoid as completely as possible those harm- 
ful influences which his calling and manner of life entail, and among which 
especially to be mentioned is the bad air in our inns and restaurants. Food should 
be easily digestible, and, in persons inclined to corpulence, sparingly taken. Alco- 
hol is to be permitted only in a moderate degree. We combat the tendency to con- 
stipation, which is often present, by dietetic remedies, by taking fruit, especially 
grapes, prunes, etc., honey, Graham bread, or by mild laxatives, such as the bitter 
waters, Friedrichshall, Ofner, etc., since any persistent constipation aggravates the 
patient's symptoms. 

If the circumstances of the patient permit and his condition requires it, we 
should send him south in the autumn in order to avoid the evils of a northern 
winter, but we must always consider whether the patient has the strength to bear 
the burden and unavoidable discomfort of such a journey without permanent 
harm. The rule is to send patients with a bronchial catarrh when there is much 
secretion to health-resorts with a dry climate — for example, to the western Ri- 
viera, San Remo, Bordighera, Mentone, etc. The somewhat dry yet cooler cli- 
mate of Meran, Gries, or Arco is suitable for patients with a stronger constitu- 
tion. Patients with dry bronchitis usually find themselves at their best in a 
warm but not too dry climate. If we wish to be sure of avoiding the winter's 
cold, we must choose Sicily, Egypt, or Madeira for a residence. Of the more 
northern winter resorts we may mention places on the eastern Riviera, especially 
Nervi. 

We must recommend, in bronchitis, a suitable summer residence, particularly 
for those who dwell in large and dusty cities. Any private country house in a 
well-wooded and protected place is suitable. If we wish to send patients to a bath, 
Marienbad, Kissingen, or Homburg are proper places for corpulent people who 
also suffer from digestive disturbances, while we may send weaker patients to 



166 DISEASES OF THE RESPIRATORY ORGANS 



Ems, Soden, Badenweiler, Ischl, Reichenhall, etc. A summer residence on the 
sea, best on the Baltic, is very serviceable for many patients. 

The inhalation treatment is much employed in chronic bronchitis', but we 
should not cherish too high hopes about its use. The best inhalations in dry 
catarrhs are simple steam, a one- or two-per-cent. solution of common salt or 
bicarbonate of sodium, Ems water, etc. In cases with marked secretion, inhala- 
tions of oil of turpentine are most to be praised. The simplest way is to pour a 
teaspoonful of oil of turpentine into hot water and inhale the vapor as it arises. 
The so-called turpentine-pipe, however, is more convenient and more efficacious 
(Fig. 23). This consists of a flask, which is filled to the height of several inches 

with water and then with a layer of oil of tur- 
pentine or of oleum pini pumilionis (P. G.), 
some two centimetres thick. Two glass tubes, 
open at both ends, are passed through the cork. 
One, straight, tube extends down into the layer 
of water : the lower end of the other is free in 
the upper part of the flask. The outer portion 
of this last tube is bent at an angle and is con- 
nected with the mouthpiece through which the 
patient inhales. The formation of turpentine 
vapor is aided by putting the flask in hot 
water. We have treated many patients in this 
way, who, for a number of hours a day, 
" smoked " their turpentine-pipes. 

In treating chronic bronchitis the pneu- 
matic method was considerably employed for a 
time; that is, the patient was made to breathe 
artificially compressed air, or to expire into air 
of less than the atmospheric pressure, by means 
of a movable pneumatic apparatus, as pro- 
posed by Waldenburg and others. Of late, 
Fig. 23.-Turpentine-pipe. however, this method of treatment has re- 

ceived less favor, inasmuch as actual results 
have fallen decidedly short of the benefit promised. In Ems, Reichenhall, and 
other places special pneumatic cabinets have been arranged, filled with compressed 
air, in which patients remain for varying lengths of time. 

One of the most serviceable remedies in dry chronic bronchitis is a large 
amount of warm drink (pectoral tea, Ems water, Seltzer, etc.). Iodide of potas- 
sium in small doses (gr. iij-v, grm. 0.2-0.3, thrice daily) often acts favorably in 
making a tough secretion fluid. Of expectorants, ipecac and apomorphine are 
most recommended in this form of bronchitis. For distressing cough we may 
give Dover's powder, morphine, or codeine. In bronchial blennorrhoea we know 
empirically that the internal use of balsams causes a distinct diminution of the 
secretion. Oil of turpentine is the most active, and may be given internally in 
gelatine capsules, or mixed with milk, in doses of ten or fifteen drops three or 
four times a day. After each dose of turpentine we should give a glass of 
milk. Lepine, G. See, and other French physicians recommend terpine as still 
more effectual. This is a derivative of turpentine, and is best employed in pills 
containing a grain and a half (gramme 0.1), of which two or even more are to 
be taken three times a day. It may also be given in solution as follows : Terpine, 
2 \ drachms (grm. 10); alcohol, q. s. ad sol. faciendam; aq. dest., 6 ounces, 6 
drachms (200 grm). Misce. Sig: Two or three tablespoonfuls daily. Myrtol, 
balsam of copaiba, and balsam of Peru are also used internally. The chief ex- 
pectorants are infusion of senega root, liquor ammonii anisatus, etc. We should 




FCETID BRONCHITIS 



167 



be very sparing of narcotics at first, but in severe cases we can not wholly dis- 
pense with them. 

[The iodide of potassium in doses of five to ten grains thrice daily is sometimes 
distinctly curative. An out-door life, free diet, moderate alcoholic stimulus, 
tonics, and woolen clothing do much to promote recovery.] 

Local applications to the chest in the form of embrocations, mustard plasters, 
dry cups, or cool or warm wet compresses are to be used, especially with severe 
dyspnoea, or with pain and a feeling of oppression in the chest. Warm baths are 
very well borne by many patients with chronic bronchitis. Sometimes, too, vapor 
baths, if taken with caution, may be of service, especially in strong and corpu- 
lent patients. In dry chronic bronchitis we often give the patient a sweat in bed. 

In all secondary chronic catarrhs our chief attention, beyond the symptomatic 
treatment of the bronchitis, must be directed to the treatment of the underlying 
disease. If we succeed in once more regulating the heart's action by digitalis 
when there is uncompensated heart disease, or in establishing diuresis when 
there is renal disease, or in improving the general physical condition by proper 
dietetic measures in the corpulent, gouty, alcoholic, etc., we may also in that way 
cause improvement in the existing bronchial catarrh. 



CHAPTER III 

FCETID BRONCHITIS 

(Putrid Bronchitis) 

^Etiology. — By putrid or foetid bronchitis we mean that form of bronchitis in 
which the secretion of the mucous membrane undergoes a putrid decomposition, 
and in which, consequently, the expectoration takes on a peculiar and extremely 
foul odor. The special agents which cause foetid bronchitis are still unknown. 

The opportunity for the agents of putrefaction to enter the bronchi with the 
inspired air is of course often given, but a foetid bronchitis naturally is excited 
only when they can remain there and increase. Foetid bronchitis therefore de- 
velops quite rarely in a previously healthy lung (primary foetid bronchitis). The 
retention and the further development of the bacteria of putrefaction are chiefly 
favored, as we know, by diseased conditions which already exist in the bronchi. A 
great number of cases of foetid bronchial catarrh therefore develop secondarily 
upon other pulmonary affections of longer standing. Thus the expectoration may 
quite suddenly change and take on a foetid character in the course of a chronic 
or rarely of an acute bronchitis or of phthisis. Bronchiectasis {vide infra) great- 
ly favors the development of this putrid change, for in it the retention and stag- 
nation of large amounts of secretion promote and occasion the putrid decom- 
position. If a putrid decomposition of the secretion begins in one part of the 
bronchial system, the further extension of the process follows from direct infection. 

In rare cases putrid bronchitis also develops as a result of an embolic pulmo- 
nary gangrene. 

Symptoms and Course ; Anatomical Changes. — If a foetid bronchitis arises in 
the course of some other chronic pulmonary disease, its appearance may be marked 
by a sudden impairment of the general condition, by high fever, often associated 
with numerous chills, and by an increase of the thoracic symptoms, such as pain 
and cough. The change in the expectoration, the peculiarity of which was first 
accurately described by Traube, is characteristic. The expectoration shows the 
same character in cases of apparently primary foetid bronchitis. 



168 



DISEASES OF THE RESPIRATORY ORGANS 



The sputum has a very repulsive, sweetish, putrid smell. The expectoration is 
usually quite abundant ; the consistency is rather thin. On standing, the sputum 
shows a very marked division into three layers. This division is due to the abun- 
dant serous exudation in the bronchial mucous membrane and to the thin fluid 
character of the expectoration, which permits an unequal division and a settling 
of the solid constituents. The upper layer consists of a very frothy, muco-puru- 
lent stratum, consisting in part of individual masses, from which a number of 
coarser or finer fibers float down into the middle layer. This middle layer con- 
sists of a dirty-green muco-serous fluid. At the bottom of the vessel is found the 
third layer, which is often the thickest, and is composed entirely of pus. It con- 
sists of pus-corpuscles which have sunk to the bottom, and is of a rather thin, 
greasy consistency. With the naked eye we generally recognize a number of 
little whitish-gray plugs and particles in it. These so-called " Dittrich's plugs," 
which are easily crushed under a cover-glass, are quite characteristic. Microscop- 
ically, they consist of decomposed pus-corpuscles, detritus, and bacteria, and 
usually contain very many needles of fat acids arranged in bundles (see Eig. 24). 

We often find also in the sputum large masses of 
fungi, especially great bunches of twisted lepto- 
thrix fibers, which, by an unpracticed eye, may 
readily be mistaken for elastic fibers. The latter 
are, of course, never found in the expectoration 
of a simple foetid bronchitis, but only in the 
deep-seated, destructive processes in the lung, 
like gangrene. On chemical examination of the 
sputum, the ordinary products of putrefaction 
may be found — volatile fat acids, especially 
butyric and valerianic acids, also sulphuretted 
hydrogen, leucine, tyrosine, etc. 
fig. 24-Crystals of fat acids. It is ver y characteristic of many cases of 

foetid bronchitis that the sputum does not have a 
putrid character at all times. Sometimes for days the patient coughs up a simple 
catarrhal secretion, and then all at once comes an outburst of intolerable stinking 
expectoration. This is probably because a circumscribed putrid focus is fre- 
quently shut off, the expectoration coming solely from the other bronchi, where 
there is merely a simple catarrh, until finally the accumulation of putrid secretion 
is all at once coughed up again in large amount by mouthfuls. 

When foetid sputum is coughed up, the patient's breath also becomes very foul- 
smelling, so that he often becomes a burden to his associates. 

The signs which foetid bronchitis gives on physical examination are those of 
an ordinary bronchitis; but it is characteristic of many cases, in distinction from 
ordinary chronic bronchitis, that the physical signs (rales, dry rhonchi) are 
limited chiefly to a definite portion of the lung, usually one lower lobe. In a 
great number of cases we also find signs of consolidation and contraction of the 
lung, of pleurisy, etc., which do not belong to foetid bronchitis as such, but are 
due to complications or sequelae. 

The most frequent of these sequelae is the development of a " reactive " lobular 
inflammation, a genuine pneumonia, which follows a catarrh of the finer bronchi. 
These pneumonias frequently run into gangrene, so that we very often find a 
number of larger or smaller nodules of gangrene besides the extensive foetid bron- 
chitis in the lungs. In many of these cases the foetid bronchitis is certainly 
the primary process, and the development of the nodules of gangrene is sec- 
ondary; yet we shall see later that the reverse may also be true. Eoetid bron- 
chitis and gangrene of the lungs run into each other so often, both clinically and 
anatomically, that there is no sharp line to be drawn between them. If the 




FCETID BEO^ T CHITIS 



109 



nodules are superficial, and reach the pleura, the infection attacks this, and we 
have a purulent or even an ichorous pleurisy. 

The smaller and medium-sized bronchi are almost always found in a condition 
of cylindrical dilatation in old foetid bronchitis. Their mucous membrane is in- 
tensely inflamed, and often ulcerated superficially. On its surface we see in the 
cadaver the greasy purulent masses and the plugs which we find in the expectora- 
tion during life. 

Whatever may .be the case with the general course of foetid bronchitis, its 
beginning is often quite sudden and acute, both in the primary and in the second- 
ary forms, as we have said. The patient is attacked with fever, which may often 
be quite high, and with a stitch in the side, cough, and expectoration. Later, 
the characteristic peculiarities described above appear. The further course of the 
disease is almost always chronic, lasting for years, but subject to many variations. 
Very often manifest improvement, and even apparent recovery, takes place, when 
suddenly there is a new attack of fever and thoracic symptoms. The general 
condition and nutrition of the patient may be quite good for a long time, 
except during the periods of marked exacerbation of the disease. Patients with 
chronic foetid bronchitis often appear somewhat bloated, but also pale and slightly 
cyanotic. Peculiar clubbed thickenings of the terminal phalanges of the fingers, 
or more rarely of the toes, gradually develop, as in many cases of bronchiectasis. 
Slight oedema of the lower extremities is also sometimes present. 

Symptoms referable to other organs may be wholly absent. We see most fre- 
quently disturbances of the stomach, loss of appetite, and nausea, which proba- 
bly comes from swallowing the foetid sputum. Patients also complain of occa- 
sional rheumatic pains in the muscles and joints, which are probably due to an 
absorption of septic matter. In conclusion it must be mentioned that, in fortu- 
nately rare cases of foetid pulmonary disease, pyogenic germs reach the brain by 
metastasis, and give rise to purulent meningitis or cerebral abscess. 

The danger of the disease, apart from the exceptional occurrence just men- 
tioned, lies in the possible extension of the process to the lungs and the develop- 
ment of pulmonary gangrene and its sequela?. We hardly ever find a simple foetid 
bronchitis in the cadaver, but we almost always see other processes besides, which 
have been mentioned above — reactive pneumonia, pulmonary gangrene, pleurisy, 
etc. All these processes develop very readily, and make rapid progress in old, 
decrepit persons, who live under bad hygienic conditions, in whom putrid processes 
in the lungs are frequent. 

The diagnosis of foetid bronchitis is not difficult in itself, for the diagnosis of 
a putrid process in the lung may be made from the stinking sputum alone. It may 
be difficult to decide whether we have to do merely with a foetid bronchitis, or 
with a pulmonary gangrene also. Decisive indications of pulmonary gangrene are 
derived from physical examination — dullness, bronchial respiration, and coarse, 
moist rales, signs of a cavity — and also the discovery of elastic fibers and frag- 
ments of parenchyma in the expectoration. 

The prognosis must be made with care in every case of foetid bronchitis. If 
the external circumstances of the patient are favorable, he may remain in toler- 
able health for years. We must always be prepared for the appearance of new 
exacerbations of the disease and of affections of the lung itself, and must also 
bear in mind the rarer sequehe (empyema, abscess of the brain). 

Treatment. — The chief aim of treatment must be to bring the putrid pro- 
cesses in the bronchi to a stand-still by the death of the agents of putrefaction. 
The difficulty of fulfilling this task lies in the impossibility of getting the disin- 
fecting material to act on the bronchial mucous membrane in the necessary 
amount and concentration. ISTevertheless, we can, without doubt, at least relieve a 
foetid bronchitis and keep it in check by the judicious use of inhalations. Inhala- 



170 



DISEASES OE THE EESPIEATOEY OEGAXS 



tions of a two-per-cent. solution of carbolic acid are most useful, given for five 
or ten minutes several times a day. These, however, are sometimes not well borne 
if long continued, and they may excite mild symptoms of carbolic poisoning — such 
as headache, malaise, and dark carbolic urine. We have often used with good re- 
sults the " carbolic mask " recommended by Curschmann, a kind of respirator 
fastened in front of the nose and mouth, containing cotton in a special receptacle 
impregnated with carbolic acid, equal parts of carbolic acid and alcohol, or other 
remedies such as turpentine or creasote. Many patients can wear these masks, 
with occasional interruptions, for many hours a day. Besides carbolic acid we 
may use inhalations of turpentine (turpentine-pipe or vapor), oleum pini pumil- 
ionis, creasote, etc. The internal use of these and similar remedies also seems fre- 
quently to be of service in putrid bronchitis. We recommend especially the in- 
ternal use of turpentine (in gelatine capsules), myrtol (also in gelatine capsules), 
also terpine hydrate (six to ten two-grain [gramme 0.1] pills a day), creasote, etc. 

In other respects all the general hygienic and symptomatic methods of treat- 
ment recommended for common chronic bronchitis (expectorants, narcotics, 
climatic health resorts, etc.) are also useful in foetid bronchitis. The sputum 
should be disinfected by putting strong carbolic acid, etc., into the sputum-cup to 
lessen the bad odor. It is a very good plan to keep the carbolic spray at work in 
the patient's room as often and as long as possible ; or the air may be impregnated 
with oleum pini pumilionis. 



CHAPTEE IV 

CROUPOUS BRONCHITIS 

(Fibrinous or Pseudo-membranous Bronchitis) 

Croupous bronchitis is a peculiar form of disease of the bronchial mucous 
membrane, of very rare occurrence, in which there is a formation of extensive 
fibrinous patches in the bronchi. Only that form of croupous bronchitis which 
occurs primarily in the bronchi is to be considered here, and not the secondary 
form, which on the one side is associated with diphtheria in the pharynx and 
larynx, and on the other with croupous pneumonia. 

The aetiology of the disease is as yet wholly unknown. Erom analogy with 
other well-known croupous inflammations of mucous membranes, we must look 
here for some noxious influence which destroys the epithelium, but up to this time 
we are entirely ignorant of its character. Individuals in youth and middle age, 
somewhere between ten and thirty years old, are the chief victims. Men are 
attacked somewhat more frequently than women. The disease comes on either in 
persons who were previously healthy — the essential fibrinous or croupous bron- 
chitis — or in those who have already suffered from some other disease, especially 
some chronic pulmonary affection — the symptomatic, secondary croupous bron- 
chitis. It is not certain whether the last-named cases have the same ^etiological 
relations as the cases of genuine primary fibrinous bronchitis. Fibrinous bron- 
chitis has been observed in the course of typhoid fever and other acute infectious 
diseases. 

Symptoms and Course. — Primary fibrinous bronchitis occurs in two forms, 
acute and chronic. The acute form begins quite suddenly, with fever, cough, pain 
in the chest, and as a rule severe dyspnoea. The fibrinous coagula, which alone 
render the diagnosis possible, appear in the expectoration either at once, or after 
the existence for some days of what is apparently simple catarrhal bronchitis. 

These coagula form complete casts of the bronchi, and are more or less branch- 



CEOUPOUS BEOXCHITIS 



171 



ing. They are of a whitish color and of quite a dense, elastic consistency. The 
main stem may be a centimetre thick, and from it the further ramifications extend, 
dividing dichotomously. The largest casts are ten or fifteen centimetres long. 
On section, we usually find a free lumen within, and generally recognize a definite 
laminated structure in the membrane. In many places they are enlarged and 
swollen. Microscopically, we find white blood-corpuscles in and upon the hyaline 
ground-substance of the casts, and also red blood-corpuscles, sometimes epithelial 
cells, and quite often the peculiar pointed octahedral crystals which are also found 
in the expectoration in bronchial asthma (vide infra). The so-called "spirals" 
(vide infra) have also been found in the expectoration of fibrinous bronchitis. 
Chemically the casts apparently consist of coagulated albumen. It is doubtful 
whether they actually consist of fibrine. Weigert's fibrine stain does not affect 
them. Their solubility in alkalies, especially in lime-water, is of therapeutic 
importance. 

On coughing, the patient usually raises a simple mucous or muco-purulent ex- 
pectoration besides the casts, and in this sputum the casts are imbedded. They 
are often first discovered- by pouring the whole amount of sputum into water, 
when they unfold and spread out. The expectoration also contains not infre- 
quently a slight admixture of blood. 

The subjective symptoms of the patient may be very violent. The dyspnoea 
sometimes attains a high and alarming degree. It ceases when a large cast is ex- 
pectorated after a severe paroxysm of coughing. Such attacks may recur every 
day or two. In other cases, however, the subjective symptoms are comparatively 
slight. 

Physical examination of the lungs reveals little that is characteristic. In un- 
complicated cases percussion shows nothing abnormal, or at most the signs of an 
acute emphysema. Auscultation gives the ordinary signs of bronchitis, not char- 
acteristic in themselves, such as rhonchi, or moist rales. If a large bronchus is 
plugged, the respiratory excursions and the respiratory murmur are almost en- 
tirely absent in the corresponding portion of the lung, but after the expectoration 
of a cast the murmur becomes once more audible. 

The duration of acute cases is sometimes only a few days, at most a few weeks. 
In favorable cases the fever, which at times is quite high, soon disappears, the 
respiratory symptoms grow milder, the expectoration of the casts ceases, and there 
is a complete and permanent recovery. In severe cases, however, death often 
ensues with all the symptoms of suffocation. The acute form sometimes becomes 
chronic, but this is rare. 

The chronic form of fibrinous bronchitis may last for years. Usually the con- 
dition grows worse periodically, at varying intervals of time, and at each exacer- 
bation casts are expectorated, while in the interval there is apparently merely a 
simple bronchial catarrh. Some observations are also recorded in medical litera- 
ture of persons who have expectorated these casts at intervals for years without 
any special disturbance of their health or their nutrition. In some cases other 
chronic pulmonary affections, such as tuberculosis, finally develop. 

The pathological anatomy of fibrinous bronchitis is not yet satisfactorily 
known on account of the rarity of the affection. The changes in the lungs 
found at the autopsy of fatal cases have usually been complications, such as pneu- 
monia, pleurisy, or tuberculosis, which stood in no direct relation to the fibrinous 
bronchitis. A loss of epithelium has been discovered in some cases in the parts 
of the bronchial mucous membrane that were attacked. 

Prognosis. — In all acute cases the prognosis should be guarded, for we know 
that about one fourth of the cases terminate fatally. The chronic cases, as has 
been said, are usually very protracted and are subject to frequent exacerbations, 
but they differ from the acute cases in being much less dangerous. 



172 



DISEASES OF THE EESPIRATOEY ORGANS 



Treatment. — We make special use for inhalations of those remedies which, as 
we have said, have power to dissolve the casts. We usually employ a two- to five- 
per-cent. solution of carbonate or bicarbonate of sodium, and above all lime- 
water, either pure or diluted with an equal volume of water. The internal 
administration of iodide of potassium, in doses of twenty to forty-five grains 
(gramme 1.5-3.0) a day, proves of advantage in many cases. Energetic inunction 
with mercurial ointment is sometimes of service. Expectoration of the casts may 
be aided in many cases by such expectorants as senega and benzoic acid, or by 
the timely use of emetics. We do not know any remedies which can prevent a 
return of the attacks in the chronic form. The treatment, except at the time of 
the attacks, is the same as in ordinary chronic bronchial catarrh. 



CHAPTER V 

WHOOPING-COUGH 

{Pertussis. Tussis convulsiva) 

^Etiology. — By the name " whooping-cough " we mean a specific disease of the 
mucous membrane of the air-passages, which is seen chiefly in children, and is 
characterized by a peculiar violent and paroxysmal cough. Sporadic cases are of 
almost constant occurrence in large cities, but the disease often appears in epi- 
demic outbreaks. Epidemics of whooping-cough follow epidemics of measles 
with remarkable frequency. 

Whooping-cough is without doubt contagious, and therefore often attacks one 
child after another in the same family. Kindergartens, orphan asylums, and day- 
nurseries aid very much in extending the disease. The contagious element seems 
to be connected with the air expired by the patient, particularly with the secretion 
from the mucous membrane expectorated after coughing. Children are most sub- 
ject to an attack up to the age of six years; from that age the liability to the 
disease decreases rapidly with increasing years. Whooping-cough is seen, indeed, 
in adults, but it is quite rare, and almost always without the pronounced features 
of tussis convulsiva. 

The epidemic onset, the contagiousness, and the whole course of the disease 
favor the theory of its infectious nature. The presence of the organisms which 
are supposed to be the poison of the disease has not yet been certainly demon- 
strated, although many have claimed to discover characteristic bacteria in the 
sputa of patients. These assertions, however, do not harmonize with one another, 
and lack well-attested and methodical proof. If a patient has once had the disease, 
he is almost invariably safe from a second attack. 

Symptoms and Course of the Disease. — Whooping-cough begins with the 
symptoms of a catarrh of the trachea and bronchi, whicli develops more or less 
rapidly, and which at first often shows nothing characteristic. We can at this 
period make a tolerably probable diagnosis only at a time when an epidemic is 
prevailing, or in case the child's associates have already been attacked with the 
disease. The cough is often very persistent, obstinate, and severe at the begin- 
ning, but it does not yet come on in distinct paroxysms. Examination of the 
chest shows nothing peculiar except a few rhonchi. There is often a coryza, with 
frequent sneezing, and there is sometimes a mild conjunctivitis. The child is 
restless and feverish, especially toward night. The temperature may repeatedly 
reach 103° or 104° (39°-40° C.) in this initial fever. The duration of this first 
so-called catarrhal stage varies, but it usually lasts a week or ten days. 



WHOOPING-COUGH 



173 



The catarrhal stage gradually passes into the second, convulsive stage, without 
any sharp boundary. The cough becomes more violent, and comes on in the 
separate paroxysms of whooping-cough which are characteristic of the disease. 
We do not know the particular reason why the cough has this paroxysmal char- 
acter, but a nervous factor probably plays the chief part in it. 

The peculiarity of the attack consists in the violent, paroxysmal fits of cough- 
ing, which are from time to time interrupted by deep, long-drawn, loud, and 
shrill inspirations, due to the occurrence of a spasmodic contraction of the glottis. 
Exceptionally there are cases without this loud whistling inspiration. The child 
becomes markedly cyanotic during the attack, the veins in the neck swell, and 
tears come into the eyes. Haemorrhage into the conjunctiva, nose-bleed, and in 
some cases haemorrhages into other organs, as the ear and the skin, often come 
on as a result of this stasis. Vomiting very often occurs either during a 
paroxysm or at its close. Involuntary evacuations of urine and faeces may also 
follow from the violent contraction of the abdominal muscles. Exceptionally we 
observe still more severe symptoms with a paroxysm : a complete spasmodic cessa- 
tion of respiration with imminent danger of suffocation, or sometimes general 
convulsions. In two cases we have seen hemiplegia in children which, accord- 
ing to the positive statements of their parents, came on suddenly during a severe 
attack of whooping-cough. It is still undetermined whether these " whooping- 
cough hemiplegias " are due to an actual cerebral haemorrhage or whether they 
come from the enormous venous stasis in the brain. 

The paroxysms vary with the severity of the disease, frequently appearing 
ten or fifteen times in twenty-four hours; sometimes with greater frequency — - 
fifty times or more. They also occur at night as often or even oftener than in 
the daytime. They come on either spontaneously or from some special predis- 
posing cause. The attacks which come on during eating cause the most dis- 
turbance, because the food taken is almost always vomited again. In chil- 
dren with whooping-cough we can often excite a spasm at any time, and this 
is important in diagnosis — by putting a spatula in the mouth, by pressing on 
the larynx, or by making the child cry. If there are several children with 
whooping-cough in the same room and a paroxysm attacks one of them, the 
others, as a rule, soon begin to cough too. Some prodromal symptoms often pre- 
cede the peculiar paroxysm, such as general uneasiness, rapid respiration, or 
vomiting. At the end of a paroxysm many children are very feeble and exhausted, 
but others recover rapidly, and are playing again quite briskly a few minutes after. 

In general the child feels quite well in the interval between the paroxysms, 
but the effects of the violent attacks of coughing may of course often be seen. 
Besides the occasional haemorrhages into the conjunctiva, we find the eyelids 
somewhat swollen, their veins dilated and blue, and showing through the skin. 
Many children grow very thin from the repeated vomiting. A small ulcer is 
quite frequently formed on the fraenum of the tongue, the origin of which is 
to be referred to mechanical causes. The tongue is violently protruded in the 
severe paroxysms of coughing, and the fraenum is thus torn, or injured by the 
sharp lower incisors. 

Physical examination of the lungs shows nothing abnormal in uncomplicated 
cases except a few moist rales or rhonchi. Sometimes the rhonchi are wanting, 
or are present in small numbers only a short time before a paroxysm, but in other 
cases an intense diffuse bronchitis is developed, which often leads to the develop- 
ment of a lobular pneumonia (vide infra). Sometimes, but not always, there is 
an acute catarrhal inflammation of the bronchi, and especially of the posterior 
wall of the larynx. 

The fever, which is usually present in the first or catarrhal stage, is absent in 
the convulsive stage. The child is free from fever for the most part. We often 



174 



DISEASES OE THE EESPIKATOEY ORGANS 



find a slight rise of temperature up to 100° or 101° (38°-38.5° C), but only 
toward night. Higher and more persistent fever points to the development of 
complications, especially on the part of the lungs. 

The convulsive stage seldom lasts less than three or four weeks, and often 
much longer, up to three or four months. The paroxysms gradually become less 
frequent and less violent (stadium decrementi), until they finally disappear 
entirely; but relapses and fresh exacerbations also occur in this stage. A cer- 
tain " irritability " of the bronchial mucous membrane remains for a long time 
after whooping-cough. Finally, however, the disease, in uncomplicated cases, 
goes on to a permanent and complete recovery. 

Complications and Sequelae. — The severe results which sometimes follow 
whooping-cough are probably due in part to the direct action of the specific causes 
of the disease, and in part to complications of a secondary nature whose develop- 
ment is merely favored by the whooping-cough. The most important are complica- 
tions in the lungs. A lobular catarrhal pneumonia often develops after a severe 
bronchitis which involves the finer bronchi. In such cases the respiration be- 
comes hurried and superficial, the fever higher, and the general condition bad 
even in the times between the paroxysms. On examination of the lungs, we hear 
numerous moist rales, especially over the lower lobes; and we can sometimes 
make out dullness on one or both sides, if there is extensive pneumonic infiltra- 
tion. Such cases are always very protracted, and many children succumb, partly 
from the disturbance of respiration and partly from general weakness and in- 
anition. 

Complications in other organs are much rarer. Among the most frequent, are 
attacks of diarrhoea which impair the child's nutrition. Many observers have 
also mentioned the quite frequent occurrence of a croupous or diphtheritic in- 
flammation in the pharynx and larynx in the course of whooping-cough. Finally, 
a case under our own observation may here be mentioned, in which death oc- 
curred with severe nervous symptoms, convulsions, and coma. At the autopsy 
very numerous capillary haemorrhages were found in the brain. 

Pulmonary emphysema is the first thing to be mentioned among the sequelae 
of whooping-cough. From the marked pressure which the severe and frequent 
outbursts of coughing exert from within upon the alveoli of the lungs, they gradu- 
ally become dilated. An acute lobular emphysema (" acute pulmonary infla- 
tion ") is set up, which sometimes passes into a typical chronic pulmonary emphy- 
sema (vide infra). Chronic bronchial catarrh may also remain for a long time 
after an attack of whooping-cough. We have already stated (see page 163) 
that many incurable cases of chronic bronchitis in adults are to be referred to 
an attack of whooping-cough in childhood. 

A third important sequel of whooping-cough is pulmonary tuberculosis. The 
bronchitis and lobular pneumonia which occur during whooping-cough some- 
times do not improve, especially in weak children with a tubercular tendency. 
The fever continues high, the child grows thin, and constantly becomes more and 
more miserable. At the autopsy we find cheesy nodules in ^he lungs, cheesy bron- 
chial glands, and at times tuberculosis of other organs. These cases signify that 
when a tubercular infection is present, but is still latent, the whooping-cough acts 
as an exciting cause for the outbreak of the disease, or that a greater receptivity 
to infection with tubercular poison is created by the whooping-cough. Mobius 
has lately reported the occurrence, in a few cases, of paralysis as a sequel of 
whooping-cough. This usually begins in the lower and extends to the upper 
extremities, and is due apparently to neuritis. 

The diagnosis of whooping-cough can not be made with certainty, as we have 
said, until the second or convulsive stage. It is easy then, however, since the 
characteristic attacks occur in no other affection of the lungs in like manner 



WHOOPING-COUGH 



175 



and with like frequency and duration. If we have no opportunity to observe the 
attack itself, and have to depend upon the description of the friends, the diagno- 
sis is sometimes more uncertain; but the accounts of the occurrence of cough, 
in individual paroxysms associated with vomiting, are usually so characteristic 
that errors are, on the whole, rare. Furthermore, the child between the parox- 
ysms usually presents certain signs : he has a bloated aspect, or we may find 
slight haemorrhages into the conjunctiva, or ulcers on the frsenum of the tongue, 
which make the diagnosis highly probable. Under some circumstances we may 
also make the attempt to bring on the paroxysm artificially (vide supra). In 
adults, as we have said, the attacks are rarely as characteristic as in children. 
There are usually the symptoms of a more or less severe bronchitis with obsti- 
nate paroxysmal cough, but without the characteristic attacks and usually with- 
out vomiting. The diagnosis of whooping-cough therefore rests mainly upon the 
existence of special serological conditions (the co-existence of the disease in 
children, etc.). 

The prognosis is favorable with the majority of children if they are previously 
strong and healthy. Very young children are in more danger than older ones. 
[Under two years there is great danger, and over five scarcely any. It has been 
said that whooping-cough causes one fourth the total mortality of children in 
London. — V.] There is danger if secondary pneumonia develops, and if the gen- 
eral nutrition and strength of the child suffer. As soon as the diagnosis is certain 
we must call the attention of the parents to the probable long duration of the dis- 
ease. Regard must also be paid to the possibility of the development of sequelae, 
especially in weak children suspected of tuberculosis. 

Treatment. — Since the disease is protracted and is not devoid of danger, it is 
our duty, when an epidemic of whooping-cough prevails, to guard children from it 
as far as possible. If one child in a family is taken ill, the other children must 
be rigorously kept away from him. If circumstances permit, we should prefer 
to send them away to another place free from whooping-cough. 

With regard to the treatment of the disease, we must first endeavor to fulfill 
general dietetic and hygienic indications. The child should breathe good, pure 
air, and for this reason it is often advisable to transfer the patient to a larger 
room, with as much air and sunlight as possible. The atmosphere should not be 
too dry, and it is advisable to employ a spray of water (carbolic solution) fre- 
quently, or to hang up moist sheets in the room. In good weather the child 
should be out of doors a large part of the time, provided fever has ceased. City 
children are to be sent, if possible, into the country. The food should be good and 
nourishing, but dry and crumbly articles should be avoided, being apt to excite 
cough. Warm or lukewarm baths frequently prove very beneficial, particularly 
when there is considerable bronchitis, as they lessen the danger of a lobular 
pneumonia. 

The medicinal treatment of whooping-cough has not yet shown brilliant 
results despite the large number of remedies recommended. During the ca- 
tarrhal stage it is usually sufficient to give a simple expectorant (ipecac, etc.) 
and plenty of warm drink. In the convulsive stage the best remedies to try are 
quinine, antipyrine, belladonna, bromide of potassium, and bromoform. The 
latter has been much recommended of late. Quinine is given in powders of one 
and a half to eight grains (grm. 0.1 to 0.5) several times a day, either in capsules or, 
in the case of smaller children, with chocolate. The earlier this remedy is em- 
ployed the more prompt is said to be its beneficial influence. Antipyrine is at 
present used more frequently than quinine, and in doses of four to eight grains 
(grm. 0.25-0.5) several times a day it often produces distinct improvement. Bella- 
donna is prescribed in powders containing one twelfth to one sixth grain (grm. 
0.005 to 0.01) of the extract of belladonna, giving three to five such powders a 



176 



DISEASES OE THE RESPIRATORY ORGANS 



day. This remedy has often seemed to the author to diminish the mimber and 
violence of the paroxysms. Bromide of potassium is employed in an aqueous solu- 
tion in the dose of fifteen to forty-five grains per diem (grm. 1 to 3). Its 
efficacy is probably due to its power to diminish reflex excitability. The same 
drug- employed in an atomizer often has a palliative effect. Bromoform is the 
remedy most used of late; two to five drops or more are given several times a 
day in sweetened water or fruit juice. It is readily taken, and it seems to act 
favorably both on the severity of the individual attacks and on the whole course 
of the disease. 

If the paroxysms are very violent we may cautiously administer small doses 
of morphine or codeia. Inhalations of chloroform and ether have also been 
recommended. The following mixture is a suitable one : 

J$ Chlorof ormi §j (grm. 30) ; 



Sig. One or two teaspoonfuls to be poured upon a pocket-handkerchief for in- 
halation. 

Finally, efforts have been repeatedly made to lessen the frequency and the 
severity of the attacks by anaesthetizing the pharynx and larynx by painting with 
a ten- to fifteen-per-cent. solution of cocaine. Michael advocates the daily in- 
sufflation into the nostrils of powdered benzoin. Neither method of treatment 
has succeeded in establishing itself in practice. 

Sprays of various antiseptic remedies have been frequently employed be- 
cause of the infectious nature of the disease. The practitioner must not expect 
too much from them, however, although they sometimes act well. A one-per- 
cent, or two-per-cent. solution of carbolic acid is most frequently employed for 
inhalation. It may be given several times a day for periods of two or three 
minutes at a time. Next to this, turpentine and benzine are most to be recom- 
mended; of these, twenty or thirty drops are poured upon a sponge previously 
moistened with hot water. Turpentine and especially terpine hydrate (grains 
vij, gramme 0.5, thrice daily) are also given internally. [Farlow and others 
report marked success from spraying the upper air-passages with a two-per-cent. 
solution of resorcine.] 

In very many cases we finally content ourselves with taking good general 
care of the child, and, if the weather permit, with keeping him as much as 
possible in the open air. Eor the treatment of the complications and sequelae 
of whooping-cough the reader is referred to the appropriate chapters of this book. 



Dilatation of the bronchi is not a separate disease, but it is a result of various 
affections of the lungs and bronchi. Nevertheless, we will speak of it briefly in 
this connection since many cases actually present the appearance of a very char- 
acteristic disease. 

We distinguish anatomically the cylindrical and saccular bronchiectases. 
Cylindrical bronchiectasis consists of a uniform dilatation of a bronchial 
tube, and occurs most frequently in the medium-sized, or rarely in the finer 



uEtheris , 

01. terebinthinsB 



§ij (grm. 60); 
oijss. (grm. 10). M. 



CHAPTER VI 



BRONCHIECTASIS 

{BroncJdal Dilatation) 



BRONCHIECTASIS 



177 



bronchi of one or more lobes of the lung. We usually find at the autopsy that, on 
slitting up the bronchi, the point of the scissors can easily be pushed through the 
dilated bronchial tube close up to the pleura. Cylindrical bronchiectasis is usu- 
ally due to a long-continued bronchitis, and develops most frequently in cases of 
emphysema, and also in whooping-cough, measles, and sometimes in phthisis, etc. 
The primary process is probably always the atrophy which follows the catarrh, 
and the diminished resistance of the bronchial walls thus occasioned. The dila- 
tation of the lumen of the bronchus is produced gradually, partly by the trac- 
tion of the thorax during inspiration, and still more by the increased pressure in 
the bronchi due to the frequent and violent fits of coughing, and finally, perhaps, 
by the constant pressure of the stagnating secretion. 

The diagnosis of cylindrical dilatation of the bronchi is only a probable one. 
We suspect that a bronchiectasis has formed if the conditions are fulfilled 
which we know lead to it. In the chronic bronchial catarrh of emphysema we 
judge that there is cylindrical dilatation of the bronchi if the secretion is very 
abundant and comparatively thin, and separates into layers on standing in a 
sputum-cup. The dilatation is usually emptied by a severe paroxysm of coughing, 
such as is apt to occur in the morning if the secretion collects in great quantity 
during the night. Physical examination usually gives numerous, low, fine, and 
medium moist rales, especially in the lower lobes. The respiratory murmur some- 
times loses its vesicular character in marked cylindrical bronchiectasis, and has a 
more indefinite and tubular quality. Sometimes it is quite obscured in the lower 
part of the lung by the abundant rales. 

Saccular bronchiectases are spherical or oval dilatations which are confined to 
a definite portion of the bronchial tube. They may attain a diameter of several 
centimetres. The bronchus passes suddenly or gradually into the dilatation, and 
it is often obliterated so that the bronchiectasis forms a completely closed cavity. 
The wall of a saccular bronchiectasis loses in great measure the character of a 
normal bronchial wall. As a rule it is atrophied to a high degree, the atrophy 
involving not only the mucous glands, but also the muscular fibers, the elastic 
elements, and even the cartilages, so that the bronchiectatic cavities seem lined 
with nothing but a thin membrane. The occurrence of many dilated vessels in 
the walls of a bronchiectasis is due perhaps to an atrophy of the vessel walls and 
is a symptom of great clinical importance (vide infra). In other cases, however, 
we find hypertrophic processes, which involve the connective tissue of the mucous 
membrane, and lead to band-like projections and swellings. Finally, ulcerative 
processes may develop on the inner surface of a bronchiectasis and attack the 
surrounding lung-tissue, and change the bronchiectatic cavity into a typical ulcer- 
ating cavity. 

Only rarely, for example in emphysema, do we find a single saccular bron- 
chiectasis surrounded by tolerably normal lung-tissue. Its origin, then, is to be 
referred to causes like those which have been given above for the much com- 
moner cylindrical bronchiectases. In the great majority of cases we find saccular 
bronchiectases, singly or in large numbers, surrounded by indurated and con- 
tracted lung-tissue. They form one of the complications of "pulmonary con- 
traction" [fibroid phthisis], which is almost always associated with contraction 
of the pleura. Since Corrigan's day we have with good reason looked upon this 
contraction as the chief cause for their origin. By the gradual shrinking and 
retraction of the lung, which as a rule has become adherent to the costal pleura, 
a traction is exerted upon the bronchial walls from without to which they grad- 
ually yield. Stagnation and pressure of the secretion work at the same time in 
like manner to dilate the bronchial tube; Thus arises the frequent combination 
of pulmonary contraction with the formation of bronchiectases. This combina- 
tion is usually unilateral, and involves the whole lung or only one of the upper 
12 



178 



DISEASES OF THE RESPIRATORY ORGANS 



or lower lobes. Our knowledge is still very defective as to the cause of this 
" chronic interstitial pneumonia " leading to contraction. It often seems to be 
a quite insidious and gradual circumscribed chronic inflammatory process; in 
other cases by careful inquiry we can discover a previous acute process (pneu- 
monia, severe acute bronchitis, etc.) as a starting-point for the disease. Inha- 
lation of dust often plays a part in the causation. 

We sometimes see the form of pulmonary contraction in question developing 
as a result of pleurisy. Laennec first advanced the opinion that in such cases the 
pleurisy was the primary trouble, and that from it an interstitial inflammatory 
process attacked the connective tissue of the underlying lung and led to contrac- 
tion and then to the formation of bronchiectases. Unfortunately we lack further 
confirmatory evidence in this regard. 

Most saccular bronchiectases are situated in the lower lobes, but genuine 
bronchiectasis is not very rare in the upper lobes. As a rule, the trouble is uni- 
lateral, or at least affects one side the most. Sometimes large portions of a 
lung may be completely transformed into a cicatricial tissue studded with many 
bronchiectatic cavities. 

" Pure cases " of bronchiectasis have nothing to do with tuberculosis. Before 
the discovery of the tubercle bacillus there was, of course, confusion between 
bronchiectatic and chronic tubercular contraction of the lungs; but we must 
remember that, under some circumstances, chronic tuberculosis may lead to the 
formation of bronchiectasis, and that, on the other hand, in bronchiectatic pro- 
cesses there is not infrequently a secondary development of tuberculosis. There 
are cases in which it is hard to decide, even at the autopsy, whether an exist- 
ing chronic contraction in a portion of the lung, with induration of tissue and 
the formation of bronchiectasis, was originally tubercular or of some other 
nature. 

The symptoms caused by saccular bronchiectasis are derived in part from phys- 
ical examination and in part from observation of the sputum, and of the gen- 
eral course of the disease. If great bronchiectatic cavities lie near the chest- 
wall, they may give the same physical signs that we shall learn to recognize 
later in the description of tubercular cavities. Bronchiectases lying within 
the lung, however, are often devoid of definite physical signs, so that at most 
we may suspect them from other symptoms, such as the peculiarities of the 
sputum. The more abundant the formation of bronchiectases the more does 
the respiration lose its vesicular character and become harsh and finally bron- 
chial. Inasmuch as there is usually a very considerable secretion of mucus, we 
generally find, upon auscultation, abundant medium and even coarse moist 
rales. The percussion note over the bronchiectatic portion of the lung is usually 
dull or dull-tympanitic, a result of the chronic interstitial pneumonia about the 
bronchiectasis. The whole thorax near an extensive bronchiectasis is often much 
retracted and distorted. 

The expectoration is, as a rule, very abundant, and it is often raised by large 
mouthfuls. On standing, as a result of its thin fluid character, it exhibits a dis- 
tinct division into an upper frothy, muco-purulent layer, a middle muco-serous 
layer, and a lower purulent layer. It usually has a peculiar stale, sweet- 
ish odor, but it may be foetid. The latter is almost always associated with 
stagnation of the secretion. So long as the expectoration is loose and easily 
evacuated, it is not foetid and the patient feels well. Then a cessation of the 
expectoration may ensue. The patient feels poorly, there may be a slight rise 
of temperature, and the expectoration becomes scanty and has a stinking foetid 
character. Periods of improvement may thus alternate with exacerbations. It 
is a favorable sign when the amount of the expectoration decreases, provided that 
it does not become foetid and that the patient does not feel worse. Since bronchi- 



BRONCHIECTASIS 



179 



ectasis may give rise to a permanent foetid bronchitis, ' and since, on the other 
hand, as we have said, foetid bronchitis itself often leads to the formation of bron- 
chiectasis, we can understand the manifold inter-relations and transitions which 
the two forms of disease present. 

The not infrequent pulmonary hEemorrhages in bronchiectasis are of great 
clinical importance. They are due to rupture of the dilated vessels (vide supra) 
in the walls of the bronchiectasis. They may also be due to ulcerative processes. 
Slight precursors may precede a severe haemoptysis. The haemorrhage may be 
very abundant, and it may be repeated during a long period — several weeks — so 
that the patient becomes extremely anaemic. Finally the haemorrhages cease and 
the patient improves quite rapidly. Such attacks of haemoptysis may be repeated 
very often in the course of the year. When we hear comparatively well-nourished 
patients with lung disease say that they have suffered for years from frequent 
and severe haemoptyses, we can usually infer, from such statements, that there 
is a saccular bronchiectasis. 

The whole course of the disease is very variable, but it usually lasts for many 
years. It is doubtful whether a saccular bronchiectasis can actually be cured; 
but if no more serious sequelae occur, many patients may live for years in a 
tolerable condition, and may even reach an advanced age. The general nutrition 
often remains very good, although a certain very characteristic, anaemic, cyanotic 
tinge of the skin gives even to corpulent patients an unmistakable morbid ap- 
pearance. A very characteristic sign is that the terminal phalanges of the fingers 
gradually become clubbed and thickened, and the nails are much bent. This 
peculiar trophic change, the cause of which is still unexplained, is much rarer in 
chronic tubercular processes (vide infra). 

The diagnosis of extensive formation of bronchiectasis in the lungs is in 
many cases easy, but in other cases it may present great difficulties. In order 
to avoid confounding it with chronic tuberculosis the following should be espe- 
cially considered : In bronchiectasis the patient does not present a true cachexia ; 
he is usually somewhat cyanotic and pale at the same time. The layer of 
subcutaneous fat often remains well marked for a long time. The terminal 
phalanges of the fingers are often clubbed, as in foetid bronchitis. Fever is usually 
absent, unless there are some special complications. The expectoration is more 
abundant and more distinctly stratified than is often seen in tuberculosis; and, 
most important of all, it contains, of course, no tubercle bacilli. Finally, bron- 
chiectatic conditions ordinarily (though, of course, not always) develop in a lower 
lobe, while tuberculosis is apt to affect an upper lobe first. 

We will refer to the appropriate chapters for the relations of bronchiectasis 
to foetid bronchitis, pulmonary gangrene, etc. 

The treatment is never directed against the bronchial dilatation as such, but 
toward its causes or sequelae. The treatment of bronchiectasis, therefore, coin- 
cides with the treatment of chronic bronchitis, foetid bronchitis, etc. Besides 
general hygienic measures (climatic resorts), balsamic remedies (turpentine, etc.) 
are chiefly used. Any pulmonary haemorrhage is to be treated symptomatically in 
the same way as haemoptysis in pulmonary tuberculosis (q.v.). 



180 



DISEASES OF THE EESPIEATOEY ORGANS 



CHAPTER VII 
STENOSIS OF THE TRACHEA AND BRONCHI 

1. Tracheal Stenosis 

etiology. — Stenosis of the trachea may be caused either by diseases in the 
vicinity of the trachea, or by diseases of the trachea itself. The first-named 
mode of origin is the more frequent. To this are due all the stenoses of the 
trachea from compression. Enlargements of the thyroid gland from simple 
struma and new growths, aneurisms of the arch of the aorta and of the in- 
nominate artery, tumors and abscesses in the anterior mediastinum, swelling of 
the lymph-glands at the bifurcation of the trachea, abscess on the anterior sur- 
face of the cervical vertebras, etc., may exert so great a pressure on the trachea 
from without that its lumen is made narrower. Besides the direct action of pres- 
sure, in most cases, a gradual atrophy and a softening of the rings of cartilage, 
due to pressure, sometimes play an important part, according to Rose, in the 
occurrence of stenosis. A collapse of the trachea may arise from this "flaccid 
softening," which may come on quite suddenly, and may cause many of the cases 
of sudden " death due to goitre." 

Changes in the trachea itself leading to stenosis are quite rare. Cicatricial 
stenosis as a result of syphilitic ulcerations is relatively the most frequent. New 
growths in the trachea are also to be mentioned, such as polypi and cancer, 
the latter almost always having invaded the trachea from the adjacent parts. 
Very rarely acute and chronic inflammatory processes such as perichondritis lead 
to a swelling of the mucous membrane sufficient to cause stenosis. In conclusion, 
we may mention that stenosis of the trachea may be due to the presence of foreign 
bodies. 

Symptoms. — If the stenosis is so extreme that there is a real hindrance to 
respiration, a very striking modification of the breathing occurs. It is difficult 
and labored, and is performed only by the help of the accessory muscles. Both 
expiration and inspiration are protracted, long drawn, and accompanied by a loud 
stridor. In many cases inspiration is more difficult than expiration, so that there 
is accordingly a preponderating inspiratory dyspnoea, and the number of respira- 
tions a minute is diminished. If the entrance of air into the lungs is incomplete 
in spite of the lengthening of the respirations, we see an inspiratory retraction of 
the lower part of the thorax, and sometimes of the throat and the supra-clavicular 
fossae. In tracheal stenosis the larynx, however, shows little or no to-and-fro 
movement on respiration. This fact is of value in diagnosis in distinguishing 
tracheal from laryngeal stenosis, for in the latter the respiratory movements of 
the larynx are quite well marked. 

We sometimes notice in the pulse during inspiration a marked fall in tension 
and in the height of the pulse-wave, the pulsus paradoxus. With the sphygmo- 
graph we can show still more plainly the changes in blood-pressure, which vary 
quite markedly with the respiration. The frequency of the pulse is usually a 
little increased, but sometimes it is diminished. 

The symptoms of the disease just described may form so characteristic a 
picture that we can recognize it at the first glance. More precise information 
as to the seat of the stenosis, or the accurate differentiation of tracheal stenosis 
from the very similar picture presented by laryngeal stenosis, demands a direct 
laryngoscopic examination of the larynx and trachea, which, of course, is hardly 
practicable in a patient with a high degree of dyspnoea. 



BRONCHIAL ASTHMA 



181 



2. Bronchial Stenosis 

Narrowing of a primary bronchus, which is the only form to be mentioned 
here, arises most frequently as a result of the presence of foreign bodies — e. g., 
bits of bone, plum-stones, buttons, etc. These may enter the air-passages by 
means of a deep inspiration, especially while eating, or during sleep. We know 
that foreign bodies get into the right bronchus, which is wider, somewhat more 
frequently than they do into the left. Stenosis of the main bronchi from pres- 
sure also arises from aneurisms of the aorta, mediastinal tumors, enlarged bron- 
chial lymph-glands, etc. Stenosis of the left bronchus from the pressure of the 
greatly dilated left auricle has been observed in mitral stenosis. 

The symptoms are not equally distinct in all cases, and they depend upon the 
shutting off of the corresponding part of the lung. The dyspnoea is usually very 
evident, especially in acute cases. The respiratory excursions are much less on 
the affected side than on the sound side. The percussion-note remains clear; 
sometimes it is very deep, because the lung beyond the narrowed bronchus is con- 
stantly inflated. Auscultation shows complete absence of the vesicular respiratory 
murmur. We either hear nothing or we sometimes hear over the whole side a 
loud whistling or humming sound, the vibration of which can in some cases be 
felt by the hand applied to the chest-wall. The vocal fremitus is diminished on 
the affected side. A vicarious emphysema soon develops in the other lung. 

Lobular pneumonia frequently develops as a result of the entrance of foreign 
bodies into a bronchus, because the agents of inflammation have entered at the 
same time with these bodies, and, as the expectoration can be evacuated only with 
difficulty, and hence is more or less stagnant, these irritants can readily establish 
themselves in it. In stenosis from pressure the condition may of course be modi- 
fied in many ways by the primary disease. 

The prognosis and treatment of tracheal and bronchial stenosis depend en- 
tirely upon the nature of the primary disease. General statements as to treat- 
ment, therefore, need not be given here. A direct mechanical treatment of tracheal 
stenosis in appropriate cases, such as cicatricial stenosis, may be undertaken ac- 
cording to the different modes of dilatation above enumerated. The methods 
for removing foreign bodies from the larger air-passages belong to the domain of 
surgery. The employment of an emetic has met with distinct success in such 
cases, but it is not without danger, for the foreign body may wedge itself into the 
glottis during the act of vomiting and occasion danger of instant suffocation. 



CHAPTER VIII 

BRONCHIAL ASTHMA 

{Exudative Bronchiolitis. Asthmatic Bronchiolitis) 

Definition and Causes of the Disease. — Bronchial asthma is the name we 
give to a morbid condition whose chief symptom is a special form of severe 
dyspnoea. The characteristic features of the dyspnoea of bronchial asthma are, 
first, that it occurs in paroxysms, or at least that it grows worse paroxysmally, 
and, second, its peculiar manner of onset. The special character of the dyspnoea 
of bronchial asthma is explained by the fact that every true bronchial asthma is 
due to an extensive and quite rapid contraction of the smaller and smallest bron- 
chial branches. This always gives rise to a form of distress for breath which differs 
materially from every other form of dyspnoea. 



182 DISEASES OF THE BESPIBATOBY OBGANS 



The question as to the origin of bronchial asthma coincides, then, with the 
question as to the origin of that extensive contraction of the bronchioles which 
is the root of the disturbance. There seems to us no doubt that the latter 
should not always be referred to the same cause. We must therefore distinguish 
several forms of bronchial asthma, which, as a result of the similar conditions 
of dyspnoea, have many points of clinical similarity. 

Formerly the so-called nervous bronchial asthma was considered to be the 
commonest form. Asthma in many cases was regarded as a pure " neurosis," due 
to paroxysms of tonic spasm of the circular muscles in the small bronchi (Trous- 
seau, Biermer). The sudden contraction of the bronchi and the consequent 
dyspnoea could, in fact, be very well explained in this way. The only thing left 
unexplained is the conditions causing the sudden onset of such a spasm. 

Many recent observations (Yoltolini, B. Frankel, Hack, etc.) have rendered it 
extremely probable that, in at least a part of the cases, reflex processes play a 
great part, and especially reflex processes from the nasal mucous membrane. 
Many patients with asthma have been found to have marked changes in the nose, 
most frequently enlargement of the so-called erectile bodies on one or more tur- 
binated bones, also nasal polypi, chronic catarrh of the mucous membrane, etc. 
The evidence of the close connection between the attacks of bronchial asthma 
and those morbid processes rest, in the first place, upon the clinical fact that the 
asthmatic attack usually begins with a marked increase of the nasal symptoms (a 
stuffed nose, greater secretion, etc.) ; and, in the second place, especially upon the 
important therapeutic observation that in such cases the asthma may be made 
permanently to disappear by removing the nasal trouble. 

Accordingly there can hardly remain a doubt that in such instances it is proper 
to speak of a reflex bronchial asthma. Certain observations which have long been 
familiar are probably connected with these facts we have mentioned — namely, 
the cases in which persons are said to have genuine asthmatic attacks from 
particular odors (ipecac, burnt coffee, violets, etc.). This is probably a reflex 
process coming from the nose. Similar relations doubtless exist in the so-called 
hay asthma (see page 135). 

Although we may not question the occurrence of a reflex bronchial asthma, 
yet we can not regard the theory that it is caused by a tonic spasm of the bron- 
chial muscles as absolutely proved. So far as our own experience goes, even in 
" reflex asthma " there are usually during the attack plain signs of an abnormal 
secretion or exudation in the smaller bronchi (expectoration, bronchitic rales, 
etc.) ; but this condition requires further explanation than by the assumption of 
a muscular spasm. We are therefore of the opinion that we should not wholly 
reject the hypothesis advanced by many authors (Weber, Stork, Frantzel). Ac- 
cording to this hypothesis, acute stenosis of the bronchioles is caused much less 
by a muscular spasm than by an acute dilatation of the blood-vessels and acute 
swelling of the mucous membrane. Such a " vaso-motor " change may very well 
be excited by reflex causes, and it would much better explain the conditions in 
an asthmatic attack than would the assumption of a purely muscular spasm. 

It is doubtful whether genuine bronchial asthma may be due to a reflex from 
any other organ than the nose. The most credible statements are those in regard 
to the connection between bronchial asthma and disease of the pharynx (hyper- 
trophy of the tonsils), but the statements in regard to the occurrence of asthmatic 
attacks in diseases of the ear, stomach ("dyspeptic asthma"), intestines, female 
sexual organs, etc., are to be regarded with the greatest skepticism. In these cases 
there is usually confusion between true asthma and other conditions of dyspnoea 
(hysterical asthma, conditions of cardiac weakness, etc.). 

Although, from what has been said, it follows that the occurrence of a nervous 
reflex asthma can not be questioned, our knowledge as to the onset of nervous 



BEOKCHIAL ASTHMA 



183 



asthma as a primary affection is still very vague. At- any rate the cases which, 
after careful investigation, allow no other explanation are very rare. It is also 
doubtful whether we have to do with a primary bronchial spasm or with vaso- 
motor conditions. The theory formerly maintained by many writers, that a tonic 
spasm of the diaphragm could be the cause of a true asthmatic attack, is at present 
almost universally abandoned. This theory is contradicted by the occurrence of 
manifest respiratory movements of the diaphragm during the asthmatic attack. 
These movements have also been demonstrated of late by the.Rontgen rays. 

Apart from the reflex asthmatic conditions, most cases of so-called " bronchial 
asthma " are undoubtedly due to a primary catarrhal inflammation of the smallest 
bronchi and bronchioles; but since not even catarrh of the finer bronchi causes 
typical asthmatic attacks, we must assume that in asthma we have to do with a 
special form of bronchiolitis or at least with special attendant conditions which 
cause the asthma. Curschmann, to whom we owe the first accurate clinical investi- 
gation of this most common form of bronchial asthma, termed the bronchial 
affection, which forms the basis of it, "exudative bronchiolitis," but we have 
ourselves for a good while usually employed the name of " asthmatic bronchio- 
litis." We would indicate by this term a peculiar disease of the smaller bronchi 
and bronchioles whose characteristic features are a peculiar sort of expectoration 
(vide infra) and characteristic " asthmatic " (vide infra) attacks of dyspnoea 
which grow worse paroxysmally. It is indeed possible, but not certain, that in 
the latter regard nervous reflex processes in the bronchioles also play a part, 
somewhat like the spasm of the glottis in whooping-cough. The causes of this 
asthmatic exudative bronchiolitis are not always evident. Sometimes, however, 
circumstances apparently play a part similar to those producing ordinary bron- 
chitis, especially the continuous inhalation of vegetable dust (wool, meal, etc.). 
Many cases of bronchial asthma may also with great probability be referred to 
some severe bronchial disease in childhood (whooping-cough, severe bronchitis of 
measles, etc.). 

Symptoms and Course of the Disease. — We will begin the account of the 
symptomatology by a description of the asthmatic " attack." In its purest form 
" nervous " bronchial asthma consists, in fact, of single attacks of dyspnoea, dif- 
fering in frequency and duration, which occur at least without special cause or 
without any discoverable reason in persons otherwise apparently healthy. In the 
intervals between the attacks the patient is perfectly well, and, in particular, 
shows no signs of disease of the respiratory organs. In most cases of " bronchial 
asthma," however, the attacks, as we have said, are only more or less sudden ex- 
acerbations of a condition which in the intervals is not perfectly normal. While 
ordinarily only the signs of a chronic bronchitis are present, often associated 
with pulmonary emphysema, from time to time exacerbations occur, usually in 
the form of long-continued asthmatic dyspnoea, lasting for days or weeks. It is 
this latter form especially which can be explained only by the assumption of a 
true bronchiolitis. 

The asthmatic attack either begins quite suddenly, or is preceded for a 
shorter or longer period by prodromata. These consist in a general feeling of dis- 
comfort, in abnormal sensations in the larynx or epigastrium, sometimes in re- 
markably frequent gaping, and often in a marked coryza associated with a good 
deal of secretion and frequent sneezing (compare the relation between many at- 
tacks of asthma and diseases of the nose, given above). The attack begins in 
most cases at night (before midnight). The patient wakes up with an intense 
feeling of pressure and anxiety. Sometimes he complains of a feeling of pain 
in the chest. He has to sit up straight, and in severe cases even to get out 
of bed. He often hurries to an open window in order to "get air." His ex- 
pression is anxious; his skin becomes pale and cyanotic, and sometimes is cov- 



184 



DISEASES OE THE EESPIEATOEY ORGANS 



ered with a cold sweat. On objective examination we are at once struck by the 
characteristic change in the respiration. Both inspiration and, especially, expira- 
tion are almost always accompanied by a high-pitched whistling sound, audible 
at a distance. Both respiratory acts are labored, requiring the aid of the acces- 
sory muscles. On inspiration, only the upper part of the thorax is elevated to 
any extent. We see in the neck the inspiratory contraction of the sterno-cleido- 
mastoids, the scaleni, etc. Still more striking, however, is the labored, panting, 
long-protracted expiration, during which the abdominal muscles are contracted 
to a board-like hardness. We therefore recognize the disturbance of respiration 
in asthma as essentially an expiratory dyspnoea. The frequency of respiration is 
in many cases normal, or even somewhat diminished, yet we have repeatedly 
counted thirty or forty respirations a minute. 

On physical examination of the lungs during the paroxysm, we find the per- 
cussion-note over them normal or even strikingly loud and deep — the " box-tone." 
The lower boundary of the lung is usually found one or two intercostal spaces 
lower than normal. Not only is this condition shown in the cases with a perma- 
nent pulmonary emphysema, but during the asthmatic attack itself there occurs 
an acute inflation of the lung. The latter is probably explained by the fact that 
the lung is much stretched by the strenuous inspirations which are made by aid 
of the accessory muscles, while the weaker expiratory force is not enough wholly 
to drive out the air again through the contracted bronchioles. Therefore it hap- 
pens in bronchial asthma, as in every other bronchial disease, that the expiration 
is usually more labored and protracted than the inspiration. On auscultation, 
high-pitched whistling and creaking sounds, which quite obscure the vesicular 
murmur, are heard over most of the lung, especially during the long expirations. 
In many places, indeed, where the bronchioles are almost completely closed, the 
respiratory murmur is entirely absent, or we hear only a low whistle on expira- 
tion. Toward the end of the paroxysm the noises become deeper and more boom- 
ing, and sometimes we hear a few moist rales. 

In brief paroxysms there may be scarcely any cough or expectoration. In 
most, particularly in the tedious cases of true asthmatic bronchiolitis, there is, 
however, a scanty tough mucous expectoration. In this are found, beside the 
ordinary constituents of simple bronchitic sputum, larger or smaller numbers of 
very characteristic clumps. These may be yellow or greenish-yellow, or, on the 
other hand, gray. The yellowish masses, which are usually very tough, and often 
consist of a bunch of thready matter, represent swollen and fatty-degenerated pus 
corpuscles, between which are very frequently interspersed a considerable number 
of pointed octahedral crystals. These crystals were first described by Leyden in 
the sputum of asthmatic patients, and are usually termed asthma crystals (see Eig. 
25). Chemically they are identical with "Charcot's crystals," which are found 
in the leuksemic spleen, the bone marrow, etc., and they probably represent the 
phosphoric-acid salt of an organic base (Schreiners base, C2H3N), although this 
has lately been questioned. As soon as the paroxysms cease the number of crystals 
in the sputum usually begins to diminish rapidly, and it is often possible to 
observe in them evident signs of disintegration. Nothing is known as to the 
origin of these crystals. Often, also, numerous ciliated epithelial cells are found, 
in addition to the crystals, in the yellow masses. The gray plugs in the sputum 
of asthmatic patients consist mainly of clumps of thready mucus, and contain 
the peculiar " spirals " which were first described by Ungar and by Cursch- 
mann. Many of these spiral threads are visible to the naked eye, but others 
demand the microscope for their recognition, through which they are seen as 
brilliant forms composed entirely of various sized bands and threads collected 
in spirals (see Eig. 25). Sometimes a brilliant central thread of small diameter 
is seen in the midst of the spiral. Around the spirals are found round cells, drops 



BEOXCHIAL ASTHMA 



185 



of fat and myeline, and sometimes ciliated epithelium, and epithelial cells from 
the pulmonary alveoli. As to the precise way in which the spirals and their 
central thread develop, the question is not yet settled, but it is certain that the 
spirals represent casts of the minutest spirally twisted branches of the bronchi, 



and therefore clearly indicate the existence of a peculiar disease of the finest 
terminal bronchial twigs. 

Of the other peculiarities of the sputum in bronchial asthma we may mention, 
first of all, the almost invariable occurrence of very many eosinophilous cells 
in the sputum, and also, apparently, in the blood. The significance of this fact is 
still unknown. We occasionally find in the sputum of asthmatics crystals of calcic 
oxalate and calcic phosphate. 

The pulse is usually accelerated during the asthmatic paroxysm, the arteries 
contracted; the bodily temperature is normal, or sometimes even subnormal. In 



protracted attacks we have repeatedly seen a slight febrile movement up to about 
102° (39° C). 



The duration of the asthmatic paroxysm is very different in individual cases, 
as has already been said. Sometimes it lasts only a few hours, but sometimes 
it lasts several days, and even weeks. Marked exacerbations and remissions of 
the disease usually alternate. The frequency of the paroxysms in ordinary 
asthma also varies exceedingly. Sometimes they come on almost every night, and 
then there are long pauses of months and years, so that we can not make any 
general statements as to the course of the disease. Many asthmatic patients make 
very remarkable statements as to the individual exciting causes of their attacks. 
Many patients claim, for example, that the attacks occur only in certain places, 
while in other places they are wholly free from the trouble, that they can live 
only in the upper storeys of the house, etc. Such statements should not remain 
unheeded, although it is certain that they are often due to imagination. Definite 
recoveries are quite rare, since long-continued asthma almost always leads to 
chronic pulmonary emphysema with all its consequences. 

Diagnosis. — The diagnosis of the bronchial asthmatic condition as such is 
not difficult if we limit ourselves strictly to the characteristic type of the disease : 
the strenuous respiration with wheezing that can be heard at a distance, the 
labored, prolonged expiration, the characteristic physical signs in the lungs, and 
the peculiar sputum. Usually we can easily distinguish bronchial asthmatic 
dyspnoea from cardiac asthma (q. v.), spasm of the glottis (q.v.), and also 
from hysterical dyspnoea with its superficial and very rapid respiration and 
normal conditions in the lungs. This latter distinction of true bronchial asthma 
from "hysterical asthma" is very important both in prognosis and treatment, 
since the two are frequently confounded. If we are sure that we are dealing 




Fig. 25.— Asthma crystals and Curschmanrfs spirals (a, central fiber). 



186 



DISEASES OF THE EESPIEATOEY ORGANS 



with true asthmatic attacks, the next question is whether it is a " purely nervous " 
reflex asthma or an asthmatic exudative bronchiolitis. Here, of course, we can 
decide only after a careful and thorough examination of the patient (especially of 
the nasal cavities) and after observing the course of the disease. Finally, we must 
also consider the possibility of a purely symptomatic asthma in chronic pulmonary 
emphysema, in the chronic bronchitis of renal disease or arthritis, etc. We must, 
however, confine our use of the term " symptomatic bronchial asthma " to those 
cases in which we actually have a dyspnoea with all the characteristic peculiari- 
ties of true bronchial asthma. 

Treatment. — In every case of asthma the first thing to be thought of is 
whether there is not a definite cause whose removal may cure the disease. In this 
connection we should examine the nose carefully, since numerous recent ob- 
servations have shown that a previously existing asthma may wholly disappear 
or at least be materially relieved after the treatment of some nasal disease which 
may be present, such as the removal of polypi, the destruction of the erectile bodies 
by the galvano-cautery, etc. Of course these results should not be over-estimated. 
It has repeatedly been claimed by nasal specialists that in many asthmatic patients 
we can find a definite spot in the nose and excite an asthmatic attack by touching 
it with a probe. This spot must then be treated first of all. We will not wholly 
reject these statements, but we are somewhat skeptical in regard to them. At any 
rate, the nose should be treated, in our opinion, only when it presents actual 
morbid changes. 

If we can not satisfy the causal indication in this way, we should always try 
next a remedy which must pass for a direct specific against certain forms of 
asthma — iodide of potassium. In doses of twenty to forty-five grains a day (grm. 
1.5-3.0), or even more if necessary, this usually causes a rapid improvement, 
which of course is not always, although it is frequently, permanent. In asthmatic 
bronchiolitis, especially, iodide of potassium in large doses often acts excellently. 
It seems to make the tough secretion more fluid, to ease the expectoration, and 
in this way to lessen the stenosis of the bronchioles. Of course a permanent and 
complete cure is only rarely obtained from iodide of potassium. If iodide of potas- 
sium has been used in vain, we must turn to the other remedies which have been 
employed against asthma, although their action is often quite uncertain. We may 
mention here the nitrite of sodium (two parts in one hundred and twenty of water, 
two to three teaspoonfuls a day), and nitro-glycerine, which has an analogous 
action (twenty drops of a one-per-cent. alcoholic solution in six and a half ounces 
[grm. 200] of water, a tablespoonful two or three times a day) ; also bromide of 
potassium, belladonna, atropine, etc. In some cases pneumatic treatment, such 
as the inhalation of compressed air, has been successful, and sometimes, too, elec- 
tricity (galvanization and faradization of the neck), or hydrotherapy, has been 
claimed to give relief. Change of climate may sometimes be of distinct service. 
Many patients bear the sea-air well, while with others a mountain residence 
exerts a favorable influence. Special resorts (Marienbad, Kissingen, ferruginous 
baths, etc.) may often be recommended with advantage if appropriate to the 
patient's general constitution. 

In severe cases a special symptomatic treatment of the attack itself is often 
necessary. Narcotics are without doubt the most effective, especially chloral and 
morphine. In severe attacks we can not avoid injections of morphine, but we 
must always be cautious in order that the patient may not form the habit of 
using this to excess. Chloral hydrate (gr. xv-xxx, grm. 1.0-2.0) often relieves the 
individual attack. Among other symptomatic remedies we may mention mus- 
tard-plasters to the chest and calves, putting the hands and feet into hot 
water, inhalations of nitrite of amyl, turpentine, chloroform, pyridine, etc. 
Fumigation with saltpeter paper — unsized paper dipped in a concentrated solu- 



PULMONARY EMPHYSEMA 



187 



tion of nitrate of potassium and dried — and the stramonium cigarettes to be 
had in most drug-stores, are much praised. The patient may also smoke with 
benefit stramonium or belladonna leaves which have previously been dipped in a 
solution of saltpeter and then dried. Many patients praise highly the different 
asthma cigarettes and smoke-producing powders or pastilles, which are sold as 
secret remedies, especially in America. Such apparent success is certainly due in 
great measure to the psychical suggestion wrought by these remedies. 

[Potassic iodide is more likely to prevent recurrence if it is given continu- 
ously, for several months at least, and it should not be thrown aside as useless 
until it has been pushed to the limit of toleration without avail. A convenient 
form of administration is in saturated aqueous solution, a minim of which repre- 
sents about a grain of the drug. 

The syrup of hydriodic acid may be substituted for potassic iodide in cases 
of intolerance of the latter. Grindelia robusta, a drachm of the fluid extract 
three or four times a day, serves sometimes to prevent recurrence of attacks. 
Marked alleviation of the paroxysms is often obtained from the inhalation of 
fifteen to thirty drops of the iodide of ethyl.] 



SECTION IV 

Diseases of the Lungs 

CHAPTEE I 

PULMONARY EMPHYSEMA 

(Alveolar Ectasis. Pneumatosis pulmonum) 

Nature and ^Etiology of the Disease —Pulmonary emphysema, the abnormal 
inflation and dilatation of the lungs, is one of the commonest pulmonary affec- 
tions. It either develops in separate parts of the lung, in which case it is subordi- 
nate to other pathological changes which co-exist in the lungs, or it involves 
almost the whole extent of both lungs, and then presents the symptoms of a char- 
acteristic affection, which it is usually easy to recognize. 

The essence of pulmonary emphysema, the condition from which most symp- 
toms are immediately derived, is the loss of elasticity in the lungs. If we com- 
pare the sound lung, with its normal elastic force, to a new and very tense rub- 
ber band, the emphysematous lung must be compared to an old and lax band that 
is stretched and pulled out. We therefore see why the emphysematous lung takes 
up a greater space than the sound one, for, on account of its lack of elasticity, it 
can no longer contract to its former volume. We may therefore call emphysema a 
permanent inspiratory distention of the lung from which it can no longer return 
to its expiratory condition. If we open the thorax of a subject with normal 
lungs, they contract, as is well known, but the emphysematous lungs remain in 
their inflated condition after the thorax has been opened. 

If we inquire into the factors which cause this loss of elasticity in the lung, 
we find that they are the same kind of influences which tend to diminish the elas- 
ticity of any other elastic body. As a rubber band, by much pulling and stretch- 
ing, gradually gets longer and less elastic, so the lungs, as a result of their abnor- 
mally frequent and severe distention, gradually become inelastic and emphy- 
sematous. Emphysema in many cases is a true wearing out of the lung. The 
normal traction of inspiration, which is continually making new demands on 



188 



DISEASES OE THE RESPIRATORY ORGANS 



the elastic powers of the lungs, finally leads to a loss of elasticity in them. In 
advanced age most lungs become more or less inelastic. The lungs of an old 
man are like an elastic band which has done its work for years but which has 
finally given out. We therefore class emphysema of the lungs in old age 
rather among the states of involution, such as develop in almost all organs in 
advanced life, than among special pathological changes. We distinguish, more- 
over, most lungs with senile emphysema from other emphysematous lungs by 
the fact that their volume as a whole is not increased, but is rather diminished 
below that of the healthy lung, since we find in them the extensive atrophic 
processes of old age. 

The condition becomes pathological, however, if the elasticity of the lung is 
deficient in earlier years and independently of the action of the special in- 
jurious influences which will soon be mentioned. In such cases of emphysema, 
developing in middle life or even in youth, the idea of a congenital weakness of 
the elastic elements in the lungs can not be set aside. It probably consists in a 
quantitative or a qualitative defect of the elastic tissue. Some observations seem 
to corroborate the statement that a disposition to emphysema may be present in 
several members of the same family. 

If a lung whose elasticity is previously subnormal can not persistently satisfy 
the ordinary demands upon it, a normal lung, on the other hand, also loses its 
elasticity if the demands made upon it are greater than it can perform. This is 
the reason why pulmonary emphysema is in some instances to be regarded as a dis- 
ease arising from the occupation. We mean here not only those influences which 
lead to chronic bronchitis and thus later to emphysema (vide infra), but more espe- 
cially the abnormal demands upon the lungs in all those callings which necessitate 
severe physical labor. We must not only regard the deeper and more rapid res- 
pirations, but also the increased pressure during expiration to which the lungs are 
often exposed in the raising of heavy weights, etc. This explains the common oc- 
currence of emphysema in the laboring classes, and also its greater frequency in 
men than in women. Besides this, we must add that in certain callings, such as 
glass-blowing and horn-blowing, the over-straining of the lungs is much more 
direct. In all such cases emphysema may be termed simply a premature exhaustion 
of the lungs. 

In very many cases emphysema develops as a result of other diseases of the 
lung, and especially as a result of chronic bronchitis. Dry catarrh of the medium- 
sized and finer bronchi when of long duration leads, as a rule, to pulmonary emphy- 
sema. The abnormal mechanical influences to which the lungs are thus exposed 
act both in inspiration and in expiration. Since the entrance of air to the alveoli 
is rendered more difficult by the swelling of the mucous membrane in the smaller 
bronchi, abnormally deep and strong inspirations are necessary, with a marked 
expansion of the alveoli, in order to draw a sufficient quantity of air into the 
alveoli. The alveolar walls are therefore exposed to an abnormal traction at each 
inspiration. On expiration, a pressure from within, which is perhaps even more 
injurious, acts on the alveoli. The ordinary expiration, which usually needs only 
the elastic power of the lungs, is not sufficient in chronic bronchitis to drive the 
air out of the alveoli through the narrowed bronchi. Thus arise the difficulty 
and delay in expiration which are present in chronic bronchitis, and which lead 
to the active participation of the muscles of expiration, the abdominal group of 
muscles. On forced expiration, however, the pressure does not act simply upon 
the contents of the alveoli, but much more upon the smaller bronchi themselves. 
The channel of exit for the air from the alveoli, therefore, becomes still narrower. 
Since the air can not at once escape, the pressure within the alveoli is raised by 
the efforts at expiration, and the alveolar wall is thus again abnormally expanded. 
The cough, which is often present in chronic bronchitis, is a further factor, which 



PULMONARY EMPHYSEMA 



189 



acts in a precisely similar injurious fashion. The attacks of coughing begin with 
a forced contraction of the muscles of expiration, which follows the closure of the 
glottis. Until the glottis opens, therefore, the lower parts of the lung especially 
are put under strong pressure. The air in them, which can not escape outward, 
is driven into the upper parts of the lung, and there leads to expansion of the 
alveoli, and finally to emphysema. 

We accordingly see that a number of injurious influences co-operate in the 
gradual development of emphysema from chronic bronchitis, and that, sooner or 
later, these influences have as their result the gradual dilatation of the lungs. 
Here, too, we must bear in mind the individual differences in the resisting power 
of the lungs. 

Conditions precisely similar to those in chronic bronchitis occur in other dis- 
eases, and lead in like manner to pulmonary emphysema. We very often see the 
development of emphysema in severe and persistent whooping-cough. The worst 
factor here, besides the existing bronchitis, is the frequent paroxysms of coughing. 
Many cases of pulmonary emphysema and chronic bronchitis may be ultimately 
referred to such a severe bronchial disease occurring in childhood. We have 
already mentioned, in the description of bronchial asthma, both the acute emphy- 
sema, which occurs during the attacks, and the final development of a permanent 
emphysema. 

In conclusion, we must here consider a theory advanced by Ereund, which 
would make the development of an emphysema dependent upon a " primary rigid 
dilatation of the thorax." It is indeed conceivable that from certain pathological 
changes in the costal cartilages, as Freund claims, a thorax, which had become 
fixed in the position of inspiration, might exert a constant abnormal traction on 
the lungs and so give rise to an emphysema. The occurrence of this hypothetical 
primary disease of the cartilages, however, has up to the present time not been 
established. It is rather considered by the majority of authors as a secondary 
change, developing as a result of emphysema or else simultaneously with it. On 
the other hand, it is certainly remarkable that we sometimes observe in children 
the " emphysematous habit " of the thorax and neck, which will be more fully de- 
scribed further on, and that in fact we can often discover in such children a 
beginning emphysema early in life. We might perhaps imagine a congenital 
failure of harmony between the size of the thorax and the size of the lungs, 
whereby the latter are from the start in constant overtension. 

Besides the already described essential or substantial emphysema, which is a 
special disease attacking both lungs uniformly, we distinguish a so-called vicarious 
or complementary emphysema. If, by any disease, certain portions of the lungs 
are incapacitated in their functions, the parts which remain healthy must then 
assume the whole business of respiration. They become excessively expanded on 
inspiration, and as a result they become emphysematous. Thus we see emphysema 
of the upper lobes in affections of the lower lobes. Emphysema of one lung is 
most frequently observed clinically when the other lung is extensively diseased, 
especially in unilateral chronic contractions of the lungs and pleuraa, usually seen 
in tuberculosis. Vicarious emphysema may also be confined to quite small por- 
tions of the lung, but then it is merely of pathological and not of clinical interest. 

Pathological Anatomy. — As we have seen, the actual abnormality of the lung 
in emphysema is not due to a pathological change, but to a change in its physical 
conditions. The loss of elasticity of the lung is shown in its greater volume, in 
its lack of contractility, and in its persistence in a position of inspiration. 

The single alveoli are of course just as much expanded as the whole lung, but 
their walls show at first no histological changes. We have here, then, a condi- 
tion which Traube has called " increased volume of the lungs," and has distin- 
guished from the " pulmonary emphysema " proper. This distinction is without 



190 



DISEASES OE THE RESPIRATORY ORGANS 



doubt justified anatomically, but clinically it can not well be maintained. As the 
distention is constant, the alveolar walls can not withstand the constant traction 
and pressure. This leads to progressive atrophy of their tissue from pressure — 
that is, it leads to a real disappearance of the elastic elements of the lung. The 
atrophy begins quite gradually. The partition-walls of the alveoli are first per- 
forated, and then they partly or wholly break down. The neighboring alveoli run 
more and more into one another, and thus finally arise alveolar ectasis and in- 
fundibular ectasis, which can be made out with the naked eye, and which may 
attain a diameter of five or ten millimetres or more. If single air-bubbles enter 
the interlobular, interstitial, or subpleural connective tissue, which may happen 
perhaps in severe fits of coughing, we speak of an interstitial or interlobular em- 
physema, in distinction from the ordinary vesicular or alveolar emphysema. 

The tissue atrophy in the septa of the alveoli affects not only the elastic tissue, 
however, but also the branches of the pulmonary capillaries in the alveo- 
lar walls. The affection of the elastic tissue adds no new conditions to the dis- 
turbed functions of the emphysematous lung, which we have just described. The 
destruction and final atrophy of the pulmonary capillaries, however, is the second 
important factor in the pathology of pulmonary emphysema, for, with the destruc- 
tion of so great a part of the vascular area in the lungs, the outflow from the 
right side of the heart is considerably impeded. There must therefore necessarily 
be a stasis in the pulmonary arteries and the right side of the heart, and the right 
side of the heart can overcome the increased resistance only by increased work, 
and thus in every chronic pulmonary emphysema there finally arise a dilatation 
and consecutive hypertrophy of the right ventricle with their further conse- 
quences. 

Symptoms and Course of the Disease 

General Course of the Disease. — Although a pulmonary emphysema may 
sometimes, as in whooping-cough, develop in a comparatively short time, still its 
course is always very chronic. In most cases the origin of the disease is quite 
gradual, as in all those instances in which emphysema develops from chronic 
bronchitis or asthma, or as a result of some injurious occupation. The symp- 
toms gradually and insidiously associate themselves with those of the chronic 
bronchitis. 

The symptoms of emphysema usually begin in middle or advanced life, but 
marked emphysema may occur in youth and childhood. The disease always lasts 
for years, unless some fatal intercurrent disease arises. 

The objective and subjective symptoms are due either to the chronic bron- 
chitis, which very often co-exists, or to the emphysema itself. Not only is the 
bronchitis, as we have seen above, very often the cause of emphysema, but, on 
the other hand, the development of chronic bronchitis is greatly favored by the 
circulatory disturbances in the lung associated with emphysema. Thus the two 
diseases, emphysema and chronic bronchitis, are closely connected clinically. 

Bronchitis causes its well-known symptoms — cough, expectoration, moderate 
dyspnoea, and a feeling of pressure in the chest. The bronchiectases, which are 
often gradually formed, especially in the lower lobes, may lend a peculiar stamp 
to the cough and expectoration (see page 178). Emphysema increases the pa- 
tient's dyspnoea to a degree which can never be caused by chronic bronchitis alone. 
The emphysematous lungs soon become incapable of satisfying any extraordinary 
demands of respiration. Many patients are only slightly conscious of the diffi- 
culty in breathing so long as they keep quiet, but whenever they make a trifling 
physical exertion, go up-stairs, or take a little longer walk than usual, the dyspnoea 
comes on. 

The variations in the intensity and extent of the bronchitis correspond to the 
frequent and quite marked variations in the patient's feelings. These variations 



PULMONARY EMPHYSEMA 



191 



depend upon the condition of the patient, his circumstances, and the possibility 
of his taking' care of himself ; the change of seasons, too, has an influence on 
him. In pleasant weather many patients live in tolerable comfort, but autumn 
and winter bring an aggravation of all their symptoms with the increase in 
their bronchitis. 

The last stage of the disease is characterized by the appearance of disturb- 
ance of compensation in the heart. We have seen above that the cause of the 
impairment of the pulmonary circulation, and of the resulting hypertrophy of 
the right ventricle, is the closure of numerous pulmonary capillaries. A further 
reason for the impairment of the circulation comes from the disturbance of res- 
piration itself, since the influence of the respiratory movements on the circulation 
is well known. The appearance of a marked disturbance of the circulation may 
be deferred for some time by the increased efforts of the right ventricle. The 
cyanosis of most patients, however, is due not only to incomplete oxidation but to 
the blood-stasis which extends backward from the right side of the heart into 
the veins of the body. Finally, the right ventricle becomes more and more 
feeble, the stasis in the veins increases, oedema of the extremities and transudation 
into the various cavities of the body ensue, and after long suffering the patient 
succumbs to dropsy. 

Emphysema is frequently combined in its later stages with other chronic dis- 
eases. Pulmonary emphysema with its sequelaB is seldom found at the autopsy 
as a single lesion, but we discover in the cadaver co-existing disease of the heart, 
the blood-vessels, or the kidneys, all a genuine wearing out of the aging body. 
Pulmonary tuberculosis is often a final development in emphysema, but it is 
usually of the chronic indurated form, and is not very extensive. 

Physical Examination. 1. Inspection. — In many patients we can detect the 
disease with considerable confidence at the first glance ; we are therefore justified 
in speaking of an emphysematous habit. The patients are usually quite well 
nourished, at least in the early stages of the disease, and are often rather cor- 
pulent. They appear plump or even somewhat bloated, and their faces are more 
or less markedly cyanotic. The configuration of the neck and thorax is especially 
characteristic. The neck is usually short and thick; the sterno-cleido-mas- 
toid muscles, which have to act as auxiliaries in inspiration, are tense and 
hypertrophied. The inspiratory contraction of the scaleni may also be seen and 
felt. The veins in the neck are visibly dilated, and in severe cases are swollen 
to thick blue cords, and we sometimes see in them evident undulating or pulsating 
movements. The thorax is rather short, but broad and strikingly deep — the " bar- 
rel-shaped thorax." The intercostal spaces are narrow, and the lower ribs incline 
only a little downward. The epigastric angle is therefore obtuse, and sometimes 
becomes almost a straight line. The respiratory movements are almost always 
accelerated in severe cases. Inspiration becomes short and labored. The excur- 
sions of single ribs are therefore slight, and the thorax is raised rigidly and more 
as a whole. Expiration is visibly prolonged. There may be a noticeable retrac- 
tion of the intercostal spaces on inspiration, in the lower and lateral portions of 
the thorax. 

This characteristic form of the thorax in emphysema is regarded as a constant 
inspiratory position of the ribs, and corresponds to the permanent inspiratory 
dilatation of the lungs. The peculiar rigidity of the thorax is probably due to 
the changes in the costal cartilages already described, which, according to 
Ereund, are primary. In many cases the emphysematous form of the thorax 
gradually develops in the course of the disease, but in other cases it seems to 
depend on some original predisposition to the disease (vide supra). 

In conclusion, we must state that the above description corresponds to the typi- 
cal form of emphysema, from which we may have many deviations. In the para- 



192 



DISEASES OF THE RESPIRATORY ORGANS 



lyzed thorax, for instance, we may meet with a high degree of essential emphysema 
of the lungs, which has often given rise to errors in diagnosis. 

2. Percussion. — Percussion gives very decided results in the diagnosis of pul- 
monary emphysema. We find the inferior border of the lungs one or two inter- 
costal spaces lower than under normal conditions, corresponding to their perma- 
nent inspiratory inflation. Clear pulmonary resonance on the right front in the 
line of the nipple extends to the lower border of the seventh, and sometimes of the 
eighth rib. On the left front it extends to the fifth or sixth rib, so that the cardiac 
dullness is lessened. The area of cardiac dullness can often not be made out at 
all; or at most, on strong percussion, it is made out in a limited extent as rela- 
tive dullness. The pulmonary resonance extends on both sides in the back to the 
first or second lumbar vertebra. These results of percussion in emphysema, how- 
ever, are frequently altered, because other conditions, such as passive congestion 
of the liver, meteorism, and ascites, may be present at the same time, and push 
up the diaphragm. Thus the detection of emphysema by percussion is made decid- 
edly difficult. 

Qualitative changes in the percussion-note may be entirely wanting in emphy- 
sema. The pitch is sometimes remarkably loud and deep — the " box-tone " [tym- 
panitic resonance] ; but in other cases, especially in the back, we find it somewhat 
raised. This may depend in part upon the poor vibratory conditions in the rigid 
chest-walls, but in other cases it is caused by the retention of an abundant secre- 
tion in' the lower lobes. 

On inspiration, the lower edge of the lung moves downward very little or 
not at all. This is an important sign in diagnosis. Since the lung is always in a 
state of abnormal inspiratory distention, and since the entrance of air is impeded 
by the accompanying catarrh of the bronchi, the difference between the inspiratory 
and expiratory expansion of the lung is much diminished. The difference caused 
by respiration in the lower limit of the lung affords a good measure of the 
respiratory disturbance in the lower lobes. 

The detection of dilatation and hypertrophy of the right ventricle by percus- 
sion is in many cases difficult, because the lungs cover the heart. A positive 
result can be obtained only by carefully defining the relative cardiac dullness [by 
very light percussion]. The epigastric pulsations frequently seen in emphysema, 
and also the marked undulating and pulsating movements in the jugular veins, are 
to be regarded as quite certain signs of dilatation of the right side of the heart. 

3. Auscultation. — The characteristic auscultatory sign of emphysema is the 
prolonged expiration. As a flabby rubber band, when it is stretched and then let 
loose, no longer snaps back quickly and strongly, so the emphysematous lung, 
when it has been stretched in inspiration, comes back again only slowly. We hear 
with it a somewhat aspirated, sonorous sound, which plainly exceeds the vesicular 
inspiratory sound in duration. The vesicular murmur itself often undergoes a 
modification in pulmonary emphysema. It sounds exaggerated, and shuffling, 
or in other cases it is rougher and more indefinite. In a high degree of em- 
physema the vesicular respiration is sometimes very faint and obscure, because 
the inspiratory current of air is reduced to a small amount in the lungs, which 
are already excessively dilated. In many cases we hear rhonchi beside the respir- 
atory murmur, dry whistling, buzzing, and creaking sounds on inspiration and 
expiration. If cylindrical bronchiectases have already formed, we hear, especially 
over the lower lobes, numerous fine and medium moist rales, but no sonorous 
rhonchi. The adventitious sounds may wholly conceal the respiratory murmur. 
With a marked retention of secretion we sometimes hear nothing but a low, sup- 
pressed rattling. 

In the heart the sounds are usually rather feeble, because it is covered by the 
lung. The " functional systolic murmur of emphysema " at the apex, described by 



PULMONAKY EMPHYSEMA 



193 



some writers, we have heard much less frequently than we should expect after the 
statements relating to it. If present, it is probably due to co-existing valvular 
changes. The pulmonic second sound in emphysema is, as a rule, markedly accen- 
tuated, as a result of the stasis in the pulmonary circulation. 

The diminution of the expiratory pressure in emphysema may be measured 
with the manometer, or with Waldenburg's " pneumatometer." The normal ex- 
piratory pressure of 110 to 130 millimetres sinks in emphysema to 100 or 80 milli- 
metres. As we should expect, the spirometer shows a diminution of the vital lung 
capacity, which can be readily explained. The normal lung capacity of about 
3,500 cubic centimetres falls to 2,000 or 1,000 cubic centimetres. 

Other Symptoms in the Lungs and in Other Organs 

In regard to the other symptoms in the lungs we have only a little to add to 
what has already been said. The intensity of the cough naturally varies in 
individual cases according to the degree of the existing bronchial catarrh. Many 
patients are troubled by a dry cough, while others have abundant expectoration. 
There is nothing characteristic of emphysema in the composition of the latter. 
All the kinds of sputa which are found in the different forms of chronic bronchitis 
are also found in pulmonary emphysema. The dyspnoea, whose predominant ex- 
piratory character we have already mentioned, increases in advanced cases to a 
most marked degree. Sometimes the increase shows itself by the appearance of 
distinctly paroxysmal dyspnoea. This is often really to be regarded as a symptom- 
atic bronchial asthma, but, on the other hand, we must not overlook the fact that 
a temporary increase of the bronchitis, retention of secretion, and cardiac failure, 
may also excite attacks of dyspnoea, which can not properly be termed asthma. 

The important changes in the heart resulting from emphysema have already 
been described. The exhausted right ventricle can no longer overcome the in- 
creased resistance in the pulmonary circulation. The difficulty of respiration is 
still greater, from the passive congestion of the pulmonary vessels. The skin be- 
comes still more cyanotic, and finally cedema and general dropsy develop. The 
fai]ure of compensation is indicated by the smallness of the pulse, its increased fre- 
quency, and sometimes by its irregularity. The difficulty of an objective exam- 
ination of the heart in emphysema has been spoken of above. 

The appearances of blood-stasis in the internal organs are shown especially in 
the liver and kidneys. The liver is swollen, and its increase in size (the liver 
of passive congestion) can frequently be made out by percussion or palpation. 
The pains in the hepatic region, of which many patients complain, are per- 
haps due sometimes to the stretching of the capsule of the liver, but they are prob- 
ably more often muscular pains excited by the frequent coughing. 

In the kidneys the effect of stasis is first shown by a diminished excretion of 
urine. The urine is more scanty in amount, more concentrated, of a higher spe- 
cific gravity, and of a darker color. It generally gives an abundant sediment of 
urates, and it may contain a small amount of albumen. Microscopically we may 
find a few hyaline casts, and a few red and white blood-corpuscles. It is evident 
that this diminished activity of the kidneys favors the development of dropsy. 

The spleen is not infrequently found congested at the autopsy. The evidence 
of this, however, is often uncertain during life, for percussion of the spleen is 
difficult on account of the emphysema, and palpation is difficult from the anasarca. 

Gastro-intestinal symptoms may be present in emphysema. The appetite 
seldom remains good throughout the disease. Many patients suffer from chronic 
constipation; and more rarely there is a tendency to diarrhoea. 

Fever is not present in simple pulmonary emphysema. Whenever fever exists 
for a long time it depends on other complications, such as severe bronchitis, pneu- 
monia, or tuberculosis. 
13 



194: 



DISEASES OF THE EE SPIKATOEY OEGANS 



Complications of emphysema with other chronic diseases are frequent. The 
old opinion that emphysema and tuberculosis, and emphysema and chronic heart 
disease, were antagonistic to each other is entirely false. These complications are 
not very rare. We may also mention the complication with general arterio- 
sclerosis and with chronic nephritis, especially the contracted kidney. Among 
acute diseases we must mention particularly the acute accidental pulmonary 
complications, to which emphysematous patients, particularly of the lower classes, 
are much exposed as a result of over-exertion, exposure to cold, etc. Acute febrile 
bronchitis and lobular pneumonia cause marked exacerbations, and attacks of 
true influenza and croupous pneumonia in aged patients are not infrequently 
dangerous to life. 

The diagnosis of emphysema can be made directly from the results of the 
physical examination, and usually presents no difficulties. We think it important 
merely to say that too much stress should not be laid upon a low position of the 
lower edge of the lung alone. Many men apparently have dilated lungs but no 
symptoms at all. The chief thing, therefore (besides the dilatation of the lungs), 
is the presence of delayed and difficult expiration and lessened power of inspira- 
tion. The diagnosis is difficult when a patient with emphysema is not examined 
until the final, dropsical stage. In such cases it is often very difficult to avoid 
confusion with heart disease (primary hypertrophy, myocarditis, mitral stenosis), 
contracted kidney, etc. It is often difficult, also, to come to a decision in those 
cases in which there are evident signs of co-existing cardiac or renal disease besides 
the emphysema. In such cases it is often hardly possible to decide upon which 
of the different organic changes the chief stress is to be laid. In all such cases 
we must place especial confidence in an accurate history as well as a careful 
physical examination. The special nature and the sequence in development of 
the individual symptoms often afford valuable data for a correct appreciation 
of the whole clinicial picture. 

Prognosis. — Pulmonary emphysema of acute origin — that is, acute infla- 
tion of the lung — like that resulting from whooping-cough and analogous affec- 
tions, may be recovered from in many cases. Otherwise, as regards the final 
curability of the disease, the prognosis is wholly bad. The duration of the dis- 
ease and the intensity of the symptoms are of course very different in individ- 
ual cases. Here almost everything* depends upon the circumstances in which the 
patient is placed. With sufficient care the disease may be tolerably well borne 
for many years, but without it the first symptoms of respiratory and cardiac 
insufficiency appear much earlier. The final termination is usually due to com- 
plications (vide supra). 

Treatment. — Since emphysema itself is only slightly amenable to treatment, 
most of our therapeutic remedies are directed to that accompanying condition 
upon which the greater part of the symptoms depend — the chronic bronchitis. 
If we succeed in improving this, or even in wholly removing it, we always obtain 
a decided improvement in all the patient's symptoms. The therapeutic agents 
mentioned in the description of chronic bronchitis are therefore of frequent use 
in emphysema. 

In the first place, we must seek the best hygienic conditions for the patient, 
and remove him from all injurious influences, such as dust, bad air, and great 
physical exertion. In dry catarrh we should use the alkaline mineral waters, 
and when there is abundant mucous secretion the balsams, such as turpentine 
internally and by inhalation. The most valuable expectorants are iodide of 
potassium, apomorphine, and ipecac when the expectoration is tough, and liquor 
ammonii anisatus and senega when it is abundant. Their action, of course, 
too often fails of the desired result, so that we frequently have to change 
our remedies. When there is a troublesome cough, disturbing the sleep, we 



PULMONARY ATELECTASIS 



195 



can not dispense with narcotics, such as morphine, codeine, or Dover's powder. If 
severe dyspnoea comes on, we may try to obtain relief by mustard plasters to the 
chest, or by immersing the hands and feet in hot water. With asthmatic attacks 
we may try iodide of potassium, besides the other remedies mentioned for asthma. 
Here, too, we must finally resort to narcotics. 

We must carefully watch the condition of the heart, and use digitalis when 
there are signs of beginning disturbance of compensation and the pulse grows 
small and irregular, and this drug may prove very useful. If symptoms of dropsy 
set in, we may sometimes prescribe diuretic remedies, such juniper-tea, acetate 
of potassium, diuretine, calomel, etc., besides digitalis. When there is persistent 
weakness of the heart we should also use digitalis and other stimulants (stro- 
phanthus, camphor, wine, etc.). 

Besides the purely symptomatic treatment thus described, the attempt has 
been made to meet the causal indications in emphysema, and especially to aid 
the patient in expiration, and thus to improve the power of the lung to contract, 
where it is possible. To this end Gerhardt has recommended assisting expiration 
mechanically by compression of the thorax. This compression must be done 
methodically by another person,* about five or ten minutes every day, by the aid 
of both hands laid flat on the lower lateral portions of the thorax. The effect of 
this manipulation in diminishing the dyspnoea and making expectoration easier 
is in many cases very satisfactory. The " breathing chair " made by Rossbach 
has a similar mechanical action. 

The employment of the pneumatic treatment has also become quite general, 
especially since the introduction of Waldenburg's portable apparatus. The expi- 
ration into rarefied air, which meets the causal indication, may procure great 
relief for the patient in many cases, and sometimes, too, may result in an improve- 
ment of the emphysema which can be demonstrated on physical examination. In- 
halations of compressed air are also employed when there is severe bronchial 
catarrh. Still, too much must not be anticipated from pneumatic treatment. 



CHAPTER II 

PULMONARY ATELECTASIS 

( Compression of the Lungs. Aplasia of the Lungs in Cases of Lvypho scoliosis) 

etiology. — Atelectasis of the lungs is a condition the direct opposite of em- 
physema. While in the latter the lungs are abnormally inflated, in the former 
they are abnormally collapsed. The air has disappeared from the alveoli and 
lesser bronchi, and in the most advanced cases even from the larger bronchi. The 
atelectatic portions of the lung are not altered histologically, but are changed to 
a firm tissue, deprived of air — so-called splenization or carnification. 

The atelectasis of the new-born is due simply to deficient respiration and to 
the consequent imperfect entrance of air into the lungs. In weak children, who 
die soon after birth, we often find the lower lobes wholly or in part in a foetal, 
uninflated condition — that is, atelectatic. By artificial inflation we can readily 

* One of the author's patients at the policlinique in Leipsic made himself a very simple but very 
effective apparatus for producing this compression of the thorax on himself, by the aid of two nar- 
row boards, which are fastened together at one end by a cord of suitable length. These boards, 
which are furnished with a pad at this end fitted to the wall of the chest, are laid flat on the two 
sides of the thorax so that their free ends project forward some six inches or a foot, and serve as a one- 
armed lever. By pressing them together the patient himself can thus, without any strain, exert a con- 
siderable pressure on his thorax with each expiration. 



196 



DISEASES OE THE RESPIRATORY ORGANS 



expand the lungs to their normal extent. In many cases of weak, newly-born 
infants there is at first an atelectasis of parts of the lung, which gradually dis- 
appears entirely and is replaced by normal conditions. 

Acquired atelectasis occurs in two ways. We may mention, as the first and 
most frequent serological factor, the plugging of the smaller bronchi. If a com- 
plete closure of a bronchus arises from the accumulation of secretion, as may 
easily happen in the narrow bronchi of children, the air can no longer enter, on 
inspiration, into that portion of lung supplied by the plugged bronchus. The air 
which is shut up in it is gradually absorbed by the blood. The adjacent parts of 
the lung expand, and the portion that is excluded from respiration collapses, 
leaving a circumscribed pulmonary atelectasis, usually rich in blood but devoid 
of air. Such atelectases, in greater or less number and extent, are very often 
found in the bodies of children who have suffered from severe bronchitis, espe- 
cially after measles, whooping-cough, or diphtheria. Besides the direct action of 
the plugging of the bronchus, the weakness of the respiratory movements and the 
cough, conditional upon the general state of the disease, play a significant part. 

The second very frequent and important cause of pulmonary atelectasis is 
compression of the lung. In all the diseases which diminish the space for the 
expansion of the lungs, the lungs are compressed to a greater or less extent, 
whereby the air is squeezed out of them. Thus arise the atelectases from pressure 
in pleuritic effusion, hydrothorax, pneumothorax, in marked cardiac hypertrophy, 
pericardial effusion, and aneurism of the aorta. Atelectasis of the lower lobes 
also arises in the same way from great upward pressure on the diaphragTn by 
ascites, meteorism, abdominal tumors, etc. 

That form of pulmonary atelectasis which arises from deformities of the thorax 
is of great practical importance. In severe kyphoscoliosis, the half of the thorax 
corresponding to the convexity of the vertebral column is much narrowed. The 
lungs are materially hindered in their expansion, and even in their growth, if the 
deformity occurs in youth. This is called " aplasia of the lungs," a condition 
which may give rise to grave results (vide infra). 

Symptoms. — In the majority of cases the symptoms of atelectasis are subordi- 
nate to the disturbance caused by the primary disease. This is especially the 
case in most of the atelectases from pressure, although the most dangerous factor 
lies in the compression of the lung. 

The atelectasis of the lungs developing as a result of diffuse capillary bron- 
chitis, especially in children, can of course not be detected by physical examina- 
tion until it is of great extent. The respiration, in extensive formation of atel- 
ectasis, often shows a very striking and characterstic deviation from the ordinary 
type, especially when the atelectasis develops in the lower lobes. It is accelerated 
and labored, and is performed chiefly by the upper and anterior portions of the 
thorax. In the lower portions we see marked inspiratory retractions, which are 
caused in part by the external pressure of the air, and in part by the exaggerated 
contraction of the diaphragm. 

Physical examination can, of course, reveal abnormal conditions, especially 
dullness on percussion, only when the atelectasis is extensive. Dullness, however, 
is usually hard to make out in children. Auscultation gives signs of existing 
bronchitis ; and sometimes, too, with more extensive consolidation, there is bron- 
chial respiration. In other cases, as may be easily seen, the respiratory murmur 
is much diminished or wholly absent. Thus, the physical signs of atelectases are 
not easily distinguishable from those of pneumonia, especially of lobular pneu- 
monia. In fact, a sharp distinction between atelectatic nodules and nodules of 
lobular pneumonia in the lung can not be drawn clinically. 

Aplasia of the lungs in kyphoscoliosis demands a special description, because it 
is of great practical significance. Many patients with kyphoscoliosis may live for 



PULMONARY (EDEMA 



197 



years without special respiratory disturbance. Careful observation, of course, 
usually shows a somewhat labored and hurried respiration, but the patients 
have not paid much attention to it. In other cases the difficulty in breathing is 
more noticeable. The person affected is incapable of any severe physical ex- 
ertion; he always feels short of breath, and often suffers from cough and expec- 
toration. In the cases first mentioned, however, which for years have had little 
or no trouble, disturbances in respiration sometimes come on quite suddenly. 
They may also frequently arise without any special cause, and may attain a very 
threatening degree. The condition may improve, or it may lead to comparatively 
or even absolutely sudden death. Examination of the lungs during life usually 
shows nothing but the signs of an extensive bronchitis. By careful percussion we 
may quite frequently detect an increase of cardiac dullness to the right. Some- 
times a moderate oedema develops. In such cases the autopsy shows nothing as the 
cause of death but the changes in the chest. The lungs are deficient in air, 
small, and compressed, but in circumscribed portions, on the contrary, emphy- 
sematous and expanded. The right side of the heart in the great majority of 
cases is dilated and hypertrophied. There can scarcely be a doubt, therefore, 
that the cause of the onset of severe symptoms and the final cause of death is to 
be sought in the cardiac failure. 

Finally, it is worthy of mention that there is a frequent form of mild atelec- 
tasis in the lower lobes, which occurs in very sick and bed-ridden patients who 
usually keep in one position — on the back — as in typhoid fever. On making such 
patients sit up we hear during the first inspirations exquisite crepitant rales over 
the lower lobes, which sometimes disappear after a few deep inspirations. Here 
we have to do with a mild atelectatic condition, with a temporary collapse of 
the alveoli and smallest bronchi. 

The treatment of atelectasis coincides in great measure with the treatment of 
the primary disease, and is therefore to be looked for in the corresponding chap- 
ters. The prophylaxis of atelectasis, by constant attention to the respiration, is of 
great practical importance. We should try to keep the patient from lying con- 
tinually on his back, and we should make him take deep inspirations. The timely 
use of tepid baths, with shower-baths, is a special preventive of the development 
of atelectasis, and it may bring about a recovery when atelectasis is already 
present. 

Tepid baths may also be used with care in the treatment of dyspnoea caused by 
kyphoscoliosis. The condition of the heart, however, deserves especial attention 
(stimulants and digitalis). The reader is referred to the consideration of the 
general treatment of circulatory disturbances in the chapters on diseases of the 
heart. In other respects the symptomatic treatment by expectorants, etc., is the 
same as in other chronic pulmonary affections. 



CHAPTER III 

PULMONARY CEDEMA 

iEtiology and General Pathology. — We have in pulmonary oedema the exuda- 
tion of a highly albuminous fluid, usually somewhat haemorrhagic, not only into 
the interstitial tissue, but also into the alveoli themselves. The danger of the 
condition is easily understood from the high degree of dyspnoea which immedi- 
ately ensues from it. In fact, pulmonary oedema is in many cases a terminal 
symptom, which comes on in all forms of acute and chronic disease. Many pa- 



198 DISEASES OE THE RESPIRATORY ORGANS 



tients are said to die with the signs of pulmonary oedema, especially patients with 
heart disease, pulmonary and renal disease, and also with other affections of the 
most different kinds. 

In rare cases pulmonary oedema is a transitory symptom. Repeated attacks 
of it may occur, especially in heart disease and chronic renal disease, and, for a 
time at least, the patient recover from them. 

In spite of much clinical and experimental work, the special causes of pulmo- 
nary oedema are still quite obscure. For one class of cases the work of Cohn- 
heim and Welch shows that pulmonary oedema is to be considered as purely the 
result of stasis. Pulmonary oedema takes place when the outflow of venous blood 
in the lung meets an obstacle which can no longer be overcome by the mechanical 
force of the right ventricle. The obstacle which plays the most significant part 
here, and which may occur in all possible forms of disease — of course more read- 
ily in those mentioned above than in others — is paralysis of the left ventricle. 
If the further progress of the blood is much hindered by this, the overfilling of 
the pulmonary circulation and a consequent pulmonary oedema will necessarily 
follow, in spite of the most vigorous action of the right ventricle. Many cases 
of terminal pulmonary oedema seem to depend upon this fact, that the left ven- 
tricle is paralyzed in its action sooner than the right. 

The paralysis of the left ventricle, however, is certainly not the only factor 
to be considered in the origin of pulmonary oedema. We must also consider 
the condition of the walls of the blood-vessels in the lungs. In many cases, 
especially in renal disease, pulmonary oedema seems to depend upon local changes 
in the vessel walls (Sahli). This form of pulmonary oedema is somewhat akin 
to true inflammatory oedema. The latter is found chiefly in the vicinity of por- 
tions of lung infiltrated with pneumonia; it is usually of limited extent, and 
therefore it is of subordinate importance as a cause of disturbances in respiration 
compared with the diffuse oedema of stasis. 

In very rare cases, as we have ourselves seen, an apparently primary acute pul- 
monary oedema, with a speedily fatal termination, develops in men who are 
apparently perfectly healthy, and the autopsy gives no explanation of its origin. 
We perhaps have to do in these cases with the sudden failure of the left ven- 
tricle, but probably with acute vascular changes as well. 

Symptoms. — Marked dyspnoea is the most striking symptom in pulmonary 
oedema. It is subordinate only when the patient is found in the death agony 
and is no longer fully conscious. 

In pulmonary oedema the respiration is hurried, labored, and rattling. All 
the accessory muscles of respiration are called into play. The patient usually sits 
upright in bed. We see on his lips and cheeks a gradually and constantly in- 
creasing cyanosis, and we often hear at a distance the moist rales originating in 
the larger bronchi. 

On examination of the lungs, the percussion is essentially normal, if there is 
no other disease of the lungs. Sometimes the percussion-note is a little higher in 
pitch, and often it is slightly tympanitic. On auscultation, we hear everywhere 
many fine and medium moist rales. If the patient can still expectorate, he 
raises a large amount of frothy, sero-sanguineous sputum. The whole picture 
of the disease is so characteristic that the condition can scarcely be mistaken. 

Treatment. — Since in most cases pulmonary oedema is not so much the cause 
as a symptom of approaching death, our remedies against it are apt to prove pow- 
erless, but it must always be our duty, at least in all cases that are not absolutely 
hopeless, to try to relieve the pulmonary circulation. Erom the pathogenesis 
of pulmonary oedema it follows that we must pay particular attention to the 
condition of the heart, especially of the left ventricle. Hence Ave should use 
energetic stimulants, especially subcutaneous injections of camphor or ether, 



CATARRHAL PNEUMONIA 



199 



every half hour or hour. Internally we give first strophanthus (ten drops of the 
tincture every hour) and also camphor, wine, and very strong cafe noir. Besides 
that, we apply strong irritants to the chest, such as large mustard plasters or 
hot sponges. Sometimes an actual improvement of the respiration, when it has 
nearly stopped, may be obtained by a bath with cold douching. When there is 
marked general cyanosis, if the patient is on the whole strong and well nour- 
ished, venesection is sometimes of manifest benefit. Emetics, however, accom- 
plish little, and are even dangerous on account of the collapse which is apt to 
come on after them. Expectorants (benzoin, liquor ammonii anisatus) are more 
frequently prescribed, and an energetic " derivation to the intestines," by senna, 
calomel, or enemata of vinegar, seems sometimes to be really of service. Acetate 
of lead in large doses, one or two grains (gramme 0.05-0.10), in powder, every 
hour, employed empirically by Traube, is deserving of trial. 

In this way, especially in acute diseases like typhoid and pneumonia, we in 
fact sometimes succeed in averting the danger of pulmonary oedema by rapid and 
energetic action. In the cases of oedema occurring in incurable chronic diseases 
of the heart and kidneys, the remedies employed are of course unfortunately 
incapable of preventing death. 



CHAPTEK IV 

CATARRHAL PNEUMONIA 

{Broncho-pneumonia. Lobular Pneumonia) 

iEtiology. — Catarrhal pneumonia is neither serologically nor anatomically 
one single, absolutely independent disease, but from a clinical standpoint we are 
perfectly justified in grouping together the catarrhal, lobular pneumonias, which 
are usually secondary to other diseases, and especially to a previous bronchitis, and 
in contrasting them with croupous, lobar, " genuine " pneumonia. In the great 
majority of catarrhal pneumonias the belief is certainly correct, that the agents 
of inflammation do not enter the pulmonary alveoli directly from without, but 
that the inflammatory process is situated originally in the bronchi, and from 
this point extends downward to the special respiratory parenchyma of the 
lung. This extension of the inflammation may take place entirely by conti- 
nuity, or it may skip some part, as the germs are often inhaled from the bronchi 
directly into the infundibula and alveoli. The last-mentioned parts must, how- 
ever, possess considerable power of resisting germs, since the danger of an exten- 
sion of bronchitis to the alveoli generally exists only in the severer and more 
extensive cases of bronchitis or under other peculiar conditions. This exten- 
sion of the process is not uniform in all parts, but it occurs first in the distribu- 
tion of some small branches of the bronchi, and this is the reason why the pneu- 
monic infiltration affects first only a few bronchial areas — that is, individual 
lobules. 

In opposition to this generally accepted theory of the method of origin of 
the true "lobular" or "broncho-pneumonic" foci, the attempt has recently been 
made to show that the inflammatory process can pass through the walls of a 
small bronchus directly into the neighboring parenchyma of the lung, and that 
it may then extend further along the lymph-channels. Clinically, however, we 
can not yet distinguish this form of focal pneumonia from the ordinary catarrhal 
pneumonia. 

If we ask what are the conditions under which we are most apt to observe the 
development of lobular pneumonia, we must first mention a number of acute 



» 



200 



DISEASES OE THE RESPIRATORY ORGANS 



infectious diseases, in which the air-passages are primarily affected, or in which 
they may very readily be involved sympathetically. Chief among these are 
measles and whooping-cough, and next diphtheria, influenza, small-pox, etc. In 
all these diseases there is either a bronchitis at the beginning, or else it can de- 
velop very easily in them. It is in these same diseases, also, that simple bron- 
chitis comparatively often develops into lobular pneumonia. 

Eurthermore, in almost all severe acute and in many chronic diseases the 
conditions favor the development of secondary bronchitis and subsequently, at 
times, of lobular pneumonia. Everywhere in the air-passages, as well as in the 
cavities of the mouth and pharynx, saliva, mucus, etc., readily collect if the 
patient is very ill. Expectoration is imperfect, and the constant dorsal decubitus 
favors the accumulation of secretion, especially in the lower lobes. The mouth 
and pharynx are harder to keep clean than under normal conditions. Eungi and 
bacteria collect in the secretion itself, as well as in the epithelium and particles 
of food which are left in the mouth, and these excite and keep up processes of 
decomposition. The inflammatory agents, which are carried into the air-pas- 
sages with the inspired air, find everywhere favorable conditions for settling and 
further development. From the upper portions they are drawn farther downward. 
From the larger bronchi the process invades the alveoli, and leads to catarrhal 
pneumonia. It is probably of significance, too, that in such very sick persons 
the vital resistance of the tissues has suffered, and that the development of such sec- 
ondary inflammation is consequently facilitated. We must also bear in mind 
that many patients who are very ill have difficulty in swallowing. They get 
choked, and particles of food, with the germs of inflammation clinging to them, 
are carried into the air-passages. These particles, which a healthy person could 
easily cough up again, remain there, are decomposed, and give rise to bronchitis 
and lobular pneumonia. 

This is the explanation of the frequent development of lobular pneumonia in 
the course of diseases which are entirely dissimilar. We observe it especially in 
severe bed-ridden cases, in all patients with stupor, in severe infectious diseases, in 
meningitis, and also in cases of nervous disease, in which coughing and deglutition 
are impaired as a result of bulbar affections. In all such cases lobular pneu- 
monia is to be considered a complication, and with reference to its origin de- 
serves the name of inhalation pneumonia or deglutition pneumonia. We shall 
soon see that this form, under some circumstances, may pass into circumscribed 
gangrene. 

Although in the preceding we have always spoken of " agents of inflamma- 
tion " in general, the precise variety is not necessarily the same in all cases. In 
the lobular pneumonias occurring in the course of measles, whooping-cough, influ- 
enza, etc., it is possible that the original specific germs may penetrate as far as 
the alveoli, and there cause an inflammatory exudation* ; but this is certainly not 
always the case, and there are many reasons why in these affections, as well as 
in all the others mentioned above, catarrhal pneumonia should be regarded as, a 
secondary complication, dependent upon the secondary inyasion of other vari- 
eties of agents which cause inflammation. Different micro-organisms may prob- 
ably act as such agents. So far as our present investigations go, streptococci 
seem most frequently to be the special cause of broncho-pneumonia, and some- 
times in other cases staphylococci, diplococci, etc. Clinically, we can not at 
present make a complete separation on a strictly ^etiological basis. 

The development of lobular pneumonia from bronchitis is most frequent, as 
we know, in children and old people. The frequency of catarrhal pneumonia in 
childhood is due in part to the limited dimensions of the bronchi. Besides 
that, however, the diseases in which it is especially frequent — namely, measles 
and whooping-cough — are children's diseases. In old people its comparatively 



CATARRHAL PNEUMONIA 



201 



easy development is due to imperfect expectoration, aiid perhaps to the dimin- 
ished resistance of the tissues. 

The mild cases of primary bronchitis scarcely ever lead to lobular pneumonia, 
but sometimes in children, and less often in adults, a severe febrile bronchitis 
may occasion the formation of pneumonic foci. In Erlangen, the author has 
seen a good many cases which can not be regarded otherwise than as primary 
catarrhal pneumonia. We may also state that the inhalation of irritating chem- 
icals may occasion lobular pneumonia as well as bronchitis. 

Pathological Anatomy. — It is characteristic of catarrhal pneumonia that the 
inflammation is usually plainly circumscribed (vide supra), being limited to the 
territory of a small bronchus. Hence the name of " lobular " pneumonia or 
broncho-pneumonia, in distinction from croupous lobar pneumonia. An atelec- 
tasis (vide supra) of the affected lobule, arising from the plugging of the 
bronchus leading to it, often, but not always, precedes the inflammation. The 
atelectasis of course becomes pneumonia only when germs enter the atelectatic 
spot. The inflammatory process itself consists of the exudation of a scanty fluid, 
which usually does not coagulate, and of numerous pus-corpuscles (white blood- 
corpuscles) into the lumen of the alveoli. With this is usually associated more 
or less marked desquamation of the alveolar epithelium, in which we often find 
necrosis or fatty degeneration. The alveolar cavities are completely filled with 
leucocytes and epithelium; few if any red blood-corpuscles are to be seen, al- 
though in some cases they may be more abundant. The vessels of the alveolar 
walls are hyperasmic, and the connective tissue also contains a few wandering 
leucocytes. 

The inflamed lobules are readily apparent to the eye and the touch by their 
firm consistence, being devoid of air. Their color at first, from the blood con- 
tained in the inflamed part, is a dark red (" splenization "), but later it becomes 
more grayish. A bit of such an inflamed spot, cut out with the scissors, does 
not float in water but sinks, because it contains no air. The lobular boundary 
of the individual nodules is usually easily distinguished from the neighboring 
healthy tissue, but, by confluence of adjacent nodules, large portions of the lung, 
and even whole lobes, may become infiltrated throughout — generalized lobular 
pneumonia. 

Symptoms. — 1. Primary Catarrhal Pneumonia of Adults. — The primary ca- 
tarrhal pneumonia which infrequently occurs in adults usually begins with the 
same phenomena as a severe attack of acute bronchitis. The patient feels pros- 
trated, and has cough, dyspnoea, and pain upon the side which is chiefly affected. 
There is almost never a pronounced initial chill, as in croupous pneumonia. The 
fever is usually not very high, from 101° to 103° (38.5° to 39.5° C), but higher 
temperatures sometimes occur, especially at the beginning of the disease. The 
expectoration is simply catarrhal or muco-purulent, never muco-sanguineous, as 
in croupous pneumonia. The physical examination gives almost invariably in 
one lower lobe many moist rales and a slight tympanitic or dull tympanitic per- 
cussion-note. Marked dullness and definite bronchial breathing are rare. In 
the lower lobe on the other, unaffected side, we often find signs of a slight bron- 
chitis ; but in general the unilateral character of the symptoms is characteristic 
of primary catarrhal pneumonia, in distinction from ordinary bronchitis and 
secondary broncho-pneumonia. In mild cases the fever lasts from four to eight 
days, but the disease may last two or three weeks or more. There is never a 
crisis; the fever ends gradually by lysis. 

The aetiology of primary catarrhal pneumonia has been little studied. Many 
cases may be streptococcus pneumonia; we must also consider the influenza 
bacilli, since catarrhal pneumonia is especially common at the time of an influ- 
enza epidemic. 



202 



DISEASES OE THE RESPIRATORY ORGANS 



2. Secondary Catarrhal Pneumonia. — Most of the cases of catarrhal pneu- 
monia develop, as we have already said, secondarily in the course of other affec- 
tions, hence the symptoms are frequently overshadowed by those of the other 
diseases. There are often found at autopsy a few foci of lobular pneumonia in 
the lower lobes which gave rise to no clinical symptoms whatever. 

In other cases, however, the development of extensive lobular pneumonia is 
of the greatest clinical significance. In many cases of chronic bronchitis, pul- 
monary emphysema, pulmonary tuberculosis, etc., in which the patient suddenly 
grows worse with a rise of temperature, the cause is certainly the development 
of foci of lobular pneumonia. Such complications may after a time completely 
disappear, or may cause a permanent aggravation of the original condition (e. g., 
tuberculosis). The onset of lobular pneumonia in other acute diseases is very 
important. The disturbance of respiration, during the patient's life, forms the 
most striking symptom of the disease, and lobular pneumonia is shown at the 
autopsy to be the immediate cause of death. The largest part of the fatal cases 
of measles and whooping-cough, and no very small part of those of diphtheria, 
scarlet fever, typhoid, small-pox, influenza, etc., are due, in the last instance, to 
the disturbance of respiration dependent upon lobular pneumonia. 

Since a diffuse bronchitis, extending into the finer bronchi, almost always pre- 
cedes the development of lobular pneumonia, and since it may also give rise in 
itself to marked disturbance in respiration, there is no sharp boundary to be 
drawn clinically between diffuse capillary bronchitis and lobular pneumonia. 
Only the experience, a hundred times repeated, that extensive capillary bronchitis 
is apt to lead to lobular pneumonia, permits us to suspect the latter, with con- 
siderable certainty, even if there is no direct clinical evidence of it. The most 
important objective physical sign of broncho-pneumonia is the not very loud, 
medium moist rales, almost always to be heard in the lower lobes. These rales 
are often high-pitched. Dullness of the percussion-note develops only when many 
lobular ' nodules coalesce and form a more extensive infiltration of the lung. 
Then we also find bronchial respiration. 

Catarrhal pneumonia is almost always associated with fever, which is mod- 
erately high and generally has a remitting character. We must, of course, judge 
of the fever in connection with the primary disease and any other complications. 

No general statements can be made as to the duration of secondary catarrhal 
pneumonia. Sometimes the acute symptoms last only a few days, in other cases 
they continue for weeks. Catarrhal pneumonia is not infrequently followed by 
pleuritic effusion, when the lobular infiltration reaches the pleura. Foci of lobu- 
lar pneumonia may develop into abscess or gangrene, but this is rare. 

3. Catarrhal Pneumonia in Childhood. — The catarrhal pneumonia of child- 
hood is very characteristic and clinically important. It is observed most fre- 
quently in measles and whooping-cough, and also in weak, atrophic, and rachitic 
children. The increased frequency of respiration is most striking. The breath- 
ing is superficial, but labored, as is shown by the contraction of the auxiliary 
muscles of inspiration and the play of the nostrils. We also notice inspiratory 
retraction of the lower lateral portions of the thorax as a result of the incom- 
plete entrance of air. The number of respirations in a minute increases in chil- 
dren to sixty or eighty, or even more. In most cases the child has a frequent 
and apparently painful cough. Expectoration is entirely absent in small chil- 
dren. When it is present it shows no characteristic peculiarities different from 
ordinary catarrhal sputum. The general condition is always bad. The child 
is restless, apathetic, and more or less stupid. Its face is usually pale, but often 
quite cyanotic. The pulse is very rapid, and in small children may attain a 
frequency of 140 to 180 a minute. Fever is almost always present. It shows 
no typical course, it is now remitting and now intermitting, and toward evening 



CATAEKHAL PNEUMONIA 



203 



it perhaps rises to 104° or 105° (39.5°-40.5° C). The occurrence of such a 
rise in temperature is not without value in the diagnosis of catarrhal pneu- 
monia. If in diffuse capillary bronchitis a high fever is present for some time, 
we may assume with considerable certainty that the lobular infiltration has already 
begun. 

Physical examination furnishes direct evidence of the affection of the lungs, 
but its results are for the most part to be referred to the diffuse bronchitis and 
not to the lobular infiltration. Auscultation gives the most valuable signs. We 
hear over the lungs, in a greater or less extent, numerous fine and medium moist 
rales, often quite high-pitched. From these signs, strictly interpreted, we can 
diagnosticate merely bronchitis, but we may suspect pneumonia with the greatest 
probability. With very confluent broncho-pneumonia, auscultation sometimes 
gives bronchial breathing and bronchophony, besides the rales. 

It goes without saying that little lobular foci, surrounded by normal lung- 
tissue containing air, give no special signs on percussion. With numerous nodules 
running into one another, the percussion-note is duller, and there is sometimes 
tympanitic resonance. The dullness is often first to be made out over a stripe 
extending along the vertebral column — so-called " stripe-pneumonia." 

An attack of extensive lobular pneumonia is usually quite protracted. Even 
in favorable cases the disease rarely lasts less than two or three weeks, and it 
may persist much longer. The course of the disease is apt to be irregular, re- 
lapses succeeding improvement. The chief danger of the disease lies in this 
tendency to a protracted course, extending over weeks and months. Many chil- 
dren finally die, not of the lobular pneumonia itself, but from the general weak- 
ness and emaciation following the tedious febrile disease. We must remember, 
however, that complete recovery may sometimes take place quite late in the 
disease. 

The " transition of catarrhal pneumonia to caseation and tuberculosis " is a 
clinical fact with which physicians have long been conversant. In fact, we often 
find true tubercular changes in the lungs of children who have died after a 
tedious illness, as a result of measles, whooping-cough, etc. There can, of course, 
be no real question, however, of an actual transition from one disease to the other. 
In such cases either we have to do with an acquired tubercular infection, which 
has found a favorable soil in an already diseased lung, or (what is probably more 
frequently the case) the disease of the lung has promoted the development of a 
previously existing tuberculosis. It is usually weak children, with a hereditary 
predisposition to tubercle, who succumb to tuberculosis as a result of the above- 
named diseases. The diagnosis of a developing tuberculosis is not always easy, 
since it is only rarely that marked phthisical changes — like dullness at the apex, 
cavities, etc., which can be made out by a physical examination — are found in 
the lungs. We can usually suspect tuberculosis only from the general conditions 
(emaciation, persistent hectic fever, hereditary predisposition, or some secondary 
tubercular disease such as meningitis, etc.), especially as absolute proof, from the 
detection of tubercle bacilli in the sputum, is only rarely possible in children. 

Treatment. — Since we have already mentioned the proper treatment, in our 
description of the various diseases in which secondary pneumonia is especially 
prone to develop, we can now be brief. We have also laid repeated stress upon 
the possibility and the great practical importance of prophylaxis, which is self- 
evident from a just comprehension of the origin of lobular pneumonia. Besides 
keeping the nose, the mouth, and the pharynx as clean as possible, tepid 
baths, perhaps with cool douching, are the best means of preventing the de- 
velopment of lobular pneumonia, or of checking its further extension. Wet 
cold packs are often used with advantage (vide infra). It is an advantage, which 
is indeed to be considered in the second rank in comparison with the improvement 



20± 



DISEASES OF THE EESPIRATOKY ORGANS 



in respiration, that by both the bath and the pack the febrile temperature is at 
the same time reduced. 

In the treatment of the lobular pneumonia of children a wet pack including 
the whole body is the best remedy. A sheet is dipped in water, wrung out, and 
wrapped around the whole of the patient except his head and arms. Outside of 
this is to be placed a dry woolen blanket or a layer of oiled muslin. The temper- 
ature of the water employed should be 68° to 77° (16° to 20° R.). The higher 
the fever the colder should the water be, and the oftener, say every hour or two, 
must the pack be renewed. In milder cases and at night it may be allowed to 
remain for three or four hours. The beneficial influence of the pack is shown 
not only by the temperature, but still more by the respiration. It is often strik- 
ing to see how much quieter the child becomes in the pack. If the breathing, 
despite this remedy, remains unsatisfactory, and the patient becomes more and 
more stuporous, the treatment must be changed to lukewarm baths of a tem- 
perature of 77° to 86° (20° to 24° R.), with douchings of colder water. It is 
sometimes advisable in severe cases to add to the water employed for bathing or 
for the wet pack a few handfuls of mustard. The stimulation thus exerted upon 
the skin is quite marked. 

Among external applications to the chest, besides mustard plasters and poul- 
tices, dry cups are to be mentioned, which often do very good service in strong, 
older children, and especially in adults. We never need to use local blood-let- 
tings, however, in catarrhal pneumonia. 

Of internal remedies, expectorants are most used. Chief among these are 
ipecac, apomorphine, senega, and benzoic acid. This last is particularly useful 
in the lobular pneumonia of children. In strong children the abundant collec- 
tion of mucus in the bronchi may sometimes be relieved by the administration 
of an emetic, but we seldom need to resort to this. We should also be cautious 
in the use of narcotics. Stimulants (camphor, wine) must be used in severe 
cases. Antipyretics may be given to reduce the temperature, but if cool packs 
be used antipyretics can be wholly dispensed with. Inhalations or sprays are quite 
valueless in lobular pneumonia, yet it is recommended to keep the air in the sick- 
chamber constantly moist by hanging up wet towels, or by sprinkling with water. 
The room should also be as large and as well ventilated as possible. The general 
hygienic treatment is of the greatest importance. One of the most important 
duties, of which the physician must always be mindful, is to keep up the patient's 
strength by sufficient and proper food. When convalescence sets in, complete 
restoration to health may be materially furthered by going to a suitable place in 
the country. 



CHAPTER V 

CROUPOUS PNEUMONIA 

{Lung Fever. Lobar Pneumonia. Fibrinous Pneumonia. Pleuro-pneumonia) 

Croupous pneumonia is a sharply defined febrile disease of the lungs, which, 
in the great majority of cases, displays a distinct individuality in its clinical, 
anatomical, and usually, also, its setiological relations. Among the severe acute 
diseases it is decidedly one of the most important and frequent, and it is univer- 
sally familiar even to the laity under the names of pneumonia or inflammation of 
the lungs. In most cases this disease appears quite suddenly, and often, appar- 
ently without any special cause, in persons up to that time in perfect health. 
Such cases are described as primary, genuine, or frank pneumonia. On the other 



CROUPOUS PNEUMONIA 



205 



hand, a case of croupous pneumonia will sometimes occur as a complication of all 
sorts of other diseased conditions (secondary pneumonia). The clinical picture 
of pneumonia in these latter cases, however, is usually obscure and not well 
characterized, and consequently the following description is especially applicable 
to the primary form of the disease : 

iEtiology. — The thought that croupous pneumonia might be an acute in- 
fectious disease had impressed the majority of physicians for a considerable length 
of time, but this suspicion did not receive satisfactory substantiation until 
the more recent investigations in bacteriology had been made. For instance, 
Friedlander demonstrated a special form of bacillus in lungs affected with 
pneumonia. Then, later, A. Frankel, and, soon after him, Weichselbaum, proved 
that while this " pneumonia bacillus of Friedlander " is perhaps to be regarded 
as the cause of croupous inflammation of the lungs in a few cases, yet in the 
overwhelming majority of instances the particular serological factor is the so- 
called diplococcus pneumoniae {diplococcus lanceolatus capsulatus) . 

The pneumonia diplococcus is characterized by its lancet-shaped outline (" like 
the flame of a candle"), and its frequent arrangement in pairs, the individuals 
of each pair having usually their broad ends apposed. Very often there are 
short chain-forms. The pairs of diplococci are usually surrounded by a delicate 
capsule. This is particularly common in preparations of the sputum. We have 
not space to describe particulars as to the pure cultures of the pneumococci upon 
agar and similar media, 

Pneumonia diplococci are among the most widely distributed of pathogenic 
organisms. They produce severe disease not only in the lungs, but in many other 
organs. With regard to the development of the pneumonic infection, it is a par- 
ticularly interesting fact that these diplococci have been not infrequently found 
in the mouths of healthy persons. This suggests the thought that the germs 
are drawn into the lungs with the inspired air, and there settle and proliferate 
when the conditions are especially favorable — for instance, if the resisting powers 
of the organism have been impaired, or perhaps if the diplococci are especially 
virulent. In animals the injection of diplococci into the lungs almost always 
excites pneumonia, but yet it is doubtful whether the incidence of the disease in 
man always bears out the surmise above mentioned. The severity of the con- 
stitutional disturbance at the very onset of many cases certainly justifies the 
supposition that at least often the infection takes place through the blood, and 
that the pathogenic organisms are carried to the lungs by way of the blood- 
vessels. Diplococci have been repeatedly found in the blood of pneumonia pa- 
tients, and the injection of diplococci into the subcutaneous cellular tissue of 
animals, particularly rabbits and mice, invariably excites a violent and fatal con- 
stitutional infection (so-called sputum-septicaemia). Certain clinical facts 
suggest that perhaps in individual cases there may be other modes of infection; 
for instance, by way of the intestine in cases with well-marked intestinal symp- 
toms. Starting from the lungs, the diplococci may invade the pleura, less often 
the pericardium, the meninges, and other organs, so that they are invariably 
demonstrable in the pus of cases of meta-pneumonic empyema, pericarditis, and 
meningitis. From a clinical point of view their almost invariable presence in 
pneumonic expectoration (Fig. 26) is of the greatest importance. They can be 
easily demonstrated by the staining of a dried preparation with gentian-violet, 
although for absolute certainty of diagnosis further investigation is required. 
Supposing the infectious nature of pneumonia to be certain, all the other alleged 
causes may of course be regarded as at most " predisposing causes." The old 
opinion, which is yet current, that pneumonia is due to catching cold, is to be 
received with great limitations, for croupous pneumonia is very frequently 
seen independently of any such influence. In many cases it will be found that 



206 



DISEASES OF THE EESPIEATOEY OEGAXS 



an exposure to cold immediately preceded the commencement of the disease; 
but in these instances the cold is probably to be regarded merely as that circum- 
stance which promoted the occurrence of the infection, possibly because of the 

resultant injury to the bronchial and pul- 




monary epithelium. This explains the fact 
that pneumonia is especially frequent in 
certain classes, for instance, among day- 
laborers and soldiers. With regard to the 
so-called " traumatic pneumonia," the state 
of the case is similar to that of pneumonia 
due to cold. Patients from the laboring 
classes sometimes assert that they were taken 
ill as a result of heavy lifting or of a blow on 
the chest, but in such cases the subsequent 



Fig. 26.-Pneumonia diplococci. (After Stitcn in the S ] de ^ aS Probably not the re- 

Vierordt.) suit of the injury, but a symptom of the 

disease which had previously begun to de- 
velop. But still, in some few cases it may be that a preceding trauma injures the 
pulmonary tissue in such a way as to promote the occurrence of the infection. 

It is a strong argument in favor of our conception of pneumonia as an acute 
infectious disease that it may rarely be endemic. Extensive endemics of pneu- 
monia, usually of quite a malignant character, have been repeatedly observed in 
single buildings, especially in barracks or prisons, as well as in tenement houses and 
other localities. It is possible that precisely these severe cases of endemic pneu- 
monia are aetiologically different from the ordinary croupous form and occasioned 
by some other pathogenic organism; but it is also true that the diplococcus of 
pneumonia itself appears to vary greatly in its virulence. 

Pneumonia does not, as a rule, show a decided epidemic character. In a 
large population sporadic cases occur at any season. It has been observed, how- 
ever, that the disease may become very frequent or almost completely disappear, 
and then again for a time be decidedly prevalent. In a limited way, therefore, 
it is quite proper to say that there are actual epidemics of pneumonia, and these, 
again, differ from one another in special peculiarities, particularly in their com- 
paratively benign or malignant character. Here again, no doubt, an important 
part is played by the varying virulence of the diplococci which we have already 
referred to, which is also very evident under the influence of different modes 
of artificial cultivation of the organism. Most attacks occur in the winter 
or spring months, without any necessary relation, however, between the frequency 
of pneumonia and the occurrence of especially bad, wet, or cold weather. 

Individual predisposition plays an unmistakable part in the disease, as we 
must suppose that it does in all infectious diseases. Like facial erysipelas and 
acute articular rheumatism, pneumonia is one of those diseases which is prone to 
attack the same individual several times. There are persons who have had acute 
pneumonia four or five or even more times in their lives. 

We can not affirm with certainty that the liability to pneumonia is due to a 
special bodily constitution. The strongest and most robust often fall ill with it, 
and, on the other hand, weak and delicate people, with a tendency to phthisis, are 
frequently attacked. Drunkards seem to have a special predisposition to the dis- 
ease, but of course it is exceedingly hard to give any definite statistics upon this 
point. 

Pneumonia occurs at any time of life, most frequently in youth or middle age; 
but it is by no means rare in early childhood, and also in more advanced years up 
to sixty or seventy. In general it is observed rather more often in men than in 
women. 



CROUPOUS PNEUMONIA 



207 



[Defective house drainage seems to be a predisposing cause of pneumonia in 
some cases. A careful inspection of the local sanitary conditions is desirable, 
especially where more than one case occurs in a house.] 

Pathological Anatomy. — The anatomical process in croupous pneumonia con- 
sists in the formation of a hemorrhagic, coagulable " fibrinous " or " croupous " 
exudation into the pulmonary alveoli and the smallest bronchi. The develop- 
ment of the exudation usually extends over one or more lobes to their whole 
extent, and, as the alveoli and finer bronchi are completely filled by the tough 
exudation, the spongy lung, filled with air, is changed to a firm tissue, devoid of 
air, except as it is penetrated by the large bronchi. 

Since Laennec's day we distinguish three stages in the development of the pro- 
cess. In the first stage (stage of inflammatory engorgement, engouement) the 
lung is very hypersernic, dark red, and the air contained in it is even now much 
diminished, but not entirely absent. The alveoli are filled with an abundant 
exudation, already hemorrhagic, but still fluid and not coagulated. 

In the second stage (stage of red hepatization) the coagulation of the exuda- 
tion is complete, and the lung has become throughout of the consistence of liver. 
The hepatized lung shows a somewhat increased volume, and is strikingly hard. 
The surface of the section has a red and manifestly granular appearance, which 
is due to the projection of the numerous little fibrinous plugs situated in the 
alveoli. With the knife we can scrape off a tenacious, creamy, grayish-red fluid 
from the surface of the section. In the small bronchi, divided by the knife, we 
find characteristic tubular bronchial casts. 

In the third stage (stage of yellow or gray hepatization), which gradually 
develops from the second, the red surface of the section changes to a yellowish- 
gray color, often mottled, while the lung grows anemic and the exudation poor 
in red but rich in white blood-corpuscles. The consistency of the lung is still 
dense but more friable. The fluid scraped from the surface of the section is 
more abundant, milky, and puriform. 

The recovery from the process begins as the exudation becomes fluid. The 
fluid is in part absorbed and in part coughed up. 

It is not necessary for every pneumonia to go through all three stages com- 
pletely. In mild cases the process may stop sooner and recovery begin. 

Concerning the finer histological processes in croupous pneumonia, the pri- 
mary change is probably to be found in the injury and partial destruction of the 
epithelium in the alveoli and smallest bronchi, produced by inflammation due to 
the specific causes of the disease. As in every croupous inflammation of a mucous 
membrane (see the chapter on diphtheria), a coagulable exudation is formed on 
the surface of the alveoli and smaller bronchi after the destruction of the epithe- 
lium. With the microscope we see the fibrinous net-work of the exudation filling 
the alveoli. Between its meshes lie numerous red blood-corpuscles — red hepatiza- 
tion. Where there is any of the alveolar epithelium left, we often notice active 
proliferation — increase and growth of cells. Later on the white blood-corpuscles 
increase, migrating from the vessels into the exudation — yellow hepatization. 
The red blood-corpuscles are dissolved unless they are removed by expectoration. 
The fibrinous exudation is also gradually dissolved as the result of chemical 
changes not yet clearly understood (peptonization of the albuminous sub- 
stances?), and is absorbed like the cells. The regeneration of the missing epi- 
thelium comes from the epithelium that has remained intact, and with that 
follows a gradual and complete restitutio ad integrum. 

The whole process is comparatively brief, usually running its course in a week 
or ten days. The most frequent termination is in complete recovery. The other 
methods of termination, as well as the complications in other organs, will be 
spoken of in connection with the clinical symptoms. We may here mention 



208 



DISEASES OF THE RESPIRATORY ORGANS 



simply that the pleura over the affected portion of the lung takes part in the 
inflammation, without exception, as soon as the disease reaches the periphery, 
and a fibrinous pleurisy, which is not very intense, may then be recognized; 
hence the former use of the terms " pleuro-pneumonia " and " peripneumonia." 

Croupous pneumonia usually spreads rapidly over a great part of the lung. It 
is very often quite sharply limited to a single lobe — lobar pneumonia " — so that 
the septum of connective tissue between two lobes also forms a strict boundary 
between pneumonic infiltration and healthy lung tissue ; but this boundary is by 
no means insurmountable, and quite frequently several lobes are wholly or in 
part attacked by pneumonia. According to all statistics, the lower lobes are more 
frequently affected than the upper. Isolated disease of the right middle lobe may 
occur, but it is much rarer than pneumonia of the upper lobes. Of the two lungs, 
the right is attacked with decidedly greater frequency than the left. We have 
ourselves seen, in 244 cases, 137 on the right, 86 on the left, and 21 in which both 
lungs were attacked to a great extent. Simultaneous affection of the lower lobe 
on one side and the upper lobe on the other — quite a rare occurrence — is termed 
" crossed pneumonia." 

General Course of the Disease. — In spite of the numerous modifications which 
the course of pneumonia may undergo in individual instances, we can still call 
pneumonia a typical disease, considering the great majority of cases. The sub- 
jective and objective symptoms dependent upon the local affection of the lung 
usually, but not always, take the chief place among the clinical phenomena. 
In this, pneumonia differs from many other infectious diseases, such as typhoid, in 
which the local organic disease is subordinated to the general infection. 

Pneumonia usually begins quite suddenly. In the majority of cases it starts 
with a pronounced chill of half an hour to an hour's duration, or at least with a 
marked and prolonged chilliness. The initial chill may attack the patient while 
in the best of health. Many patients are able to tell almost the very hour when, 
having been previously in perfect health, they were attacked by disease. The chill 
comes on in the daytime, in the evening, or even in the middle of the night, after 
a previously quiet sleep. At the same time the patient almost always feels as if a 
severe illness were beginning. Almost at once he is obliged to give up work, has 
violent headache, and loss of appetite. Not infrequently there is a single initial 
act of vomiting. Sometimes there are at once pulmonary symptoms, such as a 
-stitch in the side and cough. Usually, however, these phenomena do not develop 
:until later (vide infra). 

In other and somewhat rarer cases the beginning of pneumonia is more grad- 
ual. A prodromal stage of a few days, or even longer, precedes the severe illness. 
The symptoms are either of quite a general and indefinite nature, consisting of 
malaise, dullness, loss of appetite, and headache, or the prodromal symptoms point 
more strongly to a pulmonary affection. The patient complains several days, or 
•even weeks, before the onset of the severe disease, of cough, thoracic discom- 
fort, slight dyspnoea, and similar symptoms. At the same time it is not possible 
to determine certainly whether these prodromata are caused by an already 
existing pneumonia or not. It is undoubtedly true that in most cases we have 
merely a simple bronchitis which furnishes a favorable soil for the develop- 
ment of pneumonia; but perhaps the initiatory bronchitis may, in some cases, 
itself be an effect of the diplococcus infection, already begun, but not yet com- 
pletely developed. 

The subjective symptoms in the chest begin shortly after the onset of the 
disease, often on the very first day, but in other cases later. The patient has 
a stabbing pain in his side whenever he draws a deep breath; the respiration, 
-therefore, becomes superficial and accelerated, and often somewhat irregular ; his 
-speech is interrupted by frequent pauses. In the further progress of a severe case 



CKOUPOUS P.XEOIOXIA 



the dyspnoea becomes extreme and the respirations very frequent. With the 
stitch in the side is associated a desire to cough. The cough is painful, and 
hence short, half suppressed, and quite frequent and troublesome. From the 
second day the expectoration may assume its characteristic viscid, rusty, hemor- 
rhagic appearance. Physical examination gives on percussion and auscultation 
the signs to be described more fully below. These are rarely to be found on the 
first day, but more frequently on the second, and sometimes not till later. 

In vv-ell-marked cases the severe constitutional symptoms persist or grow worse. 
We observe general weakness, headache, and complete loss of appetite. Some- 
times there are marked nervous symptoms, such as restlessness, wakefulness, 
stupor, and delirium; herpes appears on the lips or nose; the bowels are slug- 
gish, or, again, they may be loose; the urine is concentrated, and very often it 
contains a small amount of albumen. 

Almost always the pneumonia is associated with high fever. The typical 
character of the disease and the peculiarities of the individual case are always 
well shown by the temperature chart. As the bodily temperature rises there is a 
corresponding increase in the frequency of the pulse. 

The course varies greatly according to the previous individual circumstances, 
the severity of the disease, and the existence of complications. In the majority 
of cases, after a comparatively short duration, the disease takes a favorable turn. 
The beginning of improvement is often sudden, like the onset of the disease. 
After the symptoms have lasted for some five to seven days, or in rarer cases a 
shorter or a longer time, at a constant height or with increasing intensity, there 
occurs in the regular course of the disease a critical decline of the fever — fre- 
quently associated with quite a copious perspiration — and with that a very rapid 
improvement of all the other symptoms. In a short time complete recovery 
follows. 

In other cases, however, the course is not so favorable. The disease may have 
a fatal termination. In a third small class of cases the disease finally takes a 
protracted course, which is usually due to the occurrence of sequelae in the lungs 
or pleura. 

To this brief sketch of the disease we must append a description of the special 
symptoms. 

Description of Single Symptoms and Complications 

1. Symptoms on the Part of the Lungs. — First among the subjective symp- 
toms comes the. characteristic painful feeling or " stitch " in the side. This 
probably always has its origin in the dry pleurisy which accompanies the pneu- 
monia. It is therefore absent in the cases of central pneumonia (vide infra). 
In pneumonia of the lower and right middle lobes the pain is usually more severe 
than in pneumonia of the upper lobes. One result of the stitch in the side is the 
difficulty, or even the impossibility, of deep inspiration. Hence the patient's 
dyspnoea is considerably increased, and this explains the incongruity between the 
shortness of breath and the relatively slight extent of the pneumonia in many 
cases. If the pneumonic infiltration of the lung is extensive, of course the 
dyspnoea of the patient is also referable in part to the diminution of the respira- 
tory surface. The subjective feeling of difficulty of breathing is prominent in 
the majority of cases, and it may become most distressing. 

Cough is one of the most constant symptoms in pneumonia, and is usually very 
painful ; hence the patient often tries to suppress it. Expectoration is apt to be 
very difficult at the onset of the disease, from the viscidity and scanty amount of 
the sputum; hence severe and distressing paroxysms of coughing are some- 
times observed. The cause of the cough is probably not to be found in the affec- 
tion of the alveoli, but in the co-existing bronchitis. The irritation of the pleura 
14 



210 DISEASES OE THE EESPIEATOEY OEGANS 



may also set up a reflex cough. In rare cases cough is entirely absent in pneu- 
monia. Except in the cases of limited or late localization (vide infra), we ob- 
serve this absence of cough chiefly in the pneumonia of old or very weak people, 
and also, what is of practical importance, in the drunkard's pneumonia associated 
with delirium tremens. 

The pneumonic expectoration is so characteristic that we can often make the 
diagnosis of croupous pneumonia from this alone. It consists of a very tough 
viscid mucus, which sticks fast to the bottom of the cup even when inverted, and 
contains an intimate admixture of blood, which gives it a more or less pronounced 
red or yellow hemorrhagic color. In individual cases there are numerous grada- 
tions. We usually call the pneumonic sputum " rusty," or " brick-red," or of a 
" prune-juice color," etc. Sometimes it has only a slight reddish or yellowish 
tint, and sometimes it consists almost entirely of blood. Often the sputum is 
very frothy. In some cases it assumes a peculiar grass-green [" green-gage "] 
color, which is due to a change in the blood coloring-matter, or to a mixture with 
bile pigment in " bilious pneumonia." 

The red color of the sputum, as microscopic examination shows, is due to 
numerous red blood-corpuscles, many of them still well preserved, mixed with it. 
They are, however, in part dissolved, and hence cause the uniform red color of the 
sputum. Separate spots containing much blood are often seen in it. Besides the 
red blood-corpuscles, the microscope shows numerous partly swollen or fatty-degen- 
erated pus-corpuscles. We also see long threads of mucus; sometimes large, 
round, pigmented cells (alveolar epithelium?) ; and finally, in rare cases, ciliated 
epithelium and crystals of haematoidin. 

Erankel's diplococci are, as we have said, almost always easily demonstrable 
in the expectoration, and of course numerous other bacteria besides. 

We have still to mention the bronchial casts as important constituents of pneu- 
monic sputum. Since they are usually rolled up together, we may not find them 
except by spreading out the sputum in water. They consist of the most beautiful 
casts of the small bronchi, with many dichotomous divisions, and are a product of 
the croupous inflammation extending into the bronchi. The casts of the smallest 
bronchi are sometimes found in the form of " spirals," like those in asthmatic 
bronchitis (see page 184). 

The amount of the pneumonic sputum is, as a rule, not very considerable, but 
it differs a good deal in different cases. The chemical examination of the sputum 
has so far given no remarkable results. The amount of common salt contained in 
it is quite considerable. 

In many cases the pneumonic expectoration is absent, either because there 
is no cough or because the exudation is firmly coagulated and is absorbed with- 
out ever liquefying. Sometimes it is very tough and slimy, but without any 
admixture of blood; in other cases the sputum is simply catarrhal, when present 
at all, and then, of course, it comes not from the parts infiltrated with pneu- 
monia, but from the catarrh of the larger bronchi. In many severe cases the 
hemorrhagic expectoration soon assumes more of a purulent character. We 
often find simple catarrhal sputum, too, besides the characteristic pneumonic 
sputum. 

The pneumonic sputum is sometimes seen in the first or second day of pneu- 
monia, but it may not appear until later. With the beginning of resolution it 
gradually loses its characteristic appearance. The expectoration then becomes less 
tenacious and simply muco-purulent, and finally disappears entirely. 

Physical Examination.— Inspection shows no especial anomaly in the general 
contour of the thorax. A marked bulging of the affected side occurs only when 
there is also abundant effusion into the pleural cavity. The action of the thorax 
in respiration is very important. With a limited pneumonia we often notice 



CEOUPOUS PXEUMOXIA 



211 



a very marked delay and limitation of motion of the affected side on inspiration. 
This is due in part to the pain in the side, which comes on with every deep inspi- 
ration, and also, in extensive pneumonia, of course, to the physical conditions 
resulting from the anatomical changes. The unaffected portions of the lung act 
all the more forcibly. 

The acceleration of respiration is very striking, its frequency increasing to 
thirty or forty, or even more, a minute. We have repeatedly counted sixty res- 
pirations in adults, even in cases that finally resulted favorably. The breathing 
is shallow, but yet, in all severe cases, labored, and often also irregular, as a 
result of pleuritic pain or cough. We see the inspiratory contraction of the 
sterno-cleido-mastoids and scaleni in the neck, and often in the face a marked 
dilatation of the nostrils on inspiration. If there is marked dyspnoea the patient 
sometimes reclines in bed with the upper half of the body raised. The cheeks and 
lips are cyanotic. There is often a sharp contrast between the pale portions of 
the face near the corners of the mouth and the striking feverish and slightly 
cyanotic flush of the cheeks. 

The results of percussion are directly dependent upon the changed physical 
condition in the lung, due to the anatomical processes. In the beginning of pneu- 
monia, so long as the total amount of air in the lung remains but little altered, 
the percussion-note is clear, but when the elasticity and tension of the tissue in 
the diseased portion of the lung diminish, the resonance often becomes quite 
tympanitic. With increased exudation into the alveoli and smallest bronchi the 
amount of air in the lung constantly grows less, and therefore the percussion 
resonance becomes very dull, but it usually retains its tympanitic timbre. Since 
the pneumonic lung is rarely absolutely deprived of air — for a certain amount 
is always left in the larger bronchi — the percussion resonance seldom becomes so 
completely dull or flat, as it does, for example, with a large pleuritic effusion. 
The sensation of resistance upon the percussion of a pneumonic lung is likewise 
much less marked than over a pleuritic exudation. A marked sense of resistance 
implies, therefore, an unusual degree of involvement of the pleura in the inflam- 
mation. As soon as the absorption of the exudation begins, the volume of air 
in the lung increases, and the percussion-note becomes clearer, but remains for 
some time still markedly tympanitic, until the lung has regained its normal 
tension and elasticity. We have also to note that the intensity of the dullness in 
croupous pneumonia is sometimes subject to quite marked variations, since the 
secretion retained in the bronchi is at one time abundant and at another, after 
expectoration, scanty. 

The extent of the dullness or of the tympanitic resonance is naturally depend- 
ent upon the extent of the anatomical process. Small and central infiltrations 
may entirely escape detection by percussion. 

Auscultation is of almost greater importance than percussion in the detection 
of a beginning or limited pneumonic infiltration. The auscultatory signs depend 
upon the presence of the pneumonic exudation, and upon the consequent trans- 
formation of the lung into a firm tissue devoid of air except in the larger bronchi. 
In the beginning of the disease we hear over the affected portions coarse or fine 
rales, and very often, too, the characteristic crepitant rale on inspiration discov- 
ered by Laennec. This arises because the walls of the alveoli and smallest bron- 
chi, which are glued together by the viscid exudation, are torn apart at each 
inspiration. The crepitation, however, is neither pathognomonic of pneumonia, 
nor heard in every case of pneumonia. With increasing infiltration, bronchial 
breathing replaces the vesicular. The bronchial breathing in pneumonia is usu- 
ally very loud, sharp, and close to the ear. When the infiltration is very com- 
plete there is often to be heard a pure and loud bronchial respiration, without any 
adventitious sounds; but of course there are often heard, besides the bronchial 



212 DISEASES OE THE EES PIE AT E Y OEGANS 



breathing, high-pitched, moist rales in greater or less abundance. It is especially 
true that with the commencement of " resolution " — that is, as soon as the exuda- 
tion becomes more fluid, abundant moist rales reappear, enough to obscure more or 
less the bronchial respiration. These rales are, for the most part, rather coarse, 
moist, and have a musical character. Often we hear at this time the character- 
istic crepitant rale again (crepitus redux). The rales gradually disappear, the 
respiratory murmur loses its bronchial character, becomes harsh and indefinite, 
and finally is normally vesicular once more. 

We often hear a few rhonchi over the unaffected portions of the lungs. On 
the diseased side, the respiratory murmur is often more or less diminished 
because of the diminished respiratory movement. Otherwise respiration in the 
unaffected portions of the lungs is usually completely normal. 

The auscultatory signs just described undergo an important change if the 
larger bronchi leading to the affected portion of the lung are completely plugged 
by the secretion, as they are quite liable to be. The respiratory murmur may 
then almost entirely disappear, and we hear, perhaps, only here and there a few 
obscure rales. Since such a plugging may be very transitory, we understand why 
in one day, over the same portion of the lung, we hear first loud bronchial breath- 
ing and rales, and then quite obscure and diminished breathing. 

Wherever there is bronchial breathing, we hear marked bronchophony. Some- 
times one can discover a beginning pneumonic infiltration by bronchophony 
sooner than by any other physical sign. The vocal fremitus persists or is some- 
what increased over a pneumonic lung so long as the large bronchi are open; 
but when they become plugged, as they are quite liable to be, the vocal fremitus 
is weakened or wholly abolished; and again, the voice sounds are weakened 
whenever there is a considerable amount of pleurisy accompanying the pneu- 
monia. 

We have yet to add a few remarks about the parts of the lung in which we 
may expect first to perceive the physical signs of pneumonia, especially the aus- 
cultatory signs. 

In the first place, we should never neglect to examine carefully the lateral por- 
tions of the thorax and the axillary region when we suspect a developing pneu- 
monia. We often find the first rales here in pneumonia of the lower lobes. The 
first signs of infiltration may be found in the posterior middle portion of the 
thorax — that is, in the upper part of the lower pulmonary lobes — and thence 
they extend downward. Pneumonia of the upper lobes begins just as frequently 
behind in the apices as in front in the infra-clavicular fossa?. Isolated pneumonia 
of the right middle lobe also occurs, to be made out in front, on the right, between 
the fourth and sixth ribs. This may remain confined to the middle lobe, or extend 
to the neighboring lobes. 

Few general statements can be made about the nature or the rapidity of the 
extension of pneumonia, since in these respects the greatest differences are 
observed. The infiltration may remain confined to a small portion of the lung, 
or again it may 'spread over a whole lobe or more in a short time, even in one 
or two days. We call the pneumonia, whose constant extension by contiguity 
we can follow from day to day, wandering pneumonia (pneumonia migrans), or, 
from a purely superficial resemblance, which has given rise to many wrong ideas, 
" erysipelatous pneumonia." In these cases all the signs of resolution are present 
in the parts first attacked, while the parts affected later are found still at the 
height of the disease, or in the beginning of infiltration ; but we may also find in 
the autopsies of wandering pneumonia the parts of the lung affected later in 
a more advanced stage (gray hepatization) than the parts first attacked, which 
are still in the stage of red hepatization — that is, the inflammatory process in 
such cases seems to go through a more rapid evolution in the portions of lung 



CROUPOUS PNEUMONIA 



213 



later affected. Wandering pneumonia is almost always severe and quite pro- 
tracted. 

Pneumonia in rare cases progresses by leaps. Such cases have been termed 
erratic pneumonia. In severe cases it is not unusual for both lungs to be 
affected. We then find the pneumonia either in both lower lobes, or in the lower 
lobe on one side and the upper lobe on the other side. 

2. Symptoms on the Part of the Pleura. — As we have already mentioned, 
every case of pneumonia which reaches to the surface of the lung is associated 
with a fibrinous pleurisy, and, furthermore, it is not impossible that there should 
be an infection of the pleura without any direct extension from the neighboring 
pulmonary tissue. In many instances, the mild pleurisy which attends a pneu- 
monia causes no physical signs. On the other hand, the pain in the side in pneu- 
monia is probably always referable to the involvement of the pleura. In other 
cases the dry pleurisy attracts attention by the clearly audible friction, which may 
often be very loud, and is sometimes appreciable to the touch, if the hand is 
laid upon the side. We rarely hear the pleuritic friction sound in the begin- 
ning of pneumonia, but more frequently in the later stages, and perhaps not till 
many days after the crisis has taken place. 

The cases in which pleurisy with effusion complicates pneumonia are more im- 
portant. This may occur quite early. The abnormality of the clinical course is 
shown in these cases, as a rule, by the irregular behavior of the fever. There 
will be no typical crisis, but instead a slow lysis; or after the crisis occurs, the 
temperature will rise again. In most instances the exudation is serous, but it may 
be purulent (metapneumonic empyema). Long-continued fever should arouse 
suspicion of an empyema. In the pus of such cases of empyema the pneumonic 
diplococcus above mentioned (see page 205) has been repeatedly found. In two 
fatal cases the author has seen a hemorrhagic pleurisy with a large amount of 
coagulated blood in the pleural cavity. 

The diagnosis of pleurisy with effusion complicating pneumonia is seldom 
difficult. The percussion resonance is duller, and the sense of resistance is more 
marked than in pure pneumonia (vide supra). The respiratory murmur and the 
vocal fremitus are constantly diminished and finally entirely absent. The symp- 
toms of pressure on the neighboring organs and cavities, the heart, the liver, 
and the semilunar space (see page 287), are especially important because they are 
most unequivocal. An exploratory puncture with a Pravaz's [hypodermic] 
syringe, that has been carefully cleansed and disinfected, gives a certain and 
safe method of recognizing pleurisy in doubtful cases. When there is suspicion 
that an empyema has begun, an exploratory puncture is imperative. 

A moderate degree of pleurisy may somewhat delay the course of the disease, 
but it has no special significance. Large effusions, however, may decidedly in- 
crease the difficulty in respiration and the duration of the illness. Again, the 
pneumonia may recover, leaving the pleuritic effusion quite undisturbed. In 
pneumonia of an upper lobe, too, the pleurisy may develop below and lead to 
an effusion there, while the lower lobe itself remains quite free from pneumonia. 
Metapneumonic empyema invariably requires surgical intervention, but after 
operation it almost always pursues a rapid course to recovery. 

3. Circulatory Apparatus. Blood. — The pulse is accelerated from the begin- 
ning of the disease. In cases of moderate severity its frequency reaches 100 or 
120; and, in very severe cases, a still higher rate up to 140 or 160 is seen, and is 
always a dangerous symptom. This high rate of the pulse does not have as bad 
a significance in children as it does in adults. The consideration of the quality of 
the pulse is important. Smallness, weakness, and irregularity of the pulse are 
of bad omen as symptoms of the onset of cardiac weakness. The attacks of col- 
lapse, which sometimes come on quite suddenly in severe cases of pneumonia as 



214 



DISEASES OF THE EESPIEATOEY OEGAXS 



in other acute diseases, are especially dangerous. They occasion sudden weak- 
ness of the heart with a very small and frequent pulse. The temperature sinks to 
subnormal, 95° to 93° (35°-34° C). The peripheral parts, the nose and ex- 
tremities, become cool, pale, and somewhat cyanotic. The general weakness and 
prostration become extreme. The collapse may be recovered from, especially with 
timely assistance, but patients may die in it. 

Pericarditis with fibrinous or sero-fibrinous exudation is one of the most 
serious cardiac complications. This can always be explained by a direct conduc- 
tion of the inflammatory process from the neighboring pleura, and is therefore 
somewhat more frequent in left-sided pneumonia than in right. It is a serious 
matter. Its diagnosis is seldom difficult if we make a careful physical examina- 
tion of the heart, but with very severe and extensive symptoms in the lungs a 
complicating pericarditis may be overlooked. 

A slight fresh endocarditis is sometimes found at the autopsy, but it has no 
clinical significance. Diseases of the cardiac muscle, especially fatty and paren- 
chymatous degeneration, may be discovered post mortem, but they are by no 
means frequent. In very weak persons, drunkards, etc., who die of pneumonia, we 
sometimes, indeed, find the heart remarkably flabby, with the right ventricle 
dilated, but in many cases of pneumonia we find the muscle of the heart at the 
autopsy perfectly normal. Here we almost always have to do with conditions 
of the heart which existed previously to the pneumonia, and merely became promi- 
nent during its course. "When persons of vigorous and healthy constitution die of 
pneumonia, as, indeed, seldom occurs, the myocardium is found at the autopsy 
essentially healthy. It must be emphatically stated that our present knowledge 
does not enable us to establish before death any positive relation between the his- 
tological condition of the cardiac muscle and its functional ability. Frequent 
experience has made us certain of this fact. 

With regard to the blood, there is usually a well-marked leucocytosis in 
pneumonia. The exact count shows, not infrequently, twenty to twenty-five 
thousand or more of leucocytes in a cubic millimetre. With the crisis of the fever 
the number of leucocytes also falls abruptly, while in case of a pseudo-crisis theii 
number remains high. In some instances the leucocytosis is not marked. This 
is particularly frequent in severe and fatal cases, so that the absence of leucocy- 
tosis is regarded with some justice as an unfavorable element in prognosis. 

4. Digestive Apparatus. — In severe cases of pneumonia the tongue is dry, 
coated, and quite like the tongue in typhoid. The appetite is also almost wholly 
lost from the beginning. Vomiting is not infrequent, especially in the begin- 
ning of pneumonia, and it also occurs later. It is observed with especial fre- 
quency in the pneumonia of children. Severe symptoms on the part of the intes- 
tinal canal are rare. As a rule the bowels are constipated, but there are also cases 
in which diarrhoea is so troublesome that we must believe that the mucous mem- 
brane of the intestine is considerably involved in the morbid process {vide infra). 

The complication of pneumonia with jaundice has a certain significance, but 
its causes are not always very clear. It is apparently sometimes due to an accom- 
panying catarrh of the duodenum. In other cases the veins of the liver, dilated 
from stasis, may exert a pressure on the bile-ducts. Slight jaundice has no special 
significance, and is frequent, even in mild cases; a marked jaundice, however, is 
seen only in severe cases, especially in drunkard's pneumonia. We call such 
cases, associated with jaundice, '''bilious pneumonia." They have often other 
severe gastro-intestinal symptoms, such as vomiting, diarrhoea, and meteorism, and 
severe nervous symptoms, such as stupor and delirium. 

The liver may be somewhat enlarged, usually because of passive congestion. 
The spleen is often moderately swollen, particularly in severe cases, just as in 
other infectious diseases (acute splenic tumor). 



CROUPOUS PXEOIOXIA 



215 



5. Kidneys and Urine. — The infectious character of pneumonia is also shown 
by frequent involvement of the kidneys. Careful examination of the urine almost 
always shows a trace, or even a considerable amount, of albumen. However, this 
is very seldom of serious import, and vanishes promptly after the crisis. In many 
instances the changes in the urine are so considerable as to show an acute 
nephritis. There is a large amount of albumen, with casts, epithelium, and blood, 
in the urine. But even these cases of genuine pneumonic nephritis, which usually 
develop about the third to the sixth day of the illness, seldom prove to be serious, 
and scarcely ever result in oedema, uraemia, or other complications. Usually they 
get well rapidly. In one single case the author has observed a transition into 
chronic nephritis. The way in which pneumonia causes albuminuria and ne- 
phritis — between which no sharp dividing line can be drawn — is probably by the 
production and excretion of toxines. 

Great weight was formerly laid upon the diminution of the chlorides in the 
urine in pneumonia. In fact, the precipitate of chloride of silver, when we put a 
drop of solution of nitrate of silver into the urine, may be very slight or entirely 
absent. The chief cause of this diminution of the chlorides is the small amount 
of nourishment taken by the patient, but we must also bear in mind the large 
amount of chloride of sodium contained in the pneumonic exudation, and the 
retention of the chlorides in the body. 

Great significance was also formerly ascribed to the abundant sediment of 
sodium urate (exceptionally, uric acid) which is often noticed on the day of 
the crisis. This is known as brick-dust sediment (sedimentum lateritium), and 
is perhaps due in part to a material increase in uric acid (query: through de- 
struction of the large number of leucocytes in the blood ?)> but certainly in greater 
part to the fact that the conditions for the deposition of sediment are especially 
favorable on the day of the crisis. The urine is scanty in amount because per- 
spiration is so excessive, and hence it is concentrated and relatively very acid. 
It is, therefore, natural for the urates contained in it to be deposited in the 
form of a sediment. 

Pneumonia, in common with most of the other acute febrile diseases, is at- 
tended with an increased secretion of urea during the disease. The fact is of 
theoretic interest that during the resolution of pneumonia the urine often con- 
tains a demonstrable quantity of peptone, which is, in all probability, due to the 
destruction of the cells in the pneumonic exudation and their absorption into the 
blood. 

6. Nervous System. — As in every severe febrile disease, nervous symptoms of a 
mild type are very rarely absent in any case of pneumonia. Among the nervous 
symptoms are general weakness and dullness, and especially headache, which is 
often very intense, and is usually increased by coughing. The onset of more 
severe cerebral symptoms, particularly delirium, is of great importance. Delirium 
may appear in any case of severe pneumonia, but it is most marked and has 
peculiar characteristics in alcoholic subjects. This delirium gives the pneumonia 
of drunkards (vide infra) its characteristic stamp. 

The usual cerebral symptoms in pneumonia do not correspond with macro- 
scopic changes in the brain, but result from the poisoning of the body with the 
toxines of the pneumonia diplococcus; and yet there is also a true cerebral dis- 
ease which has beyond a doubt a special relation to pneumonia, although it is an 
infrequent complication. TVe refer to purulent cerebro-spinal meningitis. This 
complication is particularly apt to appear at times when an epidemic of cerebro- 
spinal meningitis prevails, but it has been repeatedly observed at other times. The 
diagnosis of pneumonic meningitis may be obscured by the severe constitutional 
disturbances. Factors of importance are: the stiffness of the back and the 
neck; the pain in the head and in the nape of the neck; the stupor, changing to 



216 



DISEASES OF THE EESPIEATOEY ORGANS 



deep coma; and, in many cases, optic neuritis, demonstrable by the ophthal- 
moscope. The termination of a well-marked case of meningitis is probably in- 
variably fatal, but we may have milder meningeal symptoms in pneumonia, such 
as pain and stiffness in the neck, followed by complete recovery. — With regard 
to the development of this meningitis, it is probably to be regarded as a true 
metastatic inflammation, inasmuch as the pneumonia diplococci have been re- 
peatedly found in the pus of the meningitis. As to the path which the pathogenic 
germs take to reach the meninges, we are not yet certain, but suppose that they 
travel along the lymph-channels of the intercostal nerves into the meninges sur- 
rounding the spinal cord, and thence further to the membranes of the brain. 

7. Skin. — The frequent appearance of herpes in the course of pneumonia is 
characteristic, and is of diagnostic importance. It appears from the second to the 
fourth day of the disease, or sometimes later. Its ordinary seat is on the lips, 
especially at the corners of the mouth, also on the alse of the nose, and more 
rarely on the cheeks or the ear (herpes labialis, nasalis, etc.). It has been 
seen only very rarely on other portions of the body besides the face, for example, 
on the forearm and the buttock, and in some cases on the cornea and on the 
mucous membrane of the tongue or gums. The herpes does not always come 
out all at once, but in fresh crops on successive days. We have several times seen 
two eruptions of herpes separated by an interval of several days. In repeated 
instances, under our own observation, herpes labialis, with a fresh rise of tem- 
perature, appeared some days after the crisis had taken place. Herpes may be ex- 
tensive in the mildest cases, while it is particularly apt to be scanty or absent in 
123 56"~89io severe cases. We are, there- 

fore, on the whole, inclined to 
regard a well-marked eruption 
of herpes as of favorable prog- 
nosis. The true cause of the 
herpetic eruption is unknown. 
One might think of referring 
it to the action of toxines, just 
as in the herpes of other infec- 
tious diseases, such as inter- 
mittent and relapsing fevers, 
and epidemic meningitis. 
Other affections of the skin 
are of rare occurrence. We 
have seen urticaria in some 
cases. The jaundice occurring 
in pneumonia has already been 
described. 

8. Course of the Fever (see 
Figs. 27 and 28), — Pneumonia 
is, almost without exception, 
accompanied by a more or less 
high fever with a very typical course. In the beginning of the fever the tem- 
perature rises very rapidly to a high point. Even during the initial chill the 
bodily heat increases from normal to about 104° (40° C.) and over. There 
are at present no observations to show whether, in the cases of pneumonia that 
begin gradually, there is also a gradual increase of the fever. During the course 
of the disease the fever shows on the whole a continuous or remitting character, 
but there is with this a decided tendency to single deep falls of temperature. 
Since these at first may easily be taken for the actual occurrence of crises, 
although later they are proved by the renewed rise in temperature to be a mere 



40.0 C 



39.0° 



38.0< 



37.0* 



.u 3 



BOTBWMW 

■HH 
l — 

■MHB 



Pseudo- crisis. 

Fig. 27.— Example of the temperature-curve in 
pneumonia. (Personal observation.) 



croupous 



CEOUPOUS PNEUMONIA 



217 



temporary decline in the bodily heat, they are termed- pseudo-crises. Pseudo- 
crises are usually seen in the first days of the disease, but in some cases they 
appear later and, what is remarkable, they are more apt to appear on those days, 
such as the fifth or seventh, on which the true crisis is apt to occur. They may 
be repeated one or more times, giving the fever a decidedly intermitting char- 
acter. These intermitting 
pneumonias, so called from 
the course of the fever, 
have nothing at all to do 
with malaria, which fact 
must be especially noted 
because of the frequency 
of erroneous statements. 

The fever may be decid- 
edly high in pneumonia, 
often reaching 104° or 
106° (40°-41° C). The 
highest temperature ob- 
served by us was 107.8° 
(42.1° C). This was tem- 
porary. There is a cer- 
tain parallelism between 
the height of the fever 
and its severity to this ex- 
tent, that severe cases are 
often associated with per- 
sistent and especially high fever. But sometimes the most severe and even 
fatal cases have a comparatively low temperature — between 101° and 103° (38.5- 
39.5 C). The highest temperatures are especially common in the first days of the 
illness, and yet, in spite of very high fever at the onset, the general course of 
the disease may turn out to be favorable, for the crisis may occur on the 
second or third day (vide infra, rudimentary and abortive pneumonia). In 
severe cases the progress of the disease often stamps itself plainly on the 
temperature. The pseudo-crises correspond to temporary improvements, and 
the fresh exacerbations of temperature to the invasion of a fresh lobe of the 
lung. We have certainly not seen a special rise immediately before the crisis — 
the so-called perturhatio critica — so often as many statements would lead us to 
expect. We have seen a gradual decline in temperature quite frequently in the 
closing days in fatal cases, but the opposite condition also obtains. A marked 
rise before death is not peculiar to pneumonia, but it does occur when there is a 
complicating meningitis. 

The decline of the fever is the most characteristic portion of the pneumonia 
curve. The fall in temperature usually comes on in the form of a decided crisis. 
Generally in the night there is a sinking of the temperature with a more or 
less abundant perspiration, in which as a rule the temperature may reach a sub- 
normal point— 96° to 95° (36°-35° C). The critical decline is often broken by 
new and slight elevations of temperature, so that on the morning of the next day 
there may be a definite increase of fever, the so-called protracted crisis. Only in 
a comparatively small number of cases does the fever end by lysis, in which the 
temperature goes down like steps. The duration of lysis is seldom more than 
three or four days at most. A decline of temperature by lysis is most frequent in 
severe and protracted cases, in so-called typhoid pneumonia (vide infra), and also 
particularly in pneumonia migrans. 

After the final crisis has occurred, the active pneumonic process ceases. The 




218 



DISEASES OF THE RESPIRATORY ORGAXS 



day of the crisis is therefore reckoned as the last day of actual illness. The 
pneumonia makes no advance after that, but resolution and absorption of the 
exudation and the restoration of the patient's strength still take time. Hippoc- 
rates knew when the time of the crisis occurs, and that the odd days, especially 
the fifth and the seventh, have a special significance in regard to it. In an 
infectious disease that has a typical course there can be nothing strange in the 
fact that the cessation of fever, to a certain degree, is associated with a definite 
period of time ; but Hippocrates' s rule has frequent exceptions. The crisis some- 
times occurs on the ninth, the twelfth, or the thirteenth day, and even later, and, 
on the other hand, there are quite short pneumonias of but one or two days' dura- 
tion (vide infra). 

In the days following the crisis the temperature, which, as we have said, falls 
to subnormal, regains its normal height. The pulse, which usually sinks to 
fifty or sixty during the crisis, when it often shows a slight irregularity, reaches 
its normal frequency again in a few days. We are quite apt to see, in the days 
immediately following the crisis, a slight temporary increase of temperature 
again, 100° to 102° at most (38°-39° C), but this has no special significance. 

In cases which run their course regularly, the signs in the lungs upon ausculta- 
tion and percussion become normal again in about six or eight days after the 
crisis. Often the time is even shorter than this, or it may be longer. Abnor- 
mally delayed resolution will be mentioned below. 

Special Peculiarities and Anomalies m the Course of Pneumonia 

1. Pneumonia in Children. — Besides the common lobular pneumonia there is 
also a genuine, lobar, croupous pneumonia in children, which is by no means so rare 
as some authors formerly supposed. An initial chill is seen only in older chil- 
dren; initial vomiting, however, is very common in children. In many cases 
severe cerebral symptoms, like convulsions, drowsiness, or delirium, obscure the 
pulmonary symptoms at first. The further course, the development of physical 
signs, the fever, and the complications, are quite analogous to the appearances in 
adults. The pneumonic sputum is only exceptionally obtained for observation 
in children under eight years of age. In previously healthy children the prog- 
nosis of croupous pneumonia is almost invariably favorable. 

2. Pneumonia in old people is, on the other hand, always dangerous. It may 
begin suddenly, as in people of middle age, but often it begins more slowly and 
insidiously. Its course is marked by the speedy onset of great weakness and 
debility. JSTervous symptoms, like delirium, are not infrequent. Often there is 
fatal weakness of the heart. 

3. Drunkard's Pneumonia. — We see croupous pneumonia in drunkards with 
remarkable frequency. The usually severe and dangerous course of the disease is 
due to the feeble resisting powers of their impaired organs. It is characterized 
by delirium tremens, which usually develops in the first days of the disease. The 
patient's mind is disturbed, he is very restless, constantly tries to get out of 
bed, and he fumbles night and day with his bed-clothes or night-gown. The 
alcoholic character of the delirium is shown by the patient's whole manner, the 
tremor of the hands and tongue, and the cast of his thoughts, which are usually 
happy but exceptionally anxious and terrified. His mind wanders to his former 
occupation or his usual boon companions, and the like. He becomes tearful or 
raving only when forcibly restrained. He may think himself involved in the 
tavern brawls. The alcoholic delirium is almost always associated with hallu- 
cinations. The hallucinations of little moving black figures are especially char- 
acteristic. They are either animals, rats or beetles, or little black men and 
similar weird shapes, and they give him much trouble. The subjective symptoms 
of pneumonia are wholly in the background. ~No delirious patient with pneu- 



CKOUPOUS P^EUMOKCA 



219 



monia complains of cough, pain in the chest, or dyspnoea. Careful objective 
examination is the only thing that confirms the diagnosis. Very often patients 
with a happy delirium serve to entertain those about them, until suddenly very 
severe symptoms arise, and they become somnolent and succumb, with the symp- 
toms of pulmonary oedema. The prognosis of every case of drunkard's pneu- 
monia, therefore, is to be regarded as very unfavorable. 

4. Pneumonia in Pre-existing Chronic Diseases. — Croupous pneumonia is oc- 
casionally seen in all forms of chronic disease. It is especially dangerous in 
persons who are already enfeebled, or afflicted with chronic cardiac or pulmonary 
disease, such as phthisis or emphysema. The pneumonia which often attacks pa- 
tients with emphysema is clinically important, since emphysema may render the 
objective evidence of pneumonia very obscure. The croupous exudation does not 
completely fill the dilated alveoli ; hence decided dullness and bronchial breathing 
are absent. 

5. Pneumonia with Late Localization — Central Pneumonia. — Cases are quite 
often seen whose beginning, course, and subjective symptoms correspond through- 
out to a croupous pneumonia, but in which the objective evidence of pneumonic 
infiltration evades the most careful examination. The disease begins with a 
chill, the fever is high, the patient complains of pain in the chest, which is usu- 
ally slight, there is perhaps herpes, but not till the fourth, fifth, or sixth day can 
we make out anywhere any bronchial breathing or crepitant rales. In other cases 
even the crisis may set in before we are able to localize the pneumonia with cer- 
tainty. In most of these cases we probably have to do less with an actual late 
localization than with a central infiltration which nowhere approaches the periph- 
ery, and hence is made out objectively only late or not at all. A careful exami- 
nation of the sputum is of the greatest diagnostic importance, since it sometimes 
has a perfectly characteristic appearance in spite of the absence or the indefinite 
character of the physical signs. If there is no sputum, the diagnosis may of 
course remain very uncertain. The appearance of herpes and a critical fall in 
the temperature make the diagnosis of a pneumonic infection probable even in 
these cases. In one such case the author observed the development of a pleuritic 
friction rub upon the first day after the crisis, confirming the diagnosis of pneu- 
monia after the disease had run its course. 

6. Rudimentary and Abortive Forms of Pneumonia — Unusual Localizations 
of the Pneumonic Infection. — Particularly at times of a pneumonia epidemic, but 
also at other times, the author has observed illnesses of short duration but often 
with high temperature which did not seem like clear cases of pneumonia, although 
they still were, in all probability, to be regarded as pneumonic — i. e., due to infec- 
tion with the specific diplococci. Cases of this sort usually begin suddenly with a 
chill, headache, and high temperature. Generally there is a cough and pain 
in the chest. Sometimes, however, there are no thoracic symptoms at all. The 
physician expects pneumonia to develop, but instead, on the first, second, or 
third day, the fever ceases abruptly, no changes in the lung having been discov- 
ered. Very often there will be a herpes facialis in such cases, and we doubt not 
that many instances of so-called herpes febrilis, or febris herpetica, are really 
cases of pneumonic infection, without any other localization than the herpes. 
In other instances, upon careful examination there will be found, at some place 
in the lungs, a slight crepitation, or limited bronchial breathing ; but the process 
does not extend; and in a very brief time, after a day or two, the fever ceases 
(rudimentary pneumonia; abortive pneumonia). 

In this connection we may remark that the diplococcus infection may be 
localized in still other places. Thus, for example, we regard it as very probable 
that many cases of sore throat or acute enteritis, associated with the sudden 
onset of high fever and with herpes, and especially when seen at the time of an 



220 



DISEASES OE THE EESPIEATOET ORGANS 



epidemic of pneumonia, are due to diplococcus infection. Associated with these 
attacks there may also be a late development of pulmonary symptoms. 

7. Typhoid Pneumonia — Asthenic Pneumonia. — By typhoid pneumonia we 
mean those cases in which, beside the local pulmonary symptoms, which may be 
either slight or well marked, there are remarkably severe general symptoms. 
The cases do not often begin as suddenly as ordinary pneumonia, but more 
gradually, like typhoid. Even at first the general symptoms, such as great dull- 
ness, loss of appetite, or headache, predominate over the thoracic symptoms. At 
the height of the disease there is a decided typhoidal state, stupor, delirium, a very 
dry tongue, great general weakness, and also enlargement of the spleen, and fre- 
quently mild jaundice, albuminuria, etc. Such cases are to be regarded as pneu- 
monia with an unusually severe general infection (or intoxication). They some- 
times occur in epidemics. It is said that pneumonia of the upper lobes shows a 
somewhat more frequent tendency to severe nervous symptoms than pneumonia 
of the lower lobes. Recovery from this typhoid or asthenic pneumonia, which 
may last two weeks or more, often follows by lysis. Typhoid pneumonia is by no 
means a sharply defined disease. The term serves merely as a short name for the 
grave constitutional disturbance. Clinically it is impossible to distinguish it 
sharply from pneumonia migrans, bilious pneumonia, and other forms. We must 
await further bacteriological investigations to determine whether there may not 
be some other special pathogenic organism in many cases of severe character. 
For instance, Einkler is inclined to regard certain cases of especially severe pneu- 
monia that seem to be endemic or contagious, as referable to streptococcus infec- 
tion. In this connection may be briefly mentioned, also, the peculiar and severe 
pneumonia which is contracted from diseased parrots. On the other hand, it is 
not improbable that another important factor may be a variation in the virulence 
of the ordinary pneumococcus. 

Pneumc-typhoid is to be carefully distinguished from typhoid pneumonia, 
although from a clinical point of view the diagnosis between them is often no 
easy matter. By pneumo-typhoid is meant typhoid fever with a localization of 
the typhoid bacilli in the lungs (see page 14), but it is also true that ordinary 
croupous pneumonia may occasionally appear as a complication of typhoid fever. 

8. Pneumonia with Delayed Resolution. — While the resolution of pneumonia 
is complete, as a rule, in three days to a week after the occurrence of the crisis, 
there are cases in which this process demands a much longer time. ~Not infre- 
quently, and particularly in severe cases of pneumonia, one sees after the crisis 
a surprisingly rapid disappearance of all the physical signs, while, on the other 
hand, recovery is sometimes remarkably slow in apparently mild cases; but this 
rule is of course not without exceptions. The course of the disease is often 
enough precisely the opposite. Just what are the conditions upon which the 
rapidity or the slowness of resolution depends we do not know. Sometimes unfa- 
vorable constitutional conditions, such as ansemia, debility, phthisical tendencies, 
and kyphoscoliosis, appear to delay resolution. Sometimes, on the other hand, 
no such explanation can be found. It seems to us that at certain times all the 
cases of pneumonia exhibit more of a tendency to delayed resolution than at 
others, so that it is not impossible that there are variations in the pathological 
process itself. In many cases of delayed resolution it is our opinion that we have 
to do with genuine secondary diseases, or a mixed infection in the lungs for the 
development of which the precedent croupous pneumonia had prepared a favor- 
able soil. 

With regard to the symptoms of delayed resolution, there are various forms. 
In the first place, we see cases where the crisis takes place in the usual way, and 
the temperature thereafter remains permanently normal. The patients perhaps 
feel quite well, and are troubled little by thoracic symptoms; nevertheless, the 



CEOUPOUS PNEUMONIA 



221 



dullness "upon percussion remains unchanged, or diminishes at best very gradually, 
and the bronchial breathing and moist rales can still be heard. All the signs 
diminish very slowly, sometimes occupying several weeks in their disappearance, 
and then complete recovery ensues. In a few cases it is striking that, after the 
crisis, bronchial respiration and dullness persist, while there are scarcely any 
rales and no expectoration. . In these cases it seems as if the pneumonic exuda- 
tion does not really liquefy at all, and is very slowly absorbed. In other cases 
there is no distinct crisis, but the fever continues, although lower than at first, 
and the physical signs remain to a greater or less extent. At the end of two or 
three weeks, or even still later, the fever slowly ceases, and thereupon normal 
resonance and vesicular breathing gradually return. 

In still other cases the patients remain free from fever for the first few days 
after the crisis has taken place, although the pneumonia is not completely re- 
solved. Then there appears again a rise of temperature which is mostly mod- 
erate, 100.5°-103.5° (38°-39.5° C), while the dullness continues and there are 
an abundance of moist rales and catarrhal expectoration. After two or three 
weeks the fever gradually ceases and the abnormal pulmonary signs also slowly 
disappear. In such cases we may indeed suppose that some secondary infection, 
a sort of secondary catarrhal pneumonia, has developed upon the seat of the 
croupous pneumonia. The disease may take still another course somewhat dif- 
ferent from those thus far" described, and of this we have seen repeated instances 
much resembling one another. After the occurrence of the crisis the patient 
remains for about a week without fever. During this time the dullness and the 
not very loud bronchial breathing remain unchanged. Then appears a moderate 
intermitting fever, with elevations to about 102° or 103° (39.5° C). This fever 
may last two to four weeks, or even longer. Over the affected portion of the 
lungs are heard either no moist rales or only a very few. Gradually there appears 
a moderate but distinct contraction of the side involved, then the resonance 
gradually grows clear, the respiratory sounds louder and vesicular, the fever 
ceases, and finally health is completely restored. In many other cases of delayed 
resolution, as we have already said, we see this same striking absence of moist 
rales and the development of a moderate degree of contraction. Under such 
circumstances it is often very difficult to exclude a secondary pleurisy, and we 
can not make sure except by repeated exploratory puncture. Moreover, it is not 
exceptional to find delayed resolution and secondary pleurisy both present in the 
same patient. 

9. Termination of Pneumonia in Phthisis, Contraction of the Lungs, Pulmo- 
nary Gangrene, or Pulmonary Abscess. — Four terminations of pneumonia are 
ordinarily mentioned as unusual and anomalous — the termination in " chronic 
pneumonia," in tuberculosis, in gangrene, and in abscess. 

Concerning the termination in chronic pneumonia, we have already men- 
tioned a process belonging here, the termination in contraction with ultimate 
recovery. In rare cases the contraction is permanent. The anatomical process 
consists in the development of pulmonary cirrhosis, with the formation of a large 
amount of connective tissue. This proliferation, it should be said, takes place not 
only in the interstitial tissue, but also in the interior of the alveoli by extension 
from the alveolar walls. Few clinical observations of the further course of these 
cases, provided death does not shortly ensue, have as yet been published. 

When croupous pneumonia is said to terminate in pulmonary tuberculosis, of 
course the statement can be understood to mean only that the symptoms of tuber- 
culosis follow immediately upon an attack of pneumonia. When this is the 
case — it does not occur often — it is probable that the pneumonia attacked a per- 
son already suffering from tuberculosis, in whom, however, the symptoms did not 
become evident until after the pneumonia had run its course. It may also be 



222 DISEASES OE THE EESPIRATOEY ORGANS 

that exceptionally the pneumonia furnishes a soil for a secondary infection with 
tubercle bacilli. 

Pneumonia results in pulmonary gangrene in rare instances, when the patient 
is elderly, delicate, or diabetic. Here, too, in our opinion, a new infection, with 
a foul and putrid substance, must always take place, and this excites the gan- 
grene. The previous pneumonia furnishes only the occasion for the development 
of gangrene, and perhaps prepares the soil for the agents of decomposition. The 
development of gangrene is appreciated clinically (see the appropriate chapter) 
by the change in the sputum and the persistent fever. 

The transition from pneumonia to pulmonary abscess is very rare. We can 
not decide whether a further specific cause is also needed for this, or whether the 

pneumonic process may exceptionally go on 
into the formation of abscess. We know that 
the pneumococci sometimes excite purulent 
inflammation in the pleura and in the me- 
ninges, and so it would not seem impossible 
that, under peculiar circumstances, they 
should also cause the development of an ab- 
scess in the lungs. The transition to an 
abscess may be recog-nized by the character of 
the sputum, which contains fragments of pul- 
monary tissue, such as elastic fibers, besides 
abundant pus. Moreover, we sometimes find, 
on microscopic examination of the sputum in 
abscess, scales of cholesterine (Fig. 29) and 
Fig. 29.— Cholesterine crystals. haematoidine crystals; the latter may be so 

abundant as to give the expectoration a 
brownish color. Sometimes we have seen a peculiar greenish color of the sputum. 
The signs of a pulmonary cavity are found if the abscess bursts. 

Diagnosis. — No special remarks on diagnosis need to be added to the descrip- 
tion we have given of all the important symptoms which may occur in croupous 
pneumonia. In the first place, we must consider the sudden onset with a chill and 
high fever, shortly followed by subjective thoracic symptoms, such as cough and 
pain in the side; also the characteristic sputum and the objective physical signs, the 
appearance in many cases of herpes on the face, and finally the general course of 
the disease, particularly the temperature-curve with its final sudden drop. We 
will discuss the differential diagnosis between pneumonia and pleurisy with 
effusion more fully in the description of the latter affection. 

Prognosis. — Croupous pneumonia belongs in general to the benignant infec- 
tious diseases. The great majority of cases, in previously strong and healthy 
individuals, run a favorable course, and end in complete recovery. On the other 
hand, pneumonia brings a number of perils with it, the knowledge of which 
should always make us cautious in giving a prognosis. 

One grave danger lies in the extension of the process. If the advance of the 
pneumonia can not be stopped, if the whole of one lung is involved, and, besides 
that, a great portion of the other lung, the diminution of the respiratory surfaces 
may of itself occasion a fatal termination. 

A further danger lies in the onset of certain complications. An intense pleu- 
risy, with effusion, especially if purulent, causes greater difficulty in respiration, 
and thus increases the danger. Still worse is a sero-fibrinous or purulent peri- 
carditis, which, in not very rare cases, is revealed at the autopsy as the special 
cause of death. We must note, however, that recovery sometimes finally takes place 
in spite of an empyema or of a purulent pericarditis. The complication with a 
purulent meningitis, which is fortunately very rare, is probably invariably fatal. 




CROUPOUS PNEUMONIA 



223 



The dangers of constitutional infection and constitutional intoxication are, 
on the whole, much smaller in pneumonia than in other infectious diseases; e.g., 
typhoid fever; but yet, this possibility deserves some consideration, particularly 
in certain forms of pneumonia already referred to and termed " typhoid " or 
" asthenic." Such particularly severe and malignant forms of pneumonia, with 
a high rate of mortality, sometimes appear as endemics and epidemics; but it 
should be added that these cases are also often marked by the extent of the local 
process and the development of the dangerous complications above enumerated. 

The individuality of the patient plays the most important part in the 
prognosis of pneumonia. While a constitution that was previously healthy 
and uninjured usually survives the disease, one that was previously weak and dis- 
eased readily succumbs. In this fact lies the danger of pneumonia in old, weak, 
badly nourished persons, and in persons with a pre-existing emphysema, kypho- 
scoliosis, heart disease, etc. In this, too, lies the great danger of every pneu- 
monia in drunkards. Since the nervous system is much affected by chronic alco- 
holism, we very often see outbreaks of delirium tremens in pneumonia. In like 
manner the other nerve-centers are weakened and incapable of resistance, especially 
the regulatory centers for the heart and respiration. Hence we can understand 
why even moderate drinkers, though previously strong and well to all appear- 
ances, succumb to pneumonia from failure of the heart and impairment of res- 
piration. 

If we ask upon what symptoms our prognosis in any given case should depend, 
we must reply that no single factor can be given especial prominence. Chief 
stress must always be laid upon the state of the lungs and the respiration, but 
attention must also be given to the general condition, the heart's action, the 
height of the fever, etc. The worst dangers of pneumonia have just been men- 
tioned. 

Of the abnormal terminations of pneumonia, contraction gives the best prog- 
nosis; but recovery, or at least a marked subsidence of all the symptoms, may 
sometimes take place after gangrene and abscess. 

Treatment. — Many of the milder cases of typical pneumonia need no special 
active treatment when the disease takes a favorable course. Most cases get well 
under, or, we can almost say, in spite of any treatment. From the now obsolete 
method of treatment by large bleedings, and from the use of certain drugs (vera- 
trine, tartar emetic), which are even now sometimes employed, we should expect 
harm rather than any benefit, yet under such treatment many patients have 
recovered. 

We do not know of any certain means favorably to influence the pneumonic 
process. Whether we are destined to learn of some specific mode of treatment, 
perhaps by means of some serum, after the analogy of other infectious diseases, 
as diphtheria, we can not say. A few beginnings have already been made in this 
direction, but without any practical results as yet. We are at present obliged, 
therefore, to fall back upon a purely symptomatic and constitutional treatment 
of pneumonia. 

The symptoms which are usually prominent in pneumonia, even in the milder 
cases, and of which the patient is especially desirous to be relieved, are the pain 
in the side, the troublesome cough, and the difficulty and distress in breathing. 
Since the respiratory symptoms, as we have seen, are partly due to the pain, 
as this improves the patient's breathing often undergoes a decided improvement. 
For the pain, we may first mention a number of external applications to the 
skin on the affected side. An ice-bag sometimes gives marked relief. Many 
patients can not bear this, but prefer warm poultices or cold wet compresses. The 
application of mustard plasters or dry cups to the skin may be of advantage. 
Subcutaneous injections of morphine, however, are the most effective remedy, and 



224 



DISEASES OE THE EESPIEATOEY OEGANS 



are often indispensable. There is no reason why we should not use this remedy, 
with care and in moderate doses, for the relief of pain; and, as the disease is of 
short duration, we need not particularly fear the morphine habit. Small doses 
of morphine, subcutaneously or by the mouth, may also be required to alleviate 
the cough. 

Local blood-letting is a remedy the action of which can not be explained 
physiologically, and yet experience has shown that it is of undoubted advantage. 
The relief which many patients feel after the application of eight or twelve 
leeches to the affected side is very striking; but we should prescribe them only 
when there are severe symptoms at the beginning of the disease, and in persons 
who were strong and healthy before the attack. Wet cups accomplish the same 
thing, but their effect is somewhat more powerful, and hence they should be re- 
served for strong and robust persons, such as laborers. 

The tepid or cold bath serves as the most effective means of improving the 
respiration, of aiding expectoration, and of stimulating and refreshing the whole 
system. We hold it useless, if not injurious, to give a patient baths if the dis- 
ease is progressing favorably, for almost every bath has some disagreeable feature. 
These disadvantages, however, are always less, in severe cases, than the bene- 
fit and improvement which baths give the patient, and which most patients 
recognize with gratitude. The main point is that the patient should make no 
physical exertion while in the bath, that he should be lifted into it, held and sup- 
ported while in it, and lifted into bed again after it. Since the baths are given 
primarily not on account of the fever, but to improve the respiration, and be- 
cause of their favorable influence on the nervous system, their temperature need 
not be especially low. We give them from 82° to 86° (22°-24° E.) ; somewhat 
warmer with sensitive and weak people, and cooler, down to 77° or even 72.5° 
(20°-18° E.), with strong persons, or with very high fever or severe nervous symp- 
toms. We need not employ more than two or three baths a day, and at night 
we employ them only when there are threatening symptoms. The favorable 
action of the baths is seen especially in the great relief and refreshment that 
the patient feels. The respiration is quieter and slower, but deeper. The patient 
often falls into a quiet sleep after the bath. Of late years we have often re- 
placed the baths by a wet pack, even in adults. This has been almost always very 
well received, and indeed seemed to make the patients quieter, with easier respira- 
tion and less discomfort. We would particularly and strongly recommend the 
pack for private patients, in whose case the employment of baths is associated 
with many difficulties. 

Among internal remedies for pneumonia, antipyretics are frequently em- 
ployed. We do not believe they are capable of exerting any decided influence 
upon the general course of the disease, although we admit that antipyrine and, 
under some circumstances, also phenacetine and antifebrine have a good effect, 
since they not only modify the fever, but improve the nervous symptoms and the 
general condition. Antipyrine is prescribed in doses of fifteen to thirty grains 
(grammes 1-2), particularly toward night. 

To make the cough somewhat more effective, expectorants are prescribed. We 
ourselves most frequently employ infusion of ipecac, apomorphine, infusion of 
senega, liquor ammonii anisatus, and benzoin. The last two remedies are espe- 
cially favorable if the heart is feeble. It also seems to us of some importance, 
with regard to expectoration, to prescribe an abundance of liquid in the form of 
water, tea, lemonade, and similar drinks. 

The behavior of the heart should always be watched with vigilance, especially 
in elderly and delicate persons, and in the obese and alcoholic. If the pulse 
becomes very frequent, an ice-bag is placed upon the heart. If the pulse-rate is 
remarkably rapid from the start, we may order digitalis at once, either in infu- 



CROUPOUS PNEUMONIA 



225 



sion, or, still better, in powders containing 1£ to 3 grains (gramme 0.1-0.2), re- 
peated several times a day; and as digitalis acts slowly, requiring twelve to 
twenty-four hours to make its influence felt, if the weakness of the heart is dan- 
gerous, stimulants which act more promptly must be employed. As such, tinc- 
ture of strophanthus, repeated several times a day, deserves to be recommended, 
and, above all, subcutaneous injections of oleum camphoratum (1 to 4), of which 
three or four syringefuls xv), and more, may be employed (oss. to 5j). Again, 
ether injected subcutaneously is a powerful cardiac stimulant, but it should be 
employed cautiously because of its marked local effect (paralysis of the nerves), 
and the place of injection should be the skin of the abdomen or the thigh. 

We have yet to make some remarks upon the very extensive use of large 
amounts of alcohol in pneumonia. Without doubt a free use of alcohol is neces- 
sary in drunkards, especially when delirium tremens is beginning or is already 
pronounced. Since the withdrawal of any poison that is taken habitually, like 
nicotine or morphine, may excite the severest symptoms, the sudden withdrawal 
of alcohol from drunkards may have the worst results, while, if we give an abun- 
dant supply of the stimulant to which the nervous system is accustomed, we some- 
times succeed in avoiding the onset of severe nervous symptoms, such as collapse 
and failure of the heart and respiration. Likewise wine should certainly be given 
to persons who are accustomed to it and themselves desire it. It is quite a 
different matter with patients who before their illness have not been accustomed 
to take alcohol at all, or who took it only in small amounts. It may be true that 
in these cases moderate amounts of wine may have a stimulating and exciting 
action, although we never could satisfy ourselves of the often praised influence 
•of alcohol upon the action of the heart. We hold it, however, unjustifiable to 
force large amounts of alcohol indiscriminately upon every patient with pneu- 
monia, perhaps in spite of great resistance on his part. Why should we expect 
sick persons to bear doses of alcohol which have only bad results on healthy men 
unaccustomed to them ? The assertion that fever patients " bear " alcohol better 
than healthy persons lacks proof. It should be admitted that perhaps alcohol 
is more rapidly consumed in fever than in health, but it should also be considered 
that the toxic effects of alcohol are less easily noticeable in comatose patients 
than in persons possessing normal consciousness. 

[Few American physicians of any experience will accept the reasoning of 
the author on the employment of alcoholic stimulants in those not accustomed 
to their use. 

The toxic effects of alcohol are as undesirable in pneumonia as in any other 
disease, but there are few affections in which so great tolerance is shown for this 
agent. The chief indications for its exhibition are derived from the pulse and 
the first cardiac sound at the apex. A flagging heart calls for alcohol, the effect 
■of which on the symptoms and on the circulation is to be carefully watched ; the 
quantity is to be diminished, increased, maintained, or the agent is to be omitted 
entirely, according to the conditions present in the individual case. I am no ad- 
vocate of indiscriminate alcoholic stimulation ; but I believe that lives have been 
frequently saved in the past, and will be saved in the future, by the judicious and 
sometimes extremely free use of this class of remedies in acute pneumonia. In- 
halation of oxygen has won a prominent place in the treatment of severe pneu- 
monia of late years, and cases are reported in which life seems unquestionably to 
have been saved by it. In a considerable number of cases the editor has seen only 
one which could come under this class. He has seen, however, marked tempo- 
rary improvement in pulse and respiration, with diminution of cyanosis and in- 
duction of relatively quiet sleep. But the oxygen must be given in large quan- 
tities, sometimes continuously. If its inhalation fatigues the patient, the gas 
may be allowed to escape before the mouth or under the nose of the patient. The 
15 



226 DISEASES OF THE KESPIEATOKY OKGANS 



objection to the efficient use of oxygen in some cases is the expense of perhaps- 
some hundreds of gallons a day at five cents a gallon.] 

We scarcely need to lay special emphasis on the fact that the physican should 
endeavor, so far as possible, to maintain the bodily strength by means of appro- 
priate and sufficient nourishment. Soups, bouillon with toast or rusk, milk, and 
eggs are the most suitable articles of diet, and it is sometimes proper to give- 
small amounts of finely minced meat. Care should be taken that the patient 
has an abundance of refreshing beverages. Wine and also moderate amounts of 
good beer may be allowed without hesitation. 

The treatment of complications follows the ordinary rules which have been 
given under the individual affections. We must also mention that, in delirium, 
tremens, tepid baths with cold douches sometimes have a very good effect. Be- 
sides this, we may try subcutaneous injections of strychnine, seven to fifteen 
minims of a one-per-cent. solution, once or twice a day. We can not wholly dis- 
pense with narcotics, such as morphine and chloral, but we must warn against the 
imprudent use of large doses of chloral, above thirty-five grains (grammes 2.5).. 



CHAPTER VI 

TUBERCULOSIS OF THE LUNGS 

(Pulmonary Phthisis. Pulmonary Consumption) 

General Pathology and ^Etiology of Tuberculosis 

Ever since Bayle, in 1810, demonstrated the extensive distribution of peculiar- 
nodules in the various organs, and their relation to pulmonary consumption, few 
questions have so taxed clinical observers and pathologists as those relating to the- 
cause and nature of tuberculosis. Harmony could not be reached, however, so 
long as the criterion for the decision of the questions was sought in the presence of 
definite anatomical changes, which were regarded as specific of tuberculosis. 
Laennec considered the peculiar change in the tubercular products, which later 
was named caseation by Virchow, to be characteristic, and called everything 
tubercular in which it was found. He distinguished the isolated tubercle from 
diffuse, tubercular, cheesy infiltration. Thus Laennec recognized that many pro- 
cesses were allied whose affinity was often disputed afterward, and which has only 
recently been established, such as the affinity between " scrofulous " enlargement 
of the glands and tuberculosis. Another opinion became quite prevalent, after 
Virchow discovered that precisely the same anatomical process as tubercular case- 
ation was also found in inflammatory products, which were certainly not tubercu- 
lar, and in cancerous ulcerations. Hence Virchow made a sharp distinction be- 
tween tubercle and those new growths and inflammatory processes which had 
become cheesy. The anatomical criterion of tuberculosis was, in his view, the 
presence of the miliary tubercle, a gray nodule, the size of a millet-seed at the 
largest, made up of cells like lymph-corpuscles. The study of the finer structure- 
of the miliary tubercle was now pushed most eagerly by Wagner, Schiippel, Lang- 
hans, and others, but they were unable to reach perfect harmony regarding its 
origin and significance. 

As long ago as 1865, however, a discovery was made which pointed unequivo- 
cally to the only way which could lead to a correct knowledge of tuberculosis. It 
was the fact, discovered by Villemin, that tuberculosis can be produced artificially 
by inoculating healthy animals with small amounts of tubercular and cheesy sub- 
stances. Although doubted and misinterpreted at first in various quarters, the- 



TUBERCULOSIS OF THE LUNGS 



227 



fact that tuberculosis can be transmitted, and consequently the fact of its infec- 
tious character, must now be regarded as proved beyond a doubt. In the general 
change which our opinions upon the nature of infectious diseases have undergone, 
especially in the last few years, the existence of a specific, organized cause of 
tuberculosis, too, had to be assumed. Klebs, and later Cohnheim, had already 
without reserve defined tuberculosis as a specific, infectious disease and, sooner 
than we dared to hope, R. Koch discovered the special carriers of the disease in 
the shape of the tubercle bacilli, in the year 1881. The definition of tuberculosis 
no longer rests upon any external anatomical character. Every disease is tuber- 
cular which is excited by the pathogenic action of a specific kind of bacteria, the 
tubercle bacilli discovered by Koch. 

The pathogenic bacteria of tuberculosis belong to the group of bacilli. The 
tubercle bacilli are rod-like, of small diameter, slightly rounded at their extremi- 
ties, and either straight or somewhat bent. Their length is perhaps a fourth or a 
half that of the diameter of a red blood-corpuscle. In the interior of these rods it 
is not infrequently possible to distinguish very minute colorless spots which are 
probably to be regarded as endogenous spores. The tubercle bacilli have no inde- 
pendent motion whatever. Their reaction to certain coloring matters is very char- 
acteristic, and of the highest importance with regard to their recognition (vide 
infra). We know with absolute certainty that the tubercle bacilli are always 
present in all the different forms of pulmonary tuberculosis, both in the lung itself 
and in the expectoration (vide infra), and also in tubercular diseases of other 
organs, the brain, the intestines, the spleen, the liver, and the kidneys, and 
also in " scrofulous lymph-glands," in " fungous " diseases of the bones and joints, 
and in the so-called lupus, which is nothing but a local tuberculosis of the skin. 
Precisely the same bacilli are also found in the " spontaneous " tuberculosis of 
animals, such as monkeys, puppies, and guinea-pigs, and in every tuberculosis 
that is artificially produced in animals by inoculation. Finally, by the discov- 
ery of tubercle bacilli in the " pearly distemper " of cattle, the identity of this 
disease with tuberculosis — an identity which had already been established by ex- 
periments in inoculation — was confirmed anew. 

Koch, by his successful " pure cultures " and inoculations with the cultivated 
bacilli, has established the fact that these bodies, known as tubercle bacilli, are to 
be regarded as organized, and as the special cause of tuberculosis. Bacilli coming 
from any fresh product of tubercular disease may be cultivated at a constant tem- 
perature of 98° to 100° (37°-38° 0.) upon blood-serum which has been stiffened 
by heating, and upon several other artificially prepared soils. In this cultivation 
they show certain characteristic properties in their growth, which can not be 
fully described here, and they multiply to an unlimited extent. In this way we 
can keep up perfectly pure cultures of tubercle bacilli. Inoculation experi- 
ments tried with them on all sorts of creatures always give a positive result. The 
animals fall ill, lose flesh, and finally die, and at the autopsy we find undoubted 
tubercular disease of the internal organs, which may be more or less extensive. 
The most instructive inoculations are those into the anterior chamber of the eye 
in puppies or guinea-pigs, which were first tried by Cohnheim and Salomonsen. 
After an incubation of two or three weeks we see here very plainly an eruption of 
the first nodules of tubercle in the iris, and the tuberculosis spreads to the other 
organs of the body later. 

By these experiments it was first demonstrated that tuberculosis is always, at 
the start, a purely local disease, and that its further extension depends upon the 
spread of its germs. 



228 



DISEASES OF THE EESPIEATOKY ORGANS 



^Etiology of Tuberculosis in Man 

The distribution of tubercle bacilli must be remarkably extensive, for tuber- 
cular diseases occur in almost every country on earth. The predisposition of 
mankind to the disease is also very great, and thus we understand the frightful 
fact, which statistics show, that nearly one seventh of all deaths are from tuber- 
culosis ! It has neither been proved, nor is it probable, that tubercle bacilli multi- 
ply outside of the human body, like the bacilli of splenic fever, since they can 
develop only in a constant and uniformly warm temperature between 85° and 
104° (30°-40° C). We must therefore regard them as true parasites, which can 
live — that is, which can propagate and multiply — only in the bodies of animals, 
but they (or their spores) seem to preserve their virulence and their ability to 
multiply outside of the body for a long time. Phthisical sputum may be used for 
inoculation with success, even if it has been dried for several weeks. The tuber- 
cle bacilli also resist most chemical reagents, such as nitric acid, very decidedly. 

If the body becomes infected, then, with tubercle bacilli, it is always probable 
that they have come from some other individual — man or beast — with tubercular 
disease. We need not mention how numerous the opportunities for infection may 
be, considering the present general distribution of tuberculosis. The chief stress 
in this respect is to be laid upon the expectoration of phthisical patients, which 
contains the bacilli. This dries on the floor, on the linen, and on other objects, 
and then the small particles which contain the germs of infection are carried off 
by the air. The extensive investigations of Cornet have well shown how fre- 
quently it is possible to obtain tuberculous material, which is capable of causing 
infection, from the dust in the neighborhood of phthisical patients who carelessly 
deposit their expectoration upon the floor and in handkerchiefs and elsewhere. 
On the other hand, Fliigge has lately emphasized the fact that, as shown by 
experiments, the inhalation of dry sputum in the form of dust is far less dan- 
gerous than the breathing-in of fine particles of liquid expectoration. He points 
out that the consumptive with a cough can be shown to defile the surrounding air 
with numerous minute drops of sputum containing tubercle bacilli. These hover 
for a time in the air, and may be inhaled by other persons. This mode of infec- 
tion may actually be important as causing the direct transmission of tubercu- 
losis, and that such direct transmission is possible is shown by the cases of tuber- 
culosis in married couples, in nurses, and in patients who for a long time occupy 
a ward in which are many consumptives. Still, the experience of physicians 
proves that such direct infection with tuberculosis is of very infrequent occur- 
rence (vide infra). There are very many who fall sick with tuberculosis who 
have never been in close contact with other consumptives. In such cases it must 
be that the tubercle bacilli enter the body indirectly. 

The material which contains the bacilli or spores is taken into the body, in the 
majority of cases, along with the inspired air. This is probable, because, in most 
cases, tuberculosis has its starting-point in the air-passages ? the lungs, or the lar- 
ynx. Inoculation experiments show that the first extension of the process depends 
upon the point of inoculation. If it be in the anterior chamber of the eye, the first 
nodules appear in the iris, as we have said; if it be in the abdominal cavity, we 
have first a tuberculosis of the peritoneum; if the infectious matter be inhaled, 
we have first a tuberculosis of the lungs. Hence it seems very probable that, in 
tuberculosis in man, the infectious matter is taken directly into the air-passages 
by the breath. In this way it sometimes, though rarely, attacks the upper air- 
passages, as in primary tuberculosis of the nose, the pharynx, and the larynx, but 
more frequently it affects the deeper portions of the respiratory apparatus, as in 
primary tuberculosis of the lungs and bronchi. 



TUBEKCULOSIS OF THE LUNGS 



229 



We must also consider other modes of infection, first among which is the 
possibility of infection of the intestinal canal, from swallowing the infectious 
material. The transmission of tuberculosis from domestic animals to man plays 
a part in this connection which perhaps is not unimportant. Since the pearly 
distemper of cattle is identical with tuberculosis in man, the use of the flesh of 
such animals as food furnishes a possible means of infection. It is a still more 
important circumstance that, when pearly nodules are present on the udder, 
the milk of the diseased animal may be polluted by tubercle bacilli, and that the 
use of such milk as food, when it is uncooked, certainly involves the danger of the 
transmission of tuberculosis. Primary tuberculosis of the intestines, however, is 
not very frequent, probably because the tubercle bacilli which have been swallowed 
are usually destroyed in the stomach. Still, it is to be noticed that primary tuber- 
culosis of the intestine and of the abdominal lymph-glands (vide infra) is far 
more frequent in children than in adults, and that it is children who drink the 
most milk. 

In some cases the tubercular infection may probably arise from little fissures 
and excoriations of the skin. In this way either we get a local tuberculosis of the 
skin, such as lupus, or the bacilli are carried by the lymphatics to the neighboring 
glands of the neck or axilla, establish themselves there, and set up a tubercular 
disease in them. It should be stated that even when the tubercle bacilli are 
taken into the body through the lungs or the intestine, the infectious material 
often passes the primary seat of infection without fastening itself there, and does 
not take root until it reaches the nearest lymph-glands; or perhaps, often, still 
more distant regions, such as the kidneys or the bones (?). Thus arises the so- 
called primary tuberculosis of the bronchial or mesenteric glands, leading some- 
times, as we shall see later, to various severe tubercular diseases in other parts, 
such as the pleura or peritoneum. 

It remains to mention the possibility of a primary genito-urinary tubercu- 
losis. Primary infection of the uterus and ovaries might be referable to direct 
infection from without; but it is questionable whether genito-urinary tubercu- 
losis of the male, affecting the kidneys, testicles, and prostate, arises in this man- 
ner. In such cases we may be dealing with infection due to the excretion by the 
kidneys of tubercle bacilli which have got into the body in some other way. 

Considering the wide distribution of the tubercle bacilli, and the many 
chances for infection, it seems wonderful that in spite of it so many men escape 
the disease. One factor, which has been already mentioned by Koch, must be 
borne in mind, however, and that is the extremely slow growth of the tubercle 
bacilli. This is the reason why the bacilli do not always remain in the body, but 
in many cases are eliminated again before they have gained a definite foothold. 

Individual predisposition, however, is another factor which is probably still 
more important — a factor which we can not well explain, but which we can not 
get on without, at the present time, in the pathology of many infectious diseases. 
In our conception of most of the other infectious diseases, as well as of tubercu- 
losis, we must assume provisionally an unequal predisposition to disease in differ- 
ent individuals. Only a part fall ill of all who are exposed to the action of the 
poison. These are persons in whom it is particularly easy for the poison to estab- 
lish and propagate itself. 

It is very striking that the existence of the tendency to tuberculosis is often 
expressed in the general constitutional debility of the individual, and — still more 
remarkable — in certain peculiarities of his bodily frame, e. g., the shape of his 
thorax. This phthisical habitus (vide infra) is especially common in persons 
who come from families with a tendency to tuberculosis, and it is a peculiar and 
quite inexplicable expression of the predisposition to tuberculosis, due to family 
and hereditary influence (vide infra). It should be said that the hereditary tend- 



230 



DISEASES OE THE EESPIEATOEY ORGANS 



ency to tuberculosis is not invariably associated with any striking and self-evident 
weakness of the constitution. Persons who spring from tuberculous families 
may have a vigorous frame and yet fall victims to the disease; and likewise 
also, when there is no hereditary tendency, the most powerful build does not by 
any means render one invulnerable to the disease. 

We now believe that many evil influences which were once thought to be 
causes of tuberculosis act only in increasing the predisposition to the disease. In- 
sufficient food, bad air, severe illness, childbirth, want, and care — these alone, of 
course, can never produce tuberculosis ; but we can easily imagine that the body 
which has become weakened affords less resistance to the injurious influence of 
the tubercular poison than does the strong and healthy body. Thus it seems to 
us, from our own observations, to be in the highest degree probable that chronic 
alcoholism increases the liability of the individual to tuberculosis. It is surpris- 
ing how often drunkards, possessed of a naturally most vigorous constitution, 
fall victims to tuberculosis; although in this connection we ought also to con- 
sider that drunkards are so often and so long in filthy and ill-ventilated saloons 
that they are particularly exposed to the danger of infection. 

People used often to speak of the transition of other affections of the lungs 
into pulmonary consumption — that is, into tuberculosis. It was imagined that 
an old bronchial catarrh, croupous inflammation of the lungs, or the catarrhal 
pneumonia accompanying measles, or whooping-cough, could readily become 
"tubercular." Of course the proper interpretation of such a connection is that 
the precedent disease prepares a favorable soil for infection with the tuberculous 
virus, and that consequently the tubercle bacilli fasten more readily upon the 
mucous membrane, which has been previuosly affected, than under normal con- 
ditions. Moreover, many of the infections which we formerly supposed to be 
apt to change into tuberculosis are themselves tuberculous. This is true in 
most of the so-called scrofulous diseases of the lymph-glands, bones, etc., and 
also, as we shall see later, in the overwhelming majority of cases of apparently 
primary pleurisy. !N~o one will now admit the truth of the theory, which ~Nie- 
meyer once vigorously defended, that a primary pulmonary haemorrhage could 
cause the development of pulmonary phthisis. Certainly, in the cases which 
apparently support such an opinion, the pulmonary haemorrhage is not the cause, 
but a symptom, of pulmonary tuberculosis. 

ISTo single factor, however, of those which favor the predisposition to tuber- 
culosis, plays so manifest and so visible a part as does the hereditary tendency 
above mentioned — that is, the inborn predisposition of the individual. The fact 
of the heredity of phthisis meets us with such uncommon frequency that it must 
have forced itself upon the notice of the older physicians. In the great majority 
of all cases of phthisis we can make out, by close questioning, that in the family, 
either among the older members or among the brothers and sisters, one or more 
cases of tubercular disease have already occurred. The closer we investigate, and 
the more we search for some one of the different forms in which tuberculosis 
can show itself, like pleurisy, or affections of the bones and joints, the more 
frequently we can make out this hereditary predisposition. Some persons are 
indeed of the opinion that the hereditary transmission of the disease is often 
merely apparent, and not real, from the fact that the close relations between the 
children and their diseased parents, or brothers and sisters, greatly increases the 
danger of infection of the ordinary kind. Certainly this consideration should not 
be forgotten with regard to the occasional appearance of tuberculosis in families, 
but yet it would be impossible to explain in this way alone the extremely fre- 
quent development of tuberculosis in special families. 

There can be, therefore, scarcely any doubt as to the inheritance of tubercu- 
losis, but the explanation of this fact is far from clear. The hereditary charac- 



TUBERCULOSIS OF THE LUXGS 



231 



ter of tuberculosis may very well harmonize with its infectious character." \\ e 
might assume in this case a perfect analogy with syphilis — namely, a transition of 
the infectious material itself from the parent to the child before birth. There is 
only one striking difference between syphilis and tuberculosis — that the children 
of syphilitic parents very often come into the world with definite signs of infec- 
tion, while congenital tuberculosis in this sense is an extremely rare occurrence. 
We must accordingly compare tuberculosis to that form of hereditary syphilis 
(lues hereditaria tarda) in which the first symptoms of the affection come on at a 
late period. 

Since certain considerations, however, constantly oppose such a theory, we are 
of late disposed to assume that, as a rule, tuberculosis in itself is not inherited, but 
only the predisposition to tubercular disease. This opinion agrees with the facts 
that members of a family in which tuberculosis prevails very often show the so- 
called tubercular habit even without any real tubercular disease; and that they 
often have " weak lungs " — that is, that they easily get out of breath, and mani- 
fest a distinct tendency to catarrh of the respiratory organs. Another fact, 
which to a certain extent may be regarded as an argument against the assump- 
tion of a direct hereditary transmission of the disease, is that, in cases of appar- 
ently hereditary tuberculosis, as a rule those organs first show evidences of disease 
which are most exposed to an infection from the outer world — namely, the lungs 
and larynx. 

The age of the patient has an important influence upon the predisposition to 
tubercular disease. Pulmonary tuberculosis occurs with special frequency in 
youth, between fifteen and thirty. It is not rare in children. After forty it is 
much rarer in its pronounced and rapid forms, but it is seen even in the most 
advanced age. Slight tuberculous changes are very frequently found at autopsy 
in the lungs of old persons. These changes have, as a rule, no clinical sig- 
nificance. They are simply due to the inhalation of tuberculous germs with 
scarcely any tendency to further extension because of the lack of individual pre- 
disposition to the disease. It has not yet been shown that sex has a special influ- 
ence upon liability to the disease. 

Pathological Anatomy of Tuberculosis, especially of Pulmonary 

Tuberculosis 

If now we inquire wherein consists the injury which the tubercle bacilli in- 
flict upon the body, the first point to emphasize is that the action of the tubercle 
"bacilli is at first invariably purely local. Tuberculosis does not belong to the 
" general infectious diseases," in which the infection of the whole organism, the 
general infection of the body, predominates over the local disturbances. The 
essence of tuberculosis, at least in the great majority of cases, is the local disease. 
The tubercle bacilli give rise to definite anatomical changes in the organs where 
they settle, and the consequent disturbance of function in the organ has an effect 
on the rest of the body. In many cases the whole body may be so little affected 
that we may be justified in saying that there is a purely " local tuberculosis." 

The danger of tubercular diseases, however, consists in the fact that the local 
affection often attacks the most important organs, as the lungs and the brain, 
and sets up such extensive anatomical changes in them that because of these 
changes alone it becomes impossible for life to continue longer. Besides this, the 
infection in many cases does not always confine itself to one organ, but the infec- 



* Jani has made the interesting observation, that a few tubercle bacilli may be found in phthisis in 
the vas deferens and the prostate, or in the folds of the lining membrane of the tubes, without appar- 
ent disease of these parts. Whether this, howe%-er, explains the hereditary transmission of tuberculo 
sis, is as yet doubtful. 



232 DISEASES OF THE RESPIRATORY ORGANS 



tious material extends over the body by ways and means which we shall learn 
in part later on, and attacks one organ after another, or even many at once- 
Finally, it is to be said that the peculiar character of the changes caused by tuber- 
culosis explains why these are often the cause of manifold secondary processes, 
such as toxic effects and, particularly, secondary infections. Thus arise fever,, 
suppuration, secondary inflammation, and other important phenomena, which 
will be minutely considered later. 

The entire local action of the tubercle bacilli — that is, the pathological anat- 
omy of tuberculosis — is almost wholly independent of the organ attacked. Tu- 
berculosis belongs to the group of so-called " infectious tumors " — that is, the 
local action of the tubercle bacilli consists chiefly in the production of a prolifer- 
ation and accumulation of cells at their place of settlement, which is termed a 
tubercular new growth. Without going into histological details we may say, 
briefly, that the whole process consists in a primary injury of the tissue, due to 
the invasion of the tubercle bacilli, followed by a hyperplasia of the cells peculiar 
to the tissue itself, and involving not only the connective-tissue cells but also 
those of the epithelium. In this way are developed the so-called epithelioid cells 
and the giant cells. The next step in the process is the migration of numerous 
leucocytes from the surrounding blood-vessels. The leucocytes, or round cells, 
collect about the above-mentioned new-formed cells, and may finally completely 
cover them. A network, or reticulum, is found between the individual new- 
formed cells and the wandering cells. This probably represents the remains of 
the original interstitial tissue, crowded apart by the increased number of cells. 
There is no new formation of vessels. The tubercle contains no blood-vessels. 
The tubercle bacilli lie especially inside the giant cells, but also in their vicinity. 

If these changes have progressed far enough, they become visible to the naked 
eye as a small, circumscribed grayish point, which is called a miliary tubercle. 
From these minute nodules the disease itself obtained its name of tuberculosis. 
By approximation and coalescence of neighboring tubercles — for these keep devel- 
oping because of the spread of the local infection — the tuberculous formation 
continually extends itself, and thus are gradually formed the large tubercular 
nodules, and finally the diffuse tuberculous new growth or the diffuse tubercu- 
lous infiltration. 

The tuberculous new growth, as such, can scarcely ever be distinguished histo- 
logically from other infectious tumors, such as those seen in syphilis and leprosy. 
Tuberculosis, however, has a characteristic difference in its final stages of cheesy 
degeneration and eventual disintegration of the new-formed tissue, processes 
which are apparently connected with the absence of blood-vessels and the conse- 
quent deficiency of nutrition of the new formation. Both the tuberculous infil- 
tration and also the portions of the original tissues inclosed by it perish, lose their 
nuclei, and finally become disintegrated. The manner in which they are de- 
stroyed — namely, " fatty degeneration " — belongs in the group of the so-called 
coagulation necroses. This process is recognizable to the naked eye, because the 
tuberculous infiltration when it becomes thus degenerated ta,kes on a pronounced 
yellowish color. Wherever the necrotic portions of tissue are superficially situ- 
ated they are cast off, giving rise to tuberculous ulcers. 

Alongside the tuberculous new formation there are found in the organs 
affected with tuberculosis various inflammatory processes, either simple or sup- 
purative or hemorrhagic. We may therefore surmise that the tubercle bacilli 
(or the chemical toxines formed by them), besides their characteristic effects, act 
simultaneously in another role as excitants of inflammation; but it is very 
probable, and especially so in pulmonary tuberculosis, that many of the inflam- 
matory changes which arise are not peculiar to the tuberculosis as such, but are 
to be regarded as secondary processes (vide infra), for the development of which 



TUBEKCULOSIS OF THE LUNGS 



233 



the preceding tuberculous new growth, as it disintegrates, furnishes a suit- 
able soil. 

As regards the special anatomical processes and appearances in pulmonary- 
tuberculosis, the tubercular change usually begins in the walls of the smallest 
bronchi, or not rarely in the alveoli themselves. The disease does not begin, 
however, in many different parts of the lung at once, but probably in one or two 
circumscribed spots only, and in a great majority of cases in one apex. We do 
not know why the apices are so often the starting-point of phthisis, but perhaps 
it is because of their relatively slight expiratory power, which renders them a 
favorable lodging-place for the tubercle bacilli. 

The tuberculous infiltration begins in the walls of the bronchi, and thence 
gradually extends toward the periphery. The original tuberculous bronchitis 
becomes a tuberculous peribronchitis. The infectious material extends from its 
original focus by means of the lymph- and blood-channels out into the sur- 
rounding tissue; and also as soon as superficial ulceration takes place, the in- 
fectious matter is liable to be carried by the inspired air into other bronchi. Thus 
the diseased spot, small at first, keeps gradually extending. Tubercular peribron- 
chitis is usually easily recognized with the naked eye. We notice the little lumen 
of the bronchus in the middle of the " cheesy " nodule, which at first is gray and 
later yellowish. Many of the adjacent nodules run together in part, and even 
entirely. The lumen of the bronchus is either wholly plugged by the infiltra- 
tion, or the destruction of the necrotic cells begins in the midst of the peri- 
bronchitis. In the latter case the lumen is enlarged to a little irregular hole — 
the first beginning of the formation of a cavity. 

The alveolar tissue of the lung can not long remain unaffected, with such a 
disease of the smaller bronchi. Lobular atelectasis, the necessary result of 
every permanent bronchial obstruction, must arise, but this soon passes (by pene- 
tration or aspiration of the germs) into a lobular pneumonia, which from its 
specific nature later becomes caseous. We can not. go into the histological de- 
tails here. The alveoli are filled with pus-corpuscles and large epithelioid cells,, 
which are considered by many authors to be the offspring of the alveolar epithe- 
lium. The alveolar walls are also infiltrated. This finally results in the destruc- 
tion of the cheesy and necrotic tissue, and consequently in the formation of 
cavities. At other times the neighboring nodules run together, and the tuber- 
cular infiltration thus extends, giving rise to a diffuse caseous pneumonia. These 
processes may all be readily recognized by the naked eye. The earlier stages of 
atelectasis and infiltration correspond to the jelly-like, gray coloring seen in the 
so-called gelatinous infiltration of Laennec, and the transition to caseation is 
recognized by the eye from the yellowish color. 

Although all the processes thus far described are destructive in their nature, 
changes are also found in the lungs in tuberculosis which seem to have a tendency 
toward circumscribing the disease and toward healing. Prominent among these 
are the chronic interstitial processes. We meet with the formation of new con- 
nective tissue, partly about the tubercular infiltration, but especially where there 
is already destruction of tissue, and this leads to contraction and the formation of 
a firm cicatrix. The encapsulated cheesy masses may then be in part reab- 
sorbed; in part they undergo calcification. The possibility of such a halt in the 
tuberculous process depends, however, upon certain conditions. The tuberculous 
new growth and its destruction must not advance too rapidly, and the new-formed 
tissue must not itself be destroyed before it becomes cicatrized. We see the 
cicatricial formation, therefore, more especially in chronic cases; we find it in 
places which have been affected the longest, and where the tubercular process, 
perhaps, has finally come to a standstill of its own accord. Macroscopically, this 
cicatricial connective tissue is composed of a thick, firm substance, usually pig- 



234 



DISEASES OF THE EE S PIE AT OR Y OEGAXS 



merited — the so-called pigment induration. If the cicatricial formation follows a 
previous extensive destruction of the pulmonary tissue, the affected portion of the 
lung may thus be diminished to less than half its original bulk. Cavities and 
firm cicatricial tissue form the anatomical basis of such an extensive " pulmonary 
contraction." Either the cavities are formed in the usual way from the destruc- 
tion of lung tissue, or they may be simple bronchial dilatations due to the trac- 
tion of the contracted tissue — bronchiectatic cavities. 

The contractile changes in pulmonary tuberculosis teach us that the tuber- 
cular process is in itself capable of healing. The incurability of most cases of 
phthisis is due to the fact that the infectious material from every existing tuber- 
cular nodule is carried into other bronchi, and there sets up a new tuberculosis. 
Thus the disease is constantly extended. The original tuberculosis, which was 
localized in one apex only, gradually spreads to the lower portion of the lung. 
The infectious material is carried by coughing into the trachea, and from this 
point may be carried by inspiration into the other lung. This becomes diseased, 
and finally there is such an extensive destruction of the lungs as to make the 
further continuance of life impossible. 

Besides the specific tuberculous lesions in phthisical lungs, there are very often 
found simple inflammatory processes, such as bronchitis and lobular catarrhal 
pneumonia; sometimes, also, although seldom of great extent, croupous pneu- 
monia; and finally, in exceptional instances, limited foci of gangrene. These 
secondary diseases not specifically tuberculous, and yet almost always associated 
with tuberculosis, are of the greatest clinical importance. They probably are due 
in most instances to the influence of secondary pathogenic germs (particularly 
streptococci, less often diplococci, etc.), for which the tuberculosis has merely 
prepared a favorable soil. Many clinical phenomena (particularly most of the 
febrile exacerbations of the disease) depend upon these secondary inflammatory 
processes which, in their turn, promote the further extension of the tuberculosis. 
Thus, frequently, inflammatory lesions which are due to secondary infection 
finally are transformed by the invasion of tubercle bacilli into foci of tuberculosis. 

If we consider the list of anatomical processes which are found in tuberculosis 
of the lungs, and which may be combined in the most manifold ways, we can 
understand the great diversity in the anatomical picture in different cases. Pri- 
mary tuberculosis of the bronchial wall and tubercular peribronchitis, diffuse 
cheesy pneumonia, and destruction of the tubercular new growths, with the for- 
mation of cavities, on the one hand; contracting interstitial pneumonia, cicatri- 
cial formation, and pigment induration on the other — these are the compara- 
tively simple anatomical lesions from which the whole process of pulmonary 
tuberculosis in its most varied forms is composed. Besides this, we often find here 
and there one or more miliary tubercles scattered through the lungs, which are 
probably due very largely to an extension of the infectious material by means of 
the blood or lymph current; and finally the already mentioned processes of sec- 
ondary inflammation, such as bronchitis and pneumonia. 

The secondary tubercular diseases of the pleura, the bronchial glands, and 
other organs, will receive a special description. 

Clinical History of Tuberculosis in General and of Pulmonary Tuberculosis 

in Particular 

In judging of the various appearances in the clinical picture of tuberculosis 
we must especially consider the following points: The place of the first infec- 
tion is of the chief importance — that is, the place where a local affection, set 
up by the tubercular poison, first arises. One can readily understand why all those 
organs which are directly exposed to infection from without are most frequently 



TUBERCULOSIS OF THE LUNGS 



235 



affected with primary tuberculosis. Very often, as we have said, the lungs are the 
organs first attacked. Less often the upper respiratory passages — viz., the larynx 
and nose. In other cases the tubercle bacilli fasten first upon the digestive tract 
(the intestines, less often the pharynx and the tongue). In many other cases, how- 
ever, it can not be that the tubercle bacilli directly reach the organ which seems 
to be first affected. This is true of the so-called tuberculosis of serous membranes, 
of the tuberculosis of lymph-glands, of bones and joints, of the brain and of the 
genito-urinary tract. Investigators have yet to determine the paths by which 
the tubercle bacilli reach the respective organs in these cases. The glance which 
we have just taken at the organs most frequently attacked by tuberculosis shows 
the great clinical variety of tuberculous diseases viewed from this aspect. 

Another reason for the great variation in the course of tuberculosis is found 
in the fact that the extension of the local tubercular process may vary very 
greatly as regards time. Tuberculosis in one case may produce the most exten- 
sive destruction in both lungs in a few months or even weeks, and in another case 
it may remain almost quiescent for years, or advance only very slowly. We do 
not know fully on what these differences depend, but much is certainly due to the 
hygienic influences under which the patient lives. In the last analysis, however, 
we are often led to think of individual differences of constitution, which now 
check and now favor the rapid extension of the disease. 

This predisposition is, in most cases, congenital but sometimes acquired. This 
is particularly true of alcoholic subjects, who often evince a feeble power of re- 
sistance to tuberculosis, although originally of vigorous constitution, so that the 
rapidly spreading or " galloping " forms of tuberculosis are particularly common 
in drunkards. 

A third and final reason for the" differences in the course of tubercular infec- 
tion is the manner of the further extension of the tubercular poison in the body. 
As we shall see in the description of tuberculosis in single organs, there are differ- 
ent ways in which tuberculosis may pass from one organ to another. Many con- 
tingencies are involved here, and we can easily comprehend how greatly, the whole 
clinical course of the disease must be modified by the rapidity and the degree 
in which individual organs are affected. 

After these preliminary remarks we will pass on to the description of the 
clinical course of pulmonary tuberculosis. 

The onset of pulmonary tuberculosis is quite slow and gradual in the majority 
of cases. The patient can give only an approximate idea of the time when he 
began to be ill. The symptoms are referred directly to the respiratory organs 
The cough and its attendant expectoration are the chief things which affect him. 
Moreover, there is often pain in the chest, either the pleuritic stitch, or pain 
in the sternal region, or pain between the shoulder-blades. The patient is also 
apt to complain of shortness of breath, especially on severe physical exertion. 

Besides these symptoms, which point pretty directly to disease of the respira- 
tory organs, there are often quite striking general symptoms. The patient's ema- 
ciation is especially noticeable. This may be partly, though not wholly, explained 
by his loss of appetite. Besides the emaciation there is a steadily increasing pallor 
of the skin. The patient also shows a general dullness, weakness, and disinclina- 
tion to work. There is not infrequently a slight rise of temperature in the 
first stages of the disease, which causes subjective feelings of chilliness and fever. 
Severe night-sweats may also be noticed early. 

Any such constitutional disturbance should lead the physician not to regard 
the mild thoracic symptoms, which are also present, as insignificant, but to think 
of the possibility of incipient tuberculosis. It is very important to remember that 
the pulmonary symptoms may be entirely subordinate to the general symptoms 
mentioned, and that the patient himself is apt to pay little or no attention to 



236 



DISEASES OE THE EESPIKATOKY ORGANS 



them. Incipient phthisis is therefore frequently diagnosticated as simple " chlo- 
rosis " or " gastric catarrh " for a long time, and is treated as such. An early and 
careful physical examination of the lungs and of the expectoration is the only 
protection against such an error. 

Both the pulmonary and the general symptoms assume significance, if we 
have to do with a patient in whom we suspect a " tubercular predisposition." We 
very often meet persons in whose family, either in the parents or the brothers and 
sisters, several cases of phthisis have occurred. They are persons who are always 
pale and weak, and who have previously shown a special liability to catarrh and 
other diseases of the respiratory organs — e. g., pneumonia. They have perhaps 
had diseases which our present theories bring into direct relation with tuber- 
cular infection. We refer to those quite frequent cases of pulmonary tuberculosis 
in individuals who have previously suffered from " scrofulous diseases," such as 
chronic swelling of the lymph-glands, chronic affections of the eye or ear, or 
fungous diseases of the bones and joints, pleurisy, etc. (vide supra, page 230). 

Although the first symptoms of pulmonary tuberculosis often develop in those 
who were not quite well before, this is true in only a part of the cases. We 
often see precisely the same symptoms, both the pulmonary and the general, 
occurring in persons who previously seemed quite well and strong. JSTo consti- 
tution is perfectly protected against the disease. We have even seen the her- 
culean athlete of a circus die of phthisis. 

In distinction from the slow and gradual method of the development of tuber- 
culosis which has just been described, the first symptoms in other cases may be 
more sudden. A definite exposure is often given as a cause, after which the first 
symptoms of the disease have speedily developed. It goes without saying that we 
must consider these harmful influences — a chilling of the body, a cold draught, 
over-exertion, or marked mental excitement — at most, as exciting causes. 
When pulmonary tuberculosis begins somewhat abruptly, either the initial 
symptoms are from the start directly referable to the respiratory organs 
(cough, thoracic pain, dyspnoea), or the chest symptoms may be obscured by the 
severity of the constitutional disturbance. Thus we recall a number of cases in 
which young persons fell sick rather suddenly with somewhat severe, febrile con- 
stitutional disturbance. At first no cause of the fever could be found, so that 
the diagnosis was doubtful, or was supposed to be typhoid or some other disease. 
Then after a time, thoracic symptoms developed and pulmonary tuberculosis 
could be recognized. In most cases the illness would take a rather rapid course. 
That form of pulmonary tuberculosis which is termed " pneumonic " (vide infra) 
also exhibits a decidedly acute onset. 

Those cases of pulmonary tuberculosis which begin with haemoptysis are of 
special practical importance. Of course, it must be understood that the tuber- 
cular process in the lung has existed for some time before the blood appears 
(vide supra, page 230). But in the midst of apparent health, or after some 
slight constitutional disturbance, comes a cough with bloody expectoration. 
Very often the further symptoms of pulmonary tuberculosis follow directly upon 
this initial haemoptysis (vide infra). 

In conclusion, those cases are to be mentioned in which the first signs of 
tuberculosis appear not in the lungs but in the larynx. The full description of 
these cases has already been given in the chapter on laryngeal tuberculosis. 

The further course of pulmonary tuberculosis may vary so much that it is im- 
possible to give a complete enumeration of all the possibilities. 

In some cases it advances rapidly. We can make out the extension of the dis- 
ease objectively, almost from week to week. At first the apex of one lung alone 
is attacked, soon after the lower lobe of the same lung, then the other lung, either 
at the apex first or in the lower part. Besides the pulmonary symptoms, there is 



TUBERCULOSIS OF THE LUNGS 



237 



quite a high fever, rapidly increasing emaciation, and general loss of strength. 
Death ensues in a few months. We term such cases florid phthisis, or " gallop- 
ing consumption.'' 

In other cases, however, the disease has a remarkably chronic course. Its 
onset is very gradual, or else, after rather an acute onset, there is a comparative 
cessation of all symptoms. The thoracic symptoms do not disappear, but they are 
only trifling, and do not disturb the patient. Physical examination of the lungs 
does not show any extension of the process for months. The fever which accom- 
panies it is slight, if there be any. The patient remains quite well nourished, but 
in some cases there is a good deal of weakness. He feels better and worse by 
turns, his condition being greatly influenced by the care and nursing he receives. 

Trilateral contracting phthisis especially has this comparatively favorable 
course (vide supra). The affection remains confined to one lung for a long time. 
The occurrence of contraction shows the slight tendency of the tubercular process 
to advance, and with satisfactory care the patient may remain quite well for years. 

In cases, too, which have had severe symptoms for a long time, a temporary 
standstill of the affection may take place, or an actual improvement in all the 
symptoms. At other times, in cases which have made no advance for a long time, 
the symptoms suddenly grow worse. 

There are all possible varieties between the extremes of florid phthisis and the 
very chronic cases which last for years and decades. If we recall the further 
modifications which the course of the disease may assume if complications arise, 
we can appreciate the manifold character of the clinical picture of phthisis. 

Most cases with definite signs of somewhat extensive disease terminate fatally. 
Death ensues, either with the signs of general exhaustion, or as a result of the 
final failure of respiration; or it is due to the occurrence of complications, such as 
tubercular meningitis, miliary tuberculosis, pulmonary haemorrhage, or pneu- 
mothorax. Yet, on the other hand, if the tuberculosis is not extensive, the disease 
may terminate in complete recovery. To say how frequent recovery is, is diffi- 
cult, for it is probable that many insignificant cases escape diagnosis. Further- 
more, a distinction should be drawn between recovery from a standpoint of patho- 
logical anatomy, meaning complete cicatrization, with disappearance of all tuber- 
cular new growth, and recovery from a clinical standpoint [arrest], meaning dis- 
appearance of all symptoms. Often apparent recovery proves deceptive. 

Special Symptoms axd Complications 

1. Symptoms on the Part of the Lungs. — Pain in the Chest. — Extensive de- 
struction of the lungs may occur without any feeling of pain. Many cases of 
phthisis are painless throughout their course. In other cases, however, the pa- 
tient's chief complaint is of severe pains in the side or in the front of the 
chest. These are probably always due to co-existing affections of the pleura, such 
as pleurisy, or pleuritic adhesions. In patients who suffer from severe cough, 
pains sometimes arise in the abdominal muscles and at the insertion of the dia- 
phragm, due to the excessive muscular contraction. 

Cough. — In the majority of instances cough is one of the most distressing 
symptoms of phthisis, but its severity varies very much in different individuals, 
and at different times in the same patient. We sometimes see cases, particularly 
in senile, insensitive individuals, in which, in spite of advancing phthisis, cough is 
remarkably slight, or entirely absent. In cases with severe cough, it is often 
worst at night, but paroxysms of coughing of long duration are also apt to 
come on in the morning or evening hours, which are painful and very distressing, 
and exhausting for the patient. The cough is usually associated with a more or 
less abundant expectoration, but sometimes there is chiefly a dry cough. The 



238 



DISEASES OF THE RESPIRATORY ORGANS 



cough becomes very severe if the tubercular affection attacks the larynx and 
trachea (see laryngeal tuberculosis). 

Expectoration. — The amount of expectoration differs very much in different 
cases. It is most abundant when there is extensive formation of cavities in the 
lungs. In such cases it is often evacuated in the morning by persistent coughing. 
The consistency of the great part of the sputum is muco-purulent, and it differs 
little from that of simple bronchitis ; in fact, a large part of the phthisical expec- 
toration comes from the catarrhal inflammation of the bronchial mucous mem- 
brane. Usually, however, the amount of mucus as compared with the amount 
of pus is less in phthisical sputum than in that of simple bronchitis. The 
sputum is therefore less viscid and more fluid. The amount of mucus in the ex- 
pectoration is also apt to be greater in chronic bronchitis than in tuberculosis, 
although mucus is seen in the latter. The expectoration which comes from cav- 
ities is almost pure pus, with only a slight amount of serum and mucus inter- 
mixed. Such sputum consists often of large separate masses described as num- 
mular, or coin-shaped. If received in water, the uneven, rough surface of these 
masses is often evident, and suggests their formation in the irregular pulmonary 
cavities. 

The admixture of blood with the sputum is of great diagnostic and practical 
importance. Since no other disease so often gives rise to the presence of blood 
in the expectoration, coughing of blood (haemoptysis) is almost synonymous with 
consumption among the laity. Little streaks of blood in the expectoration are 
quite frequent. They have no great significance, but, of course, they may some- 
times be the precursors of severe haemorrhages. Profuse haemoptysis takes place 
when the wall of a little pulmonary vessel — almost always a branch of the pul- 
monary artery — is infiltrated, destroyed, and finally eroded, by the tubercular new 
growth. The reason why haemoptysis is not more frequent is because the con- 
tents of the vessels usually undergo thrombosis. Severe haemorrhages very often 
have their origin in little aneurisms of the branches of the pulmonary artery, 
which penetrate into the interior of the cavities. In the cases of fatal 
h&emoptysis we frequently succeed in finding the little aneurism and its point 
of rupture. 

Pulmonary haemorrhage occurs in all stages of phthisis. The initial haemopty- 
sis has already been mentioned (page 236). This may be followed by other symp- 
toms of pulmonary tuberculosis, or the haemoptysis may cease without any imme- 
diate sequels. Pulmonary haemorrhage may also occur at any time in the further 
progress of the disease. The amount of blood raised is variable. There may be 
one or more tablespoonfuls, or one or more pints. The blood is bright red, usually 
quite frothy, but little clotted, and in part mixed with other constituents of the 
sputum. After the first well-marked haemoptysis, the expectoration usually is 
mixed with blood for several days. Again, there may be repeated haemorrhages in 
a short time. Sometimes the haemoptysis begins abruptly, not infrequently at 
night, without any occasion. In other cases, the haemorrhage is referable to some 
distinct cause, such as bodily exertion, a violent paroxysrn of coughing, strain- 
ing at stool, mental excitement, and the like. Many cases of phthisis are char- 
acterized by a special tendency to haemorrhage, while in many others haemoptysis 
never occurs. Severe haemoptyses are, of course, always an undesirable and dan- 
gerous complication, since they weaken the patient very much, and also depress 
his spirits. Many patients maintain their peculiar careless indifference, which 
is almost characteristic of the disease, despite the spitting of blood. The haemop- 
tysis may sometimes be the direct cause of death, but, as a rule, the patients sur- 
vive it. We have no better means of determining with certainty the influence 
which hsemoptysis has upon the progress of tuberculosis than by the bodily tem- 
perature. If there was no fever before, and the haemoptysis also has an afebrile 



TUBEKCULOSIS OF THE LUNGS 



239 



course, or only a very brief rise of temperature, then we may hope in general that 
the patient may fully recover from the haemorrhage and be as well as before. If, 
however, the haemoptysis is followed by persistent fever, or if the fever which 
may have previously existed becomes higher and more persistent, we have every 
reason to suppose that the tuberculous process is making more rapid advances 
subsequently to the haemoptysis. We here append a temperature chart (Fig. 30) 

* Haemoptysis. 









SSHSBSSSSSBSSSSS35SSS3SS 


SSSS33SII 

nun 
mm 
mm 


!!! 


■ 

i 

mrs* 


!! 
1 


muuwHnu 

iHiinnm 

Mi l H IS 


li! 
II 


in 



Fig. 30.— Influence of a pulmonary haemorrhage upon the bodily temperature. (Erlangen medical clinique.) 

illustrating the temporary influence of a haemoptysis upon the temperature in a 
stationary afebrile case of pulmonary tuberculosis. The fact that the fever 
preceded the haemorrhage by a few days is probably due to the tuberculous arte- 
ritis, because of which material capable of exciting fever entered the circulation 
before the process had caused complete destruction and bursting of the arterial 
wall, and consequent pulmonary haemorrhage. 

A purulent sputum intimately mixed with blood is quite frequent and charac- 
teristic in many cases of phthisis with extensive formation of cavities. This is 
formed in the cavities from the mixture of the purulent secretion with little 
capillary haemorrhages. In this way the sputum, which is often nummular, 
assumes a greasy character and a reddish-brown or chocolate color. 

If foetid or gangrenous processes develop in the lungs, the sputum becomes 
foetid. In some cases we see temporarily in phthisis the characteristic sputum 
of croupous pneumonia, which comes from portions of the lung attacked with 
secondary pneumonia. 

Microscopic examination of the sputum may show — besides the ordinary mor- 
phological elements, such as pus-corpuscles, red blood-corpuscles, and epithelium 
— two constituents which are of decided diagnostic importance: elastic fibers 
and tubercle bacilli. 

The demonstration of elastic fibers in the expectoration permits us to decide 
with certainty that there is a destructive process in the lungs, and thus it usually 
is direct proof of tuberculosis. Elastic fibers are also found in pulmonary gan- 
grene, and in the very rare cases of pulmonary abscess, as well as in tuberculosis, 
but gangrene is easily recognized by the other peculiarities of the sputum. The 
search for elastic fibers in the expectoration of tubercular patients demands a cer- 
tain amount of practice. We are most sure to find them if we look in the sputum, 
when it is spread out, for little lentiform particles, which can easily be discerned 
with the naked eye. These consist of necrotic shreds of tissue torn off from the 
walls of cavities. If we press one of these " kernels " under a cover-glass we find, 
in the midst of the granular detritus, beautifully twisted elastic fibers, which 
often have quite a definite alveolar arrangement (see Fig. 31). The elastic tissue 
is the only one spared in the general destruction. There is a special method of 
looking for elastic fibers. The sputum is boiled in sodic hydrate, diluted with 



240 



DISEASES OF THE KESPIEATOKY OEGAXS 



water, and we look for elastic fibers in the precipitate which then forms. We are 
never justified, however, in deciding that pulmonary tuberculosis is absent because 
we do not find elastic fibers in the sputum. Their presence is the only thing that 
has real diagnostic significance. 

The discovery of tubercle bacilli in the expectoration of phthisical patients is 
of much greater importance, and often this alone is decisive (see Fig. 32). They 
were first demonstrated by Koch, but Ehrlich devised the first simple method for 
their discovery, which can be easily employed by any physician. 

The simplest method and the one which we now employ almost exclusively 
for staining the bacilli, is as follows: Some of the sputum is rubbed between two 
cover-glasses, which are then slowly separated, leaving upon each cover-glass a 



very thin layer of sputum. In order to fasten this sputum upon the cover-glass, 
the latter is passed three times slowly through a gas flame. The cover-glass is 
now held with a pair of forceps and covered with the following staining-fluid 
(carbol-fuchsine solution), which was first proposed by Ziehl and Neelsen: Dis- 
tilled water, 100 parts; crystals of carbolic acid, 5 parts; fuchsine, 1 part; mix, 
filter, and add alcohol, 10 parts. This staining solution upon the cover-glass is 
heated to boiling for a short time, and then the staining is completed. The cover- 
glass is now washed, first in absolute alcohol, then in distilled water, then placed 
for about two minutes in a solution of 2 parts of methyl-blue in 100 parts of a 
twenty-five-per-cent. solution of sulphuric acid. The acid bleaches out the dif- 
fused fuchsine stain, leaving the tubercle bacilli still colored, while the pus-cor- 
puscles are colored blue. The preparation is now rinsed in water, dried between 
two pieces of filter paper, and examined in Canada balsam. The whole process, 
when one has had a certain degree of experience, requires four or five minutes. 
The number of bacilli in different cases, and at different times in the same case, 
varies considerably. The more abundant the bacilli, the more reason have we to 
suppose there is a rapidly advancing process of ulceration, but of course we 
can never draw a broad conclusion as to the extent of the tuberculous disease 
from the number of bacilli in the sputum. Our only information on this point 
must come from the physical examination, and other clinical observations. On 
the other hand, the diagnostic significance of the demonstration of bacilli with 
regard to the recognition of a pulmonary tuberculosis can not be overrated. 




Fig. 31.— Elastic fibers. 



Fig. 32.— Tubercle bacilli in the sputum. 



TUBEKCULOSIS OF THE LUNGS 



241 



Every positive result is absolutely decisive, aud the diagnosis of tuberculosis of 
the lungs ought certainly never to be made unless the bacilli have been demon- 
strated. Very frequently bacilli may be found in the sputum in early cases, at a 
time when no other certain sign of tuberculosis can be detected. On the other 
hand, we scarcely need to point out that the physician should be cautious in the 
interpretation of negative results. In all suspicious cases we must repeat the ex- 
amination of the sputum over and over again. 

Dyspnoea. — Many patients hardly ever complain of their breathing in spite of 
extensive destruction in the lungs. A patient who is much emaciated manifestly 
needs little oxygen, and the increased frequency of respiration, which is almost 
constant, can satisfy his needs. If there is a greater demand upon the respiration, 
a subjective feeling of dyspnoea may of course very readily occur, especially on 
a slight bodily exertion. In many cases, however, the patient complains of a dif- 
ficulty in breathing even when quiet, especially if pleuritic pains or adhesions 
between the surfaces of the pleura prevent him from taking a deep breath; and 
in the final stages the dyspnoea may be extreme. 

2. Symptoms on Physical Examination. — In many cases inspection gives us 
that general impression of the patient which we term the " phthisical habit." The 
special signs of this are as follows : A slender but often quite a tall frame, weak 
muscular development, a thin layer of fat, a pale and perhaps very delicate skin 
with a bluish translucence, sometimes a circumscribed " hectic " flush in the 
cheeks, a long and slender neck, a long and flat thorax, small, thin hands, etc. Of 
course this characteristic constitutional habit is not equally well marked in all 
cases. The inspection of the thorax is of special value. The phthisical or " para- 
lytic " thorax is generally noticeable from its length, but it is narrow and flat. 
Unusual width of single intercostal spaces, and acuteness of the epigastric angle, 
are associated with a long thorax. The sternum is also long and narrow, and the 
sternal angle — Louis's angle — is sometimes particularly prominent. The supra- 
clavicular and infra-clavicular fossae are sunken, the neck is wasted, and the 
shoulder-blades stand out from the thorax. On comparing the two halves 
of the thorax we very often observe a distinct drawing-in and flattening (con- 
traction) on the side most affected. This change is most frequent in the upper 
and anterior portions of the chest, but it is not rare even in the posterior and 
lower. 

The paralytic form of thorax is very often seen in phthisis, but it may be en- 
tirely absent. 

The respiration is usually somewhat accelerated, and sometimes quite mark- 
edly so in women with disease of the apices. The feminine type of high thoracic 
breathing is largely changed to low thoracic or diaphragmatic breathing. A 
unilateral impairment of respiration is of greater importance; in such a case 
the apex in front or even the whole side, if there be phthisis of the lower lobe, 
lags in inspiration. The respiration is sometimes irregular, especially if there be 
pleuritic pains. 

The results of percussion are, of course, entirely dependent upon the sort of 
anatomical changes in the lungs, and hence differ very greatly in different cases. 
Since the phthisical process begins in the apices in the majority of cases, our 
chief attention is turned to the condition of the upper portions of the lungs on 
percussion. Slight changes in percussion may wholly escape discovery. Only 
when the air contained in the lung-tissue in the part affected is replaced to a cer- 
tain degree by the tubercular infiltration does the percussion-note become dull. 
Unilateral dullness at the apex is therefore one of the most frequent physical 
signs of phthisis. We can usually make it out most plainly in the upper anterior 
intercostal spaces first, and in incipient cases often in the supra-clavicular fossae 
only, but it is also observed sometimes in the back in the supra-scapular fossae. 
16 



242 



DISEASES OF THE EESPIEATOEY ORGAXS 



As the infiltration advances the dullness becomes more extensive. For the accu- 
rate determination of the limits of dullness in the upper portions of the lungs,, we 
recommend that percussion should be practiced in such a way as to proceed from 
the normal resonance of the lower portions upward toward the affected area. This 
method is particularly useful for the back of the chest. Often the dullness takes 
a tympanitic quality as a result of diminished tension in the lung, or more or less 
pulmonary retraction. Changes in tension may render the resonance, in begin- 
ning tuberculosis, deeply tympanitic without any accompanying dullness. 

The formation of cavities in tuberculosis has a great influence on the percus- 
sion-note. The dullness on percussion may thus become decidedly less, the degree 
of resonance depending, of course, upon the fullness of the cavity and the char- 
acter of the surrounding tissue. We often find a decided tympanitic resonance 
or a combination of dullness and tympany over a cavity. The different modifica- 
tions of the percussion-note in cavities are given below. The " cracked-pot reso- 
nance," or buckram sound, is met with in percussing over cavities, but we also find 
it in many other pathological conditions, and in children not infrequently when 
the lung is normal. 

Auscultation also gives no special pathognomonic signs of phthisis. Varying 
with the character and extent of the tubercular changes, abnormal respiratory 
sounds and adventitious sounds are heard in place of the normal vesicular mur- 
mur. With slighter changes the vesicular breathing is merely modified; it seems 
remarkably diminished or interrupted, or sometimes exaggerated, with prolonged 
expiration. When the infiltration of the lungs increases, we find bronchial res- 
piration in place of the vesicular breathing-; but, on the other hand, the forma- 
tion of a cavity is a frequent cause of bronchial respiration. 

Various sorts of moist rales are among the most frequent and diagnostically 
important of the auscultatory signs of phthisis. They are caused by the collection 
of secretion in the bronchi, or in pulmonary cavities. The more abundant and 
liquid the secretion is which is set in motion by the air current which traverses 
it, the more abundant and moister the rales. The larger the space is in which 
they develop, the coarser they are. Besides the true moist rales, there are also 
dry bronchitic rales (sibilant or sonorous) occasionally to be heard in portions of 
the tuberculous lung. In general, we may say that the extent of the tuberculous 
disease in the lungs can be determined by no symptom so surely as by the auscul- 
tatory signs relating to the respiration, and the adventitious sounds which may 
be present. 

Physical Diagnosis of Incipient Phthisis. — The importance of the diagnosis 
of early phthisis is so great that we will briefly sketch its most important physical 
signs. Xow that the examination of the sputum for tubercle bacilli plays by far 
the most prominent part in the recognition of incipient tuberculosis, and is the 
only decisive evidence, the physical signs of this condition have lost much of their 
former importance. Still, even now. the determination of the seat and extent 
of the early process is extremely desirable. The auscultatory signs in the begin- 
ning of the disease are in general more certain and easier t ( o recognize than those 
from percussion. He who lays too much weight on the so-called " slight dullness 
at the apex " will often make a false diagnosis. We will mention the following 
symptoms: 1. Constant and evident diminution of the respiratory murmur at 
one apex, especially if it. is associated with marked deficiency of the respiratory 
movement on the affected side. In some cases the respiratory murmur on the 
diseased side is not weaker, but it has a more indefinite and harsher character; 
or again it may be rude, sharp, and " puerile." 2. Markedly interrupted respira- 
tion at one apex. 3. A prolonged expiratory murmur, which has a harsh charac- 
ter. 4. The discovery of dry rhonchi or moist rales at one apex is most important, 
since we know by experience that " apex catarrhs " are, as a rule, tubercular. 5. 



TUBERCULOSIS OF THE LUXGS 



243 



Definite dullness, apparent on repeated examinations, or tympanitic dullness or 
tympany at one apex. 6. Evident contraction at one apex, as revealed by inspec- 
tion or percussion above the clavicles. 7. Some authors lay stress upon a systolic 
murmur in the subclavian artery, especially loud on expiration. This may occur 
in the beginning of phthisis, if the caliber of the vessel is narrowed by processes 
of contraction in the neighboring apex, but this symptom is neither frequent nor 
of great practical importance. 

The chief rule in the diagnosis of incipient phthisis must be held to be this 
— not to give a definite opinion until repeated examinations have been made. 
The other portions of the lungs are to be carefully examined as well as the 
apices, since in not very rare cases tuberculosis may begin in the lower lobes. 
We must always consider the patient's general symptoms as well as the physical 
signs (vide infra, diagnosis). 

Diagnosis of Cavities. — The positive diagnosis of pulmonary cavities by 
means of physical examination is often very difficult. Any one who will compare 
the discoveries at autopsies with the results of previous physical examination of 
consumptives will be in a position to confirm the truth of this statement. We 
may mention as the chief symptoms of a cavity : 1. Loud bronchial respiration, 
perhaps of an amphoric character, in places where the percussion-note is only 
slightly or not at all dull, but perhaps tympanitic. Such a condition means that 
the bronchial respiration is not due to an infiltration of lung-tissue. Bronchial 
respiration, however, may of course be heard over cavities which are surrounded 
by thickened lung-tissue, and hence give dullness on percussion. Pure amphoric 
respiration is very characteristic of a cavity, particularly if there is a clear, 
metallic quality to the sound ; but this sort of respiratory murmur is heard only 
when the cavity is comparatively large, of regular shape, and with smooth walls. 
Under these circumstances the moist rales, if there are any, also have a clearly 
metallic sound (tinkle), and the percussion resonance may also be distinctly 
metallic. This last should be demonstrated by rod percussion with simultaneous 
auscultation. In many cases of this sort the differential diagnosis, between a 
large cavity and a sacculated pneumothorax (see page 298), is very difficult. 
2. The so-called metamorphosing respiration, which begins as vesicular and sud- 
denly becomes bronchial, is heard especially over cavities, and hence has a diag- 
nostic value. 3. The different kinds of " changes in the percussion-note " over 
cavities are important signs. The most frequent and of greatest practical im- 
portance is Wintrich's change of note. This is when the tympanitic resonance, 
which is obtained over the cavity, becomes, on opening the mouth, more decided- 
ly tympanitic, louder, and especially much higher. The respiratory change of 
pitch of Eriedreich usually consists of a higher pitch on inspiration, but here 
there are numerous variations. Gerhardt's change of pitch (Weil) consists in a 
change of the tympanitic resonance when the patient changes his position, the 
pitch usually being higher when the patient sits up than when he is lying down. 
4. Loud, bubbling rales are one of the most frequent signs of a cavity. They 
are definite indications of the occurrence of rales in a larger space than is nor- 
mally present in the apices of the lungs. If we have coarse and metallic rales in 
the apices of the lung, there is considerable probability of the existence of a cav- 
ity, inasmuch as the normal apices can not produce such sounds. 

Contraction of the Lungs [Eibroid Phthisis]. — Unilateral contraction of the 
lungs, much more frequent on the left than on the right, is a form of tuberculosis 
which is made apparent both by special physical signs and also by certain clinical 
peculiarities. It is usually recognized at once by inspection of the thorax, one 
side of the thorax being remarkably retracted. The upper anterior portions of 
the thorax, and, in all cases of a high degree of disease, the lower lateral and 
posterior portions, are much less tense than the corresponding parts on the other 



2M 



DISEASES OE THE EESPIEATOEY OEGAXS 



healthy side. The fossae and intercostal spaces on the affected side are deeper, 
the shoulder-blade is drawn nearer the vertebral column, and the latter is even 
sometimes drawn over to the contracted side (scoliosis). The resonance is dimin- 
ished to a greater or less degree, over the affected side, which either lags behind 
or remains almost wholly at rest on respiration. The respiratory murmur is quite 
loud, and bronchial; and we also hear many rales, which are usually bubbling. 
Exceptionally the rales are few and the respiratory murmur feeble and indis- 
tinct. Anatomically, we have to do with a marked process of contraction of the 
interstitial connective tissue in the lungs, which is almost always associated with 
extensive formation of cavities, partly of an ulcerative, partly of a bronchiectatic 
character. The pleura is involved in the process almost without exception, but 
almost always secondarily; it is also thickened and contracted. If the pleuritic 
thickening is marked, the respiratory murmur and the vocal fremitus are de- 
cidedly weakened. 

The influence of the contraction on the neighboring organs is very decided, 
and usually it is easy to discover. The heart especially, whose external peri- 
cardium is in most cases very adherent to the pleura, is drawn well over to the side 
of the contraction. The apex-beat and the cardiac dullness are correspondingly 
displaced. With left-sided contraction the heart may be drawn over to the line of 
the left axilla, and with right-sided contraction it may be drawn to the median 
line, or even to the right of the sternum. With contraction of the left upper 
lobe the anterior surface of the heart comes into immediate contact with the an- 
terior chest-wall over a larger area than normal. We therefore see the motions 
of the heart over an abnormal extent, and we can often feel very plainly in the 
second left intercostal space the pulsation and the closure of the valves in dias- 
tole of the pulmonary artery. The upward traction of the diaphragm may be 
recognized by the position of the liver, or, in left-sided contraction, by the in- 
crease of the " semilunar " tympanitic space on the left. We usually find the 
sound lung on the other side quite emphysematous, as shown by the downward 
displacement of the lower boundary of the lung, and also by the drawing over of 
the anterior median edge of the lung to the contracted side. In a part of the 
cases we can make out by percussion the development of consecutive dilatation 
and hypertrophy of the right ventricle. 

These are the chief physical signs of the so-called unilateral form of chronic 
pulmonary contraction. We would add here a few clinical remarks. These 
cases often, but of course not always, run a very chronic course, lasting for years. 
The general condition and the nutrition of the patient may thus remain com- 
paratively undisturbed for a long time. The patient looks somewhat pale and 
cyanotic, yet he is so well nourished as to present a very marked contrast to the 
appearance of the ordinary cases of phthisis. The appetite remains good, the 
fever is entirely absent, or else a slight degree of fever may be at times discov- 
ered by careful examination. The cough and expectoration, too, though often 
quite troublesome, are at other times very slight, especially when the patient 
has good care and nourishment. We need not wonder* then, that formerly 
many physicians did not consider that these cases had anything to do with phthi- 
sis — " consumption " ; and yet we are convinced by many clinical and anatomical 
observations that, serologically, they are in by far the greatest part tubercular. 
They represent a very slow form of tuberculosis, which has time to develop inter- 
stitial processes which lead to contraction — that is, to local healing. If such 
cases come to autopsy, their tubercular character is usually definitely confirmed. 
We find undoubted tubercular lesions in the other lung and also in the remaining 
organs — e. g., the intestines. Sudden changes for the worse may occur in every 
" pulmonary contraction," even those cases which seem favorable ; the other lung 
may become highly tubercular, a miliary tuberculosis or a tubercular meningitis 



TUBEKCULOSIS OE THE LUNGS 



215 



may develop, etc. On the whole, however, the slow course of this form of chronic 
tuberculosis is characteristic and of great practical significance, and its prognosis 
is therefore comparatively favorable. 

We can not deny that a non-tubercular unilateral contraction of the lung 
may occur. As a result of bronchitis (particularly in cases due to the inhalation 
of dust), and also after pleurisy, processes of contraction develop, which are 
associated with the formation of bronchiectasis, and certainly have nothing to do 
with tuberculosis. In rare cases also croupous pneumonia is followed by unilat- 
eral contraction of the lung; and finally there is a rare and by no means satis- 
factorily investigated form of unilateral chronic interstitial pneumonia, with 
contraction, often associated with the formation of bronchiectasis. The differ- 
ential diagnosis of these conditions from tuberculous contraction rests in part 
upon the clinical history, which should be carefully taken, but mainly upon the 
absence of tubercle bacilli in the expectoration. 

In conclusion, we must mention that there are very many transitional forms 
between pulmonary contraction and the other varieties of pulmonary tuberculosis. 
We find more or less extensive processes of contraction in one apex in most cases 
of phthisis. 

Disseminated Pulmonary Tuberculosis. — There is a form of pulmonary tuber- 
culosis which it is very hard to make out on physical examination. In this we 
have to do with numerous peribronchial nodules disseminated over the whole 
lung. As there is still a good deal of normal tissue, containing air, between these 
nodules, percussion affords no dullness, and auscultation gives at most diffuse 
rhonchi ; hence this form is often confused with chronic bronchitis or pulmonary 
emphysema. The diagnosis can seldom be made from the physical signs, but only 
from the other symptoms, such as fever, emaciation, striking pallor of the skin, 
and the sputum. 

This form of phthisis sometimes runs a chronic course, but usually it is quite 
rapid. It occurs in elderly people, and also in children. Many forms of " dis- 
seminated, coarse granular " tuberculosis are transitional forms between this and 
genuine acute miliary tuberculosis. 

Pneumonic Form of Pulmonary Tuberculosis. — A special clinical interest 
attaches to that form of pulmonary tuberculosis termed pneumonic, which 
we have already briefly mentioned. The disease begins in a decidedly acute 
manner with dyspnoea, frequent cough, and pain in the side. Sometimes we 
observe even a distinct initial chill. The expectoration is scanty, viscid, 
mucous, and often reddish or hsemorrhagic. It sometimes also has a peculiar 
greenish color. Even after a few days of illness we find, on examination, the 
well-marked signs of lobar infiltration. There is first pneumonic resonance, then 
a dull tympany, with fine moist rales and bronchial breathing. In most cases, 
but not all, a lower lobe is involved. The disease is almost invariably regarded 
at first as a croupous pneumonia, but the expected crisis does not appear. The 
fever remains high, the infiltration does not undergo resolution, the rales become 
coarser, the patient looks pale and wretched. Now, suspicion of tuberculosis 
being aroused, the sputum is carefully examined, and soon, although perhaps not 
at the first examination, tubercle bacilli are found. All cases of this sort take 
a rapid and unfavorable course. They may be called galloping consumption. 
Upon autopsy we find diffuse tubercular infiltration, and usually incipient cavity 
formation in numerous places. Other portions of the lungs than that first 
and most violently attacked ordinarily present considerable tuberculous change. 
In these instances it is evident that we have to do with an acute infection of a 
large portion of the lung with tubercle bacilli, which of themselves exert a pow- 
erful inflammatory action, with unusual virulence. In rare cases there may also 
be a mixed infection, due to the pneumococcus. 



246 



DISEASES OF THE KESPIKATORY OKGAXS 



3. General Symptoms in Pulmonary Tuberculosis. — In the description of the 
general course of pulmonary tuberculosis we have already mentioned the value 
of the constitutional symptoms in diagnosis and prognosis. 

Fever. — Only a few cases of phthisis run their course entirely without fever, 
but it may be absent for a time, even for weeks and months; and indeed, in 
cases with a very slow and favorable course (e. g., where there is unilateral con- 
traction), there may be no fever at all for years. The more carefully we measure 
the temperature the more often shall we find a slight evening rise up to 100° or 
101° (38° to 38.5° C), or at least between 99° and 100° (37.5° to 38° C), even 

at times when the patient is doing 
well. Many cases that pursue a com- 
paratively favorable course have for 
a long while a so-called sub-febrile 
condition. That is, the bodily tem- 
perature is normal in the morning, 
but in the evening invariably rises to 
about 100° or 100.7° (37.8° to 3S.2° 
C), or even higher. (See Fig. 33). 

Very often, particularly in the 
more rapid cases, there is consider- 
able elevation of temperature, and 
the varieties and course of the fever 
are more or less characteristic. We 
should first mention the " hectic fe- 
ver " (see Fig. 34) which is often 
observed. For months the tempera- 
ture chart may present a uniform ap- 
pearance with a morning temperature approaching or reaching the normal, while 
there is a regular elevation every evening to 102° or 104° (39° to 40° C). In 
general, the higher the evening exacerbations the more unfavorable the case. 
In other cases the temperature chart is quite irregular; longer or shorter per- 
sistent periods of elevation alternate with periods when there is no fever. Particu- 
larly toward the end of the disease, as the bodily weakness increases, the previously 
regular, intermitting temperature grows 
irregular. At this time the intermis- 
sions often become more marked, and 
not infrequently general collapse tem- 
peratures— 95° to 93° (35° to 34° C.)— 
are observed. Again, the fever may for 
limited periods take on a more continu- 
ous character, probably in connection 
with exacerbations of the tuberculous 
process. In some few cases with acute 
onset {vide supra) we have also seen, 
in the beginning of the disease, a toler- 
ably high and approximately continuous 
fever, passing gradually into the ordi- 
nary fehris hectica. The cause of the 
fever in pulmonary tuberculosis is not 
yet settled. The special question is 
whether the tubercular process causes 
the fever of itself (by production of toxines), or whether the fever is due to the 
secondary inflammatory processes, such as the absorption of septic and toxic 
material from the decomposing contents of the bronchi and the pulmonary cav- 





Fig. 34.— Hectic fever in chronic pulmonary 
tuberculosis. 



TUBERCULOSIS OF THE LUNGS 



247 



ities, The practical importance of the fever in pulmonary tuberculosis is very 
great. The emaciation and weakness of the patient are caused mainly by fever 
(vide infra), as are many subjective symptoms, including headache, chilliness, 
and perspiration. It is important to remember that in observations of the fever 
we possess one of the most positive means of forming an opinion as to the course 
of pulmonary tuberculosis. In cases which are either completely stationary or 
very chronic there is no fever at all. The sub-febrile condition shows a slow, but 
still continuous, advance of the disease. Continuous hectic fever is an unfavor- 
able sign, and indicates a comparatively rapid march of the disease — the more 
rapid, the higher the evening temperature. In the florid or galloping forms we 
find tolerably high fever, at times continuous and at times remittent. Subnor- 
mal temperatures are almost always of bad omen. 

All changes in the general course of the disease for better or worse stamp them- 
selves clearly oh the temperature chart. The onset of complications and secondary 
disease is often first indicated by the thermometer. Whether an attack of haem- 
optysis passes over without permanent damage, or whether it is followed by an 
aggravation of the disease, can usually be told by the temperature sooner than in 
any other way (vide supra, page 238). Thus we see that the persistent and careful 
observation of the temperature in consumption deserves to rank as one of the 
most important means of estimating the status and course of the illness. 

Emaciation. — The great emaciation of the patient is very striking in most 
cases of phthisis. The muscular system and the fatty tissue are affected in equal 
degree. The soft parts of the thorax are often especially involved. The emacia- 
tion is due in part to the patient's loss of appetite, and to the small amount of 
food which he takes in consequence thereof, but the chief cause lies in the per- 
sistent fever and the increased metamorphosis of tissue. Quite a high degree of 
emaciation, however, may appear in the beginning of the disease with no fever. 
This we are wont to ascribe to the " general illness," but the special cause of it is 
unknown. Under favorable external conditions phthisical patients may make 
quite a decided gain in weight, especially at the times when they are free from 
fever. In very chronic cases, which run their course from the first without fever, 
the nutrition of the patient may remain good for a long time. Toward the end 
of the disease emaciation sometimes reaches its highest degree, and many phthis- 
ical patients die " wasted to a skeleton " in the true sense of the word. 

Anaemia — Color of the Shin. — In most cases anaemia appears in the course of 
the disease, to be recognized by the pale and sallow color of the skin and of 
the visible mucous membranes. The anaemia only rarely reaches that degree of 
peculiar waxy pallor that is found in idiopathic pernicious anaemia. If the pallor 
is extreme, however, there is usually some special reason, such as profuse haemop- 
tysis or the complication of amyloid degeneration. The existence of the anaemia 
is also the reason why the phthisical patient does not look cyanotic in spite of 
the respiratory disturbance. In the more chronic forms, where the general nutri- 
tion suffers less, we often see a cyanotic coloring of the lips and cheeks. Some- 
times the skin of phthisical patients assumes a dirty, dusky hue. We have already 
spoken of the circumscribed " hectic flush of the cheeks " seen with the fever. 

General Weakness — Night-Sweats — Nervous Disturbances. — We need not say 
that the general emaciation and anaemia are accompanied by a marked decline in 
the patient's power of endurance. He finally becomes so helpless that he can 
scarcely move alone in the bed. 

The tendency which very many patients have to severe night-sweats is uni- 
versally acknowledged but not wholly explained. It may have some connection 
with the fall from the evening febrile temperature to the morning remission, and 
perhaps it is due to the greater accumulation of carbonic acid in the blood from 
the disturbance of respiration. 



DISEASES OF THE EESPIEATOEY ORGAXS 



The disease lias remarkably little influence upon the higher nervous functions, 
especially those of the mind. Most patients have a perfectly clear intellect to 
their latest breath. We all know the contented, hopeful, sanguine disposition of 
many patients, who do not recognize their own danger until the last stages of the 
disease. Occasionally the anaemia and the general disturbance of the nutrition 
of the brain lead to mental alterations, such as confusion, distraction, or melan- 
cholic conditions. 

We find, more frequently, disturbances in the peripheral nerves and muscles. 
Among these are neuralgic pains, and pains of an indefinite character, which have 
their seat in the legs, or sometimes in the arms, especially in the ulnar region and 
the sciatic nerve. These may be very distressing. Marked hypersesthesia of the 
skin and deeper parts is also not uncommon. The cause of such disturbances is 
probably often to be looked for In the degenerative changes in the peripheral 
nerves (Vierordt and others). Well-marked multiple neuritis has been repeat- 
edly observed in tuberculous patients (see section on nervous diseases). 

We very often see an increased reaction upon direct mechanical irritation in 
the emaciated muscles, and great liveliness of the so-called idiomuscular contrac- 
tions, which is shown, for example, on percussing the pectoral muscles on the an- 
terior wall of the chest. The phenomena grouped under the name of tendon re- 
flexes are also much increased in phthisis. 

4. Symptoms and Complications on the Part of Other Organs. — 1. Pleura.— 
In pulmonary tuberculosis the pleura is also involved as a rule. The affection is 
almost always the result of a direct extension of the process from the lung to the 
pleura. At the autopsy, we find in the pleura a few or many miliary tubercles, 
besides the simple inflammatory process — tubercular pleurisy. 

In many cases, in which we have to do only with an adhesive pleurisy and 
with pleuritic contraction, we can merely suspect the disease of the pleura, but it 
can not be directly made out and differentiated clinically from the pulmonary 
affection. In other cases we can diagnosticate a dry pleurisy in phthisis from the 
occurrence of the pleuritic friction-rub. The symptoms of pleurisy become more 
marked if there is a pleuritic effusion, which is usually readily discovered by a 
physical examination. The patient's pain and dyspnoea are usually much in- 
creased by such a complication. Besides a simple sero-fibrinous effusion we quite 
frequently find purulent and even hsemorrhagic effusions in tuberculosis of the 
pleura. 

The formation of pneumothorax is an important complication in the pleura in 
phthisis. This is due to the rupture of a superficial pulmonary cavity into the 
pleural cavity, and the entrance of air into the latter. The different forms of 
pneumothorax and its symptoms will be described under diseases of the pleura. 

2. Larynx, Pharynx, and Trachea. — The symptoms of laryngeal tuberculosis 
and their relation to pulmonary tuberculosis have already been given under dis- 
eases of the larynx (see page 148). We saw there that, although there is a primary 
laryngeal tuberculosis, most cases are secondary in their development to a pulmo- 
nary tuberculosis. , 

The same holds true in regard to the much rarer tuberculosis of the pharynx. 
In some cases this may be of primary origin, but it is usually a result of re-inocu- 
lation with tuberculosis by means of the sputum, or of a direct extension of the 
tubercular process from the larynx to the pharynx. Tubercular ulcers of the phar- 
ynx are found most frequently on the soft palate, on the tonsils, on the root of 
the tongue, and on the boundary between the pharynx and the larynx; they 
are rare in other parts of the pharynx. In exceptional cases tubercular affections 
are seen in the mouth — on the tongue. The local discomforts which all these 
ulcers cause is usually very considerable. Disseminated miliary tubercles, too, 
have been repeatedly seen in the mucous membrane of the pharynx. 



TUBERCULOSIS OF THE LUXGS 



249 



3. Stomach and Intestinal Canal — Peritoneum. — Tubercular ulcers in the 
mucous membrane of the stomach are exceedingly rare, but we very often notice 
some symptoms on the part of the stomach. Loss of appetite is a particularly 
common symptom in phthisis. Vomiting occurs often in phthisical patients, 
especially when the larynx is involved. It is usually brought on by paroxysms 
of coughing. Less frequently the cause of the vomiting is gastric catarrh, occa- 
sioned by the irritation of the sputa which have been swallowed; but in some 
cases the gastric symptoms depend upon the general condition — e. g., the anaemia. 

Although the tubercle bacilli swallowed with the sputum hardly ever infect 
the stomach, probably from the acid reaction of its contents, they very often at- 
tack the intestinal canal. In the majority of the cases of phthisis we find tuber- 
cular ulcers, either singly or in considerable numbers, in the vicinity of Bauhin's 
valves [the ileo-caecal valve], in the lower part of the ileum, and the upper part 
of the large intestine. 

Intestinal tuberculosis does not always cause very marked clinical symptoms, 
but as a rule we find diarrhoea in patients with tubercular ulcers of the intestine. 
They may have three or four stools in the twenty-four hours, and even more, but 
the stools have nothing characteristic. We rarely see a slight admixture of pus 
or blood in them. Tubercle bacilli have been repeatedly discovered in the de- 
jections, but the search for them is rather difficult. We must call attention, how- 
ever, to the fact that many patients have diarrhoea during life in whom we find 
at the autopsy no intestinal tuberculosis, but only a simple intestinal catarrh. 
Severe diarrhoea of a persistent and refractory character may also occur in asso- 
ciation with amyloid degeneration of the intestine, which is not infrequently 
seen in connection with other amyloid changes. Sometimes tuberculous ulcera- 
tions of the intestine are found at autopsy which, during life, had caused no 
diarrhoea. 

In cases of severe intestinal tuberculosis we sometimes meet with meteorism. 
With deep ulcers, extending to the peritoneum, we often see marked tenderness 
of the abdomen. 

The peritoneum may be affected by the tubercular ulcers of the intestine in a 
twofold manner. Genuine peritonitis from perforation, with a purulent or even 
a sanious exudation, is quite rare, and is excited by the rupture of an ulcer and 
the entrance of the contents of the intestine into the abdominal cavity. An in- 
fection of the peritoneum with the tubercular poison is more frequent. This 
may arise from deep-seated ulcers, which do not reach actual perforation, so that 
we have a peritoneal tuberculosis, or a tubercular peritonitis. During life peri- 
tonitis from perforation and that from tuberculosis are not always to be distin- 
guished. We must also mention that simple ascitic fluid is sometimes found in 
the abdominal cavity in phthisis, which may lead to a false diagnosis of peritoneal 
tuberculosis. 

Another way in which we may have a peritoneal tuberculosis in the course of 
phthisis is from the extension of the process in a tubercular pleurisy, through the 
diaphragm to the peritoneum. 

4. Liver and Spleen. — We very often find a few or even many tubercles in the 
liver in phthisis, but they have no clinical significance. The liver is almost always 
infected with the tubercular poison from tubercular ulcers in the intestines, from 
which the poison passes to the branches of the portal vein and then to the liver. 
Fatty liver and amyloid or lardaceous liver are more important clinical changes. 
We can sometimes recognize the former by making out on physical examination 
the increase in the size of the organ, and by feeling its characteristic blunt lower 
edge. Moreover, we must emphasize the fact that, in our experience, fatty infil- 
tration of the liver is found much more rarely at the autopsy of consumptive 
subjects than the statements of many earlier authors would lead one to expect. 



250 



DISEASES OF THE EESPIEATOEY OEGAXS 



Amyloid degeneration of the liver appears almost always in association with 
amyloid change in other organs (kidneys, spleen, intestine). If the amyloid 
degeneration is advanced, the liver is considerably enlarged, and it is usually pos- 
sible to feel distinctly its sharp and resistant edge; and, not infrequently also, 
its firm upper surface. 

Miliary tubercles or single large tubercular nodules in the spleen have a patho- 
logical interest only. Great splenic enlargement is found in amyloid degen- 
eration. 

5. Kidneys, Urinary Passages, and Sexual Organs. — The presence of miliary 
tubercles in the kidneys is the first change in them to be mentioned, but it has no 
clinical significance. Extensive tuberculosis of the genito-urinary apparatus, 
however, may produce marked symptoms, such as pyuria. Genito-urinary tuber- 
culosis will be discussed in a later part of this work. In regard to the symptoms 
of amyloid kidney, which may develop in the course of phthisis in connection 
with amyloid disease in other organs, we will refer to the section on renal 
diseases. 

Genuine cases of nephritis, both acute and chronic, are also found quite fre- 
quently in phthisis, often combined with amyloid disease. These can not escape 
notice if the urine is carefully examined. Their development is probably always 
referable to the excretion of toxic material, arising from the disease in 
the lung. 

6. Circulatory Organs. — The rate of the pulse is often increased in consump- 
tion. This increase in frequency may be merely proportional to the fever, if any 
exists. It is also usually seen and it may be considerable when there is no 
fever. A persistently rapid pulse, when the temperature is little, if at all, ele- 
vated, may therefore be an important diagnostic sign of pulmonary (and all 
other) tuberculous diseases. The increase of the pulse, which readily comes on 
from comparatively trifling external causes, is especially noteworthy. It may 
be seen after slight physical exertion, or upon mental excitement, as during the 
physician's visit. 

Anatomical changes in the heart are rare, except that it is often remarkably 
small and flaccid. Moderate fatty degeneration of the heart, slight endocarditis 
of the valves, or occasional tubercles in the heart, causes no symptoms. The oc- 
currence of tubercular pericarditis, however, is important. This almost always 
arises from the extension of the tubercular process from the adjacent pleura, but 
in exceptional cases pericarditis has been seen as a result of rupture of a tuber- 
culous lymph-gland or a pulmonary cavity into the pericardium. 

7. Lymph- glands. — The lymph-glands are a favorite seat for tubercular 
changes. We have stated above that the so-called scrofulous, cheesy lymph- 
glands, which are seen chiefly in the neck and the axillae, are affected with tuber- 
cle in the majority of cases. The tubercular infection probably develops here 
from slight injuries and excoriations of the skin, by which the bacilli enter the 
body and reach the neighboring glands by means of the lymph-current. In 
other cases the infection comes perhaps from the mucous membrane of the phar- 
ynx. In tuberculosis of internal organs, too, we very often find the corresponding 
lymph-glands enlarged and more or less cheesy. The bronchial lymph-glands 
are swollen as a result of pulmonary tuberculosis, the mesenteric and retroperito- 
neal glands as a result of intestinal tuberculosis. The tuberculosis of the bron- 
chial lymph-glands is of especial importance in children. Indeed, the tubercular 
virus which has gained access to the lungs may apparently reach the bronchial 
glands by means of the lymph-channels even without affecting the lungs them- 
selves, and occasion a tuberculous disease of the glands. Glands thus diseased 
break down and discharge into the lungs, and in this way generate a secondary 
pulmonary tuberculosis. This is one reason why the pulmonary tuberculosis of 



TUBEKCULOSIS OF THE LUNGS 



251 



children so often begins not in the apex but in the middle or lower portion of 
the lung. 

Pressure from the enlarged glands may affect the air-passages, the branches of 
the pulmonary artery, the veins, the recurrent nerve (paralysis of the vocal cords), 
and even the aorta. Perforation of the cheesy bronchial glands into the oesoph- 
agus, the blood-vessels, etc., has also been observed. Tuberculosis of the bron- 
chial glands does not present any definite type of disease, however, and, although 
we may sometimes suspect it when there is pulmonary tuberculosis, we can only 
rarely diagnosticate it with certainty. The author himself observed a note- 
worthy case of tuberculosis of the bronchial glands, with compression of one 
vagus nerve in a patient who, during life, for weeks coughed up large amounts 
of a purely sero-mucous expectoration containing no bacilli. 

8. Nervous System. — We have already mentioned various nervous symptoms 
in the description of the general symptoms. We must also add that tubercular 
meningitis is seen in the course of phthisis (see page 1059), and that large soli- 
tary tubercles may occasionally develop in the central nervous system. 

9. Skin. — We have spoken of the great tendency which many patients have to 
severe sweats, especially at night. The frequent appearance of pityriasis versi- 
color, especially on the skin over the thorax, is also worthy of note. We often 
see moderate oedema of the legs and ankles, which is due to weakness of the 
heart. More marked oedema of one leg sometimes arises from thrombosis of the 
femoral vein. We must also mention here, in conclusion, the specific tubercular 
disease of the skin — lupus. This occurs alone, as a rale, without a co-existing 
pulmonary tuberculosis ; but, on the other hand, the old term " scrofulous lupus " 
had reference to the fact that we often find other tubercular affections in lupus 
besides the disease of the skin. Thus it does not seem strange that lupus and 
phthisis have been repeatedly observed to co-exist. Cutaneous tuberculosis may 
develop not only in the ordinary form of lupus, but also in nodules of consider- 
able size, or in rather extensive ulcers. Certainly some of the cases of so-called 
corpse-tubercle belong to true tuberculosis. We have seen a similar tuberculous 
cutaneous disease in a woman who for a long time had washed the soiled handker- 
chiefs of a consumptive patient. We have also seen a tuberculous affection of 
the skin upon the chin of a patient very ill with consumption. In this case, no 
doubt, the skin became infected by the sputum. 

Diagnosis. — The diagnosis of pulmonary tuberculosis has become absolutely 
certain, since the discovery of the tubercle bacilli, by the demonstration of their 
presence in the sputum (vide supra). In all incipient cases, in which the other 
symptoms of the disease have not yet made themselves manifest, but the sus- 
picion of incipient phthisis has been aroused by a persistent cough, by marked 
pallor and emaciation, by slight hoarseness, by an evening rise of temperature, 
by the appearance of night-sweats, by the presence of a hereditary predisposition, 
and similar symptoms, the finding of tubercle bacilli in the sputum is often the 
sole deciding factor. Still, it must not be forgotten that the examination for 
bacilli is decisive only when its result is positive, and that the greatest attention 
should be given also to all the other symptoms. To form an opinion as to the 
severity of a particular case, and as to its exact distribution and the variety of 
the tubercular process, is at present possible only by means of a consideration of 
the other symptoms, and in particular of the results of physical examination. 
The latter, therefore, has lost none of its importance by the discovery of the 
tubercle bacilli. 

Confusion between phthisis and other diseases is twofold. Where the consti- 
tutional symptoms are predominant, and there are no marked pulmonary symp- 
toms, an existing tuberculosis may be overlooked. In the beginning, especially, 
many cases of phthisis are considered to be merely anaemia, chronic gastric 



252 



DISEASES OF THE EESPIKATOEY OKGANS 



catarrh, or simple bronchitis. If a continuous or intermitting fever appears in 
an early stage of phthisis, before any marked pulmonary symptoms have devel- 
oped, the disease may be mistaken for malaria or the like. On the other hand, 
it is by no means rare to consider patients phthisical who are suffering from 
some entirely different affection. He who lays too great stress on the uncertain 
results of percussion will often make a false diagnosis. Severe latent diseases 
of the stomach, or certain general diseases, such as anaemia, diabetes, or chronic 
nephritis, may be mistaken for phthisis. Other pulmonary affections, too, may 
be confounded with tuberculosis, especially chronic bronchitis, emphysema, 
bronchiectasis, foetid and gangrenous processes, and carcinoma of the lungs. A 
careful, unprejudiced, and complete examination of the patient is the only pos- 
sible protection against such errors. It is very important for the physician to 
know that there is such a thing as hypochondriacal phthiseophobia. Some nerv- 
ous individuals are tormented by a constant dread of becoming consumptive. 
Such persons complain of thoracic pain, dry cough, weakness, and other imagi- 
nary symptoms, which might readily mislead the physician into supposing that 
they actually have incipient pulmonary tuberculosis. Of course, the correct 
interpretation of such conditions is usually no difficult matter to the experienced 
physician, who is guided by the general impression of " nervousness," and by the 
complete absence of any objective physical signs. 

In this connection we ought, furthermore, to express our opinion of the diag- 
nostic value of Koch's tuberculine (vide infra). Koch made the important dis- 
covery that tuberculous patients, particularly those suffering with pulmonary 
tuberculosis, exhibit a particular " reaction " after the injection of small amounts 
of tuberculine (gramme 0.001 to 0.002 of Koch's preparation). When this reac- 
tion occurs there develops, some four or five hours after the injection, a fever of 
102° to 104° (39° to 40° C), associated with chilliness, headache, pain in the 
limbs, nausea, and languor. This constitutional reaction passes off after some 
twelve or fifteen hours. If the tuberculous process is located in the skin, trachea, 
or some other part where it is accessible to direct observation, a very decided 
local reaction may usually be observed besides the constitutional disturbance. 
The tuberculous tissue becomes swollen, red, and finally in part necrotic. In 
patients with tuberculosis of the internal organs, also, this local reaction probably 
takes place, but of course it can not be actually seen, although it may perhaps be 
inferred because of the secondary phenomena. Thus, in pulmonary tuberculosis 
there may be an increase in the cough and expectoration. On the other hand, if 
an injection of tuberculine is made in a person who is healthy, or who is suffering 
from some disease other than tuberculosis, then, according to Koch, there will 
be no reaction at all to small doses. To obtain any reaction in persons who are 
healthy, or, at any rate, not tuberculous, it is said that the dose of Koch's prepa- 
ration must be increased to the amount of gramme 0.01. If these statements 
were true, the appearance or the absence of a reaction after the injection of a 
small amount of tuberculine would be an important and, indeed, a decisive factor 
in determining whether tuberculosis did or did not exist in iany given case. 

These statements of Koch have been shown, however, by extensive investiga- 
tions, to be true only in general, and not in every case. Other observers as well 
as the present author have occasionally found that healthy persons, or persons 
free from tuberculosis, have reacted to doses of one or two milligrammes of tuber- 
culine ; while, on the other hand, patients with indubitable pulmonary tuberculo- 
sis have shown no distinct reaction even to considerable doses of tuberculine. 
Consequently the result of an injection of tuberculine can never be completely 
decisive from a diagnostic point of view, and in practice, therefore, the employ- 
ment of tuberculine for diagnosis has been adopted by only a few; but still, it 
would be a mistake to discard this means of diagnosis completely. In doubtful 



TUBERCULOSIS OF THE LUNGS 



253 



cases when we can not be sure of the diagnosis, the ' injection of about two 
milligrammes of tuberculine is of real importance, and the result of the test 
is certainly a valuable factor in summing up such a case; yet the verdict is 
never so unimpeachable as in cases in which the tubercle bacilli have been dis- 
covered. 

Prognosis. — It is very difficult to make a general statement as to the prog- 
nosis of pulmonary tuberculosis. There is no doubt that tuberculous foci in the 
lungs, if of limited extent, may become completely healed, at least from a clinical 
point of view. Indeed, such recovery probably takes place oftener than many 
suppose; at least, it is not very exceptional to find at the autopsy of elderly 
persons cicatricial contractions in the apices of the lungs which may, without 
doubt, be regarded as healed tuberculosis. In many of these cases the previous 
tuberculosis had never come to the knowledge of any physician. At the pres- 
ent day the discovery of tubercle bacilli in the sputum has rendered the diag- 
nosis of even very limited tuberculous processes an easy matter, and, consequent- 
ly, cases of recovery from pulmonary tuberculosis are now recognized much more 
often than formerly. 

Nevertheless, the prognosis of pulmonary tuberculosis must always be re- 
garded even now as very serious, and when the disease has made any great prog- 
ress the prognosis is decidedly unfavorable. Many cases of apparent recovery 
exhibit merely a temporary improvement, to grow worse again, and the assertion 
that treatment is absolutely hopeless in almost all cases in which the disease has 
reached an advanced stage is, unfortunately, too well established to require elab- 
orate argument. 

There is, however, one fact of extreme importance which should never be dis- 
regarded in the prognosis of pulmonary tuberculosis. There is a great difference 
in the duration of the disease. It is possible for the process to go on for years, 
while the patient feels tolerably well, and yet the disease smoulders. Erom this 
point of view cases may be distinguished as " benign," compared with those of 
rapid progress, and this prognostic distinction has the greatest importance in 
practice, although it is often very difficult to recognize. Many a consumptive, 
when first examined, gives one the impression that he can not live a fortnight 
longer, and yet the disease lasts many months, with improvement in most of the 
symptoms and general alleviation of the patient's condition. Again, one believes 
the disease to be incipient, encourages the family, and the patient dies in a few 
weeks of galloping consumption. 

Certain complications may occur which it is impossible to foresee, such as 
pulmonary haemorrhage, pneumothorax, tubercular meningitis, and miliary tu- 
berculosis. Apart from these, however, there are certain conditions which lead us 
to, expect a comparatively favorable course for the disease : such are a vigorous 
constitution unimpaired by bad habits, of which drinking is particularly un- 
favorable; a good weight; freedom from hereditary taint; limited extent of the 
local process ; later life ; the absence of complications ; and, finally, the persistent 
absence of fever. This last factor is so important that we must lay special stress 
upon it. If there is no fever whatever in a case of pulmonary tuberculosis, the 
patient is at that time in a condition in which the disease is quiescent; and a 
decided improvement, perhaps even cure, may be expected if appropriate means 
are employed. On the other hand, whenever fever appears we know that the dis- 
ease is not quiescent, but is actively advancing with more or less rapidity. The 
important points about the temperature in this regard have been already empha- 
sized (see page 246). It is self-evident, also, that the worldly circumstances of 
the patient, as well as the factors which we have just alluded to, are of great 
prognostic importance. On these, for instance, depends the possibility of proper 
care, of abundant nourishment, and, it may be, of a change of climate. 



254 



DISEASES OF THE EE SPIE AT OEY ORGANS 



Treatment. — 1. Prophylaxis. — The question of what prophylactic measures 
may effectually prevent the extension of the disease has entered upon a new 
stage since our definite knowledge as to the infectious nature of tuberculosis. We 
can no longer doubt the contagious character of phthisis, in support of which 
isolated examples were previously brought forward. Even if, according to all 
experience, the danger of contagion is not very great, still it is foolish to ignore 
it entirely. We must therefore call the attention of the relatives of phthisical 
patients to the possibility of this danger, and we should not permit the children 
of such patients to be uselessly exposed to it. We should take satisfactory pre- 
cautions for isolation, and also for disinfection of the sputum. Suitable sputum 
cups should be employed, and care should also be taken to prevent the dissemina- 
tion of the expectoration, either in its fresh state or after it has become 
dry. The future will teach us whether much evil may not be averted by such 
measures. 

The " prophylaxis " till now employed was almost exclusively confined to 
hardening and strengthening the threatened individual as much as possible. We 
should try to strengthen the bodies of children of a weak habit, with " scrofulous " 
symptoms, and children from families in which cases of tuberculosis have already 
occurred, and thus to arm them against the enemy that threatens them. Good 
food, fresh air, and a diminution of the sensitiveness of the body by cold spon- 
ging and cold baths — these are the factors whose favorable influence is generally 
recognized. 

The removal of certain foci of tubercular disease, already existing, from the 
body may prove of great prophylactic importance. We refer to the timely treat- 
ment or extirpation of scrofulous — that is, tubercular — swellings of the lymph- 
glands, healing or resection of tubercular bones and joints, etc. Although in 
individual cases we can of course never know whether the part removed is the 
sole focus of disease in the body, still we are undoubtedly justified in trying 
to remove at least one possible source of some later general infection. A fuller 
discussion of this important point must be left to the works on surgery. 

2. Therapeusis. — Physicians have often thought that they had discovered a 
specific remedy for tuberculosis, but apparently they have thus far been mistaken. 
Formerly, the inhalation of antiseptic substances, such as carbolic acid, benzoate 
of sodium, and iodoform, was recommended, but this practice is now almost en- 
tirely given up. Arsenic was for a time much used, best given in pills containing 
£ T - to (gi*m. 0.003) repeated several times a day; but this practice, again, has 
not held its own. Arsenic may be tried in incipient cases, particularly those 
associated with marked ansemia, but great curative influence is not to be expected 
from it. Creasote has won far more advocates. Continued for a considerable 
time in large doses (fifteen to thirty grains, grammes 1 to 2, or more, in the course 
of twenty-four hours), it is regarded by many physicians as an excellent remedy 
in incipient and even in advanced pulmonary consumption. It is best prescribed 
in gelatine capsules, or in a mixture of one part of creasote to two parts of the 
tincture of gentian, of which twenty to eighty drops may be given three times a 
day in a considerable amount of milk, or in wine. This remedy is usually f airly 
well borne, and the patients are pleased with the improvement it causes in their 
appetite and general condition. Of late, physicians have employed guaiacol, the 
active ingredient of creasote, instead of the drug itself, especially since carbonate 
of guaiacol has been brought forward, a preparation which has very little of the 
disagreeable odor and taste of creasote itself. Carbonate of guaiacol is admin- 
istered in powders containing about eight grains (gramme 0.5), in daily doses at 
first of twenty-five grains (gramme 1.5), gradually increasing to thirty or forty- 
five grains (grammes 2 to 3). Dyspeptic disturbance sometimes follows the use 
even of guaiacol, but still this remedy is, in general, better borne and more read- 



TUBEECULOSIS OF THE LUNGS 



255 



ily taken than creasote. As to the specific and therapeutic use of guaiacol in pul- 
monary tuberculosis, it is not easy to form a decided opinion. It is certain that 
many patients praise these remedies, and improve considerably while using- them ; 
but, on the other hand, the indiscriminate laudation of many authors is decidedly 
unjustifiable. When the disease is slowly progressing with persistent sub-febrile 
temperatures, the author has scarcely ever felt sure of any distinct influence ex- 
erted by guaiacol or creasote upon the temperature and the disease. Neverthe- 
less, it is often advisable in practice to make trial of these remedies, particularly 
of the carbonate of guaiacol. The remedy must be employed for months and, if 
possible, in increasing doses. Among the remedies which are recommended as 
having a specific influence, we will also mention cinnamic acid, which is con- 
tained in Peruvian balsam. This has been employed extensively by Landerer in 
the treatment of various tuberculous diseases, and particularly in pulmonary 
tuberculosis. He gives it in the form of small subcutaneous injections of a five- 
per-cent. emulsion, made up of the sweet oil of almonds and the yolk of egg. The 
results obtained by Landerer, in the institute of Krahenbad, in the Black Forest, 
appear very favorable, but as yet they lack confirmation. The method has not 
yet been generally adopted. 

At the end of 1890 great interest was excited, as is well known, by the state- 
ment of B. Koch that he had extracted from pure cultures of tubercle bacilli, 
by means of glycerine, a substance called tuberculine, by which he was able to 
heal tuberculous processes both in animals and men. This assertion aroused 
the thoughtless enthusiasm which is unfortunately so common with regard to 
therapeutic questions, and which indeed in this case was rendered excusable by 
the high authority of the discoverer. In fact, within a few weeks after the 
remedy was made known, numerous reports were published of cures due to tuber- 
culine. But the longer the experiments were pursued the more evident it became 
that these extravagant opinions were not substantiated, and there set in a revul- 
sion of sentiment which has led to many adverse criticisms, perhaps equally un- 
justifiable with the early praise. It is absolutely impossible to speak of tubercu- 
line as an established remedy for tuberculosis. In many patients there does in- 
deed appear a decided improvement under treatment, but these cases are such as 
were favorable any way, and therefore they may owe their improvement to the 
general symptomatic treatment and regimen which they have also enjoyed. At 
any rate, tuberculine has done no harm in such cases. Then, again, we have seen 
numerous cases of rather severe disease, in which it was not possible to notice any 
distinct influence of the tuberculine upon the general course of the illness. Per- 
haps the condition of the patient improved, or remained unchanged; or, again, it 
grew worse. Yet, whatever the change, it was such as might have occurred inde- 
pendently. Finally, there are, in the third place, cases which have been seen by 
the author as well as other observers, in which there was such a decided change 
for the worse shortly after the commencement of treatment, that one might 
really suppose that the remedy had exerted an actually harmful influence. We 
refer especially to cases in which the patient, previously without fever, exhibited 
after the injection a persistent elevation of temperature, with a more rapid ad- 
vance of the local process in the lungs. 

Consequently, we may say that, in all advanced cases, we can expect nothing 
from tuberculine. In incipient cases we may make trial of it, but we should be ex- 
tremely careful in our dosage, so as to avoid any chance of doing injury. Koch's 
rule at first was that the physician should begin with injections of gramme 
0.001, and gradually increase. In this way was discovered the interesting fact that 
the necessary dose for the production of the "reaction" (vide supra, page 252) 
became greater and greater. Many patients would finally bear the injection of 
one hundred milligrammes of tuberculine without any reaction at all. At first 



256 



DISEASES OE THE EESPIEATOEY ORGANS 



it was regarded as the object of treatment to reach this point of tolerance, but 
the practice is now abandoned. One should begin with very small doses, about one 
fourth to one half a milligramme, and increase so slowly and by such minute gra- 
dations as to avoid any marked reaction. By such a method we can almost en- 
tirely exclude any harmful effect, and it may not be impossible that some of the 
patients who have had a favorable result actually owe their improvement to the 
tubereuline, but it is extremely difficult to make sure of this. It would require 
the continuous observation of many patients for years, to enable one to form a 
reliable opinion with regard to this question. 

It may be seen that at present we can only speak with great reserve as to the 
possible therapeutic value of tubereuline, but nevertheless, its discovery was an 
event of the greatest value and interest, regarded from a therapeutical stand- 
point. There is no doubt of the specific influence of this substance upon tuber- 
culous processes. There is scarcely any sight more astonishing to the physician 
than the reaction of a patch of lupus upon the skin to a tiny dose of tubereuline 
introduced into the circulation! Taken into consideration with other bacterio- 
logical facts, this affords us a clear glance into a future when we shall succeed 
in making the wonderful influence of the material produced by the growth of 
bacteria available for the cure of infectious disease, and, in particular, of tuber- 
culosis. Perhaps there are the same possibilities for tuberculosis as in the case 
of diphtheria, the treatment of which, by means of the antitoxic serum pre- 
pared by Behring, is apparently so very successful; but with regard to tuber- 
culosis our methods are as yet incomplete, and a final opinion as to their value 
would be premature. Meanwhile, therefore, we physicians must continue to lay 
the greatest stress in the treatment of tuberculosis upon those methods which are 
termed in the widest sense hygienic and constitutional. It is undeniable that, by 
the correct and faithful employment of such methods, many very satisfactory 
successes may be obtained. For the present, we must be discreet, and seek to in- 
fluence the disease in the old accustomed manner by those therapeutic measures 
which have come down to us from ordinary medical observation and expe- 
rience. 

The hygienic and constitutional method of treating consumption has for its 
object the greatest possible promotion of the natural powers of healing. We 
aim at this, in the first place, by avoiding as much as possible all influences which 
might cause a further extension of the disease, and by re-enforcing, so far as we 
can, all influences which increase the resisting powers of the individual, and the 
processes of spontaneous cure. The factors which are of most importance in this 
connection are, first, diet; second, rest; and third, the uninterrupted enjoyment 
of good air. To obtain these three therapeutic factors all at once requires the 
renunciation by the patient of his calling, and his usual mode of life. The 
treatment of tuberculosis, therefore, should begin with the demand that the 
patient, for as long a time as possible, should devote himself exclusively to the 
care of his health. The next point is the choice of the place in which the " cure " 
shall be carried on. In many cases the proper management of the patient may 
be pursued under the ordinary surroundings of home. Often, however, this is 
not the case because the last two, or even all three, of the essentials named can 
not be provided at home. It, therefore, is the duty of the physician in every indi- 
vidual case to determine how the desiderata are best to be obtained. According 
to the patient's means we consider respectively a residence in the country (if pos- 
sible, in a picturesque and wooded region) ; a special health-resort ; or, finally, 
a suitable sanitarium. Erom a therapeutic standpoint, there is no doubt that 
treatment in a specially adapted sanitarium is chiefly to be recommended. In 
this all the requirements for recovery can be best carried out, and the patient 
constantly remain under medical observation. In most cases it is only exter- 



TITBEKCULOSIS OF THE LUNGS 



257 



nal considerations, for instance, pecuniary, which keep the patient from a sani- 
tarium. It is a true philanthropy, therefore, which has of late led everywhere 
to efforts to render the benefits of institutional treatment accessible to the less 
wealthy classes. The requirements for proper treatment are also partially ful- 
filled in the so-called public health-resorts for pulmonary consumptives. These 
resorts, however, have the disadvantage that the patient is left far more to his 
own resources, and is consequently apt to be incautious, and hence jeopardize 
his recovery. A public health-resort would, therefore, be especially chosen for 
patients who have already been in an institution, and have learned what mode 
of life is proper for them; or for those who have already so far recovered that 
they may be allowed a certain degree of freedom. 

With regard to the minutise in carrying out the above-enumerated essen- 
tials of treatment, we would add as follows : 1. Diet. This should be as nourish- 
ing and abundant as possible. Meat, milk, eggs, farinaceous foods, and butter are 
chiefly to be recommended, care being taken that the body should receive a 
sufficient amount of carbohydrates and fats, as well as an abundance of albumen. 
Many special " cures " for pulmonary consumption have a value, in so far as they 
lead to the ingestion of an abundant amount of easily assimilated nourishment. 
Such are cures with milk, koumyss, or kefir. It has even been proposed to in- 
troduce large amounts of such nourishment as milk and pulverized meat into 
the stomach by means of a stomach-tube, and thus accomplish " overfeeding." 
This method has not become very popular, although it may be indicated in some 
cases. It is very important to see that the patient has a diet that is not only 
abundant, but also palatable and varied. If pure milk is not readily taken, we 
may try the addition of coffee, tea, common salt, or brandy. With regard to the 
prescription of alcohol we recommend, unhesitatingly, moderate amounts of beer, 
and particularly such beer as is rich in extractive matter; and perhaps also 
extract of malt, and porter. Small amounts of good wine may contribute to the 
improvement of the appetite and the general condition. On the other hand, we 
think it useless and, in some circumstances, harmful, to order large amounts of 
the stronger alcoholic beverages, such as port wine and brandy, as prescribed in 
many sanitariums. Artificial foods, such as various preparations of meat, soma- 
tose, neutrose, and the like, should be used merely as makeshifts. The employ- 
ment of cod-liver oil to the amount of two to four tablespoonfuls a day is some- 
times not inappropriate, if it is well borne. 

2. The two other factors of cure — rest, and the continuous enjoyment of good 
air — are best fulfilled by the fresh-air treatment, which is of late gaining in 
importance and popularity. The patients spend the greatest part of the day lying 
in the open air on comfortable reclining chairs. At the same time they avoid 
any unnecessary bodily exertion, any great demands upon respiration, and any 
irritation of the respiratory passages. Gain in bodily weight is promoted. The 
limitation of the diseased processes in the lungs is favored. Of course, in such 
matters also the individual should be considered, for moderate exercise in the 
open air is certainly for many patients not harmful, but rather beneficial. Often 
the methodical carrying out of the open-air treatment under suitable conditions 
demands the resources of a sanitarium, but we may find in a garden or on a 
veranda a sunny spot, screened from the wind, where the patient may lie com- 
fortably and pass the entire day till near sunset in the open air. In case of 
necessity the patient must content himself with a place by an open window. The 
advantages of the climatic health-resorts {vide infra) consist principally in the 
fact that they render possible a continuous enjoyment of the open air, even during 
the colder part of the year. It has been maintained that climatic factors, par- 
ticularly elevation, exercise a specific influence upon the healing of pulmonary 
tuberculosis; but this has not yet been proved. The best-known sanitariums for 
17 



258 



DISEASES OF THE RESPIRATORY ORGANS 



pulmonary disease are found in Falkenstein in the Taunus, Gorbersdorf, St. Bla- 
sien, Reiboldsgriin, Hohenhonnef, and Andreasberg in the Hartz Mountains, and 
Davos and Arosa in Switzerland. Of the public health-resorts which are particu- 
larly suitable for consumptives, we would name for summer use the acidulated, 
alkaline, and chloride-of -sodium waters of Ems, Obersalzbrun, and Reinerz; the 
chloride-of-sodium waters in Reichenhall, Salzungen, and Soden; the mud springs 
in Lippspringe, Inselbad, and Weissenburg in Switzerland. For summer climate, 
the following are to be recommended : Beatenberg, Heiden, Engelberg in Switzer- 
land; Badenweiler, St. Blasien, Rippoldsau in the Black Forest, and many others. 
For the colder portion of the year we have, in their lofty situation, Davos, 
Arosa, and others. The more vigorous the constitution of the patient, the more 
proper it is to recommend him to go to a great elevation in the winter; while 
delicate subjects are usually better suited in the southern resorts. 

Of course only the very distant health-resorts in Algiers, Egypt, Malta, and the 
much-praised Madeira, can furnish a certain guarantee of constant mild weather. 
The Sicilian health-resorts (Catania and Palermo), and also Ajaccio, afford fa- 
vorable climatic conditions; while the health-resorts of the Riviera, Meran, Gries, 
Arco, Gardone, Lugano, Pallanza, and Montreux, are much more uncertain in 
this respect, and therefore are to be used merely as stopping-places by the way 
during the spring and autumn months. 

We must also "state that, in incipient cases, a residence by the sea, or a long 
sea-voyage, may sometimes be of great help. We have ourselves known several 
young physicians who have become ship surgeons on account of incipient phthisis, 
and who have returned from the voyage much stronger, and some of them appar- 
ently entirely well. 

We can not go into a full description here of all the health-resorts mentioned. 
We can not omit, however, calling special attention to the fact that we should 
always ask ourselves, in choosing a health-resort, whether the expense and incon- 
venience thus imposed upon the patient can be balanced by the possible benefit. 
The earlier the stage of the disease and the better the general condition of the 
patient, the more will his physician be justified in urging him to make every 
sacrifice in order to regain his health. 

We must particularly insist with the patient that no cure of tuberculosis can 
be accomplished by a single visit to any health-resort, but that recovery must be 
achieved by living continuously for years in accordance with all the demands of 
hygiene. On the other hand, it is wrong, both from a medical and from a humane 
standpoint, to send away consumptives in the last stages of their disease, to perish 
far from home and friends. Consumptives with fever should never be sent from 
home, unless they find refuge in a real sanitarium where they may enjoy the con- 
stant observation and treatment of a physician. 

[Our own health-resorts for consumptives are too well known to demand ex- 
tensive consideration here. The prime object is to secure for the patient a pure 
air, with such climatic conditions that he can pass the largest amount of time out 
of doors, at the same time that within doors his comfort /is provided for, and a 
sufficiency of suitable and well-cooked foods is attainable. In Colorado, JSTew 
Mexico, and California, large numbers of former consumptives are leading active 
lives. Florida, Aiken, Thomasville, Asheville, and some other southern resorts, 
are good winter asylums for many cases, but patients should not return to ISTew 
England before June 1st. An out-door life in the Maine or Adirondack woods 
during the warmer months is highly to be recommended for early and otherwise 
suitable cases. Saranac, N. Y., affords every comfort during the colder months, 
combined with the very best medical attendance, and many people do well there. 
A relative disadvantage under which nearly all American health-resorts labor, as 
compared with those of Europe, consists in the greater difficulty in providing oc- 



TUBEKCULOSIS OF THE LUNGS 



259 



cupation and thus securing a mental attitude most favorable to recovery. In gen- 
eral, the northern sea-board is much less favorable than the interior, and early 
cases often do well during the winter removed from the dampness of the coast, 
with its alternations of freezing and thawing. A change of climate is a very im- 
portant step, and should receive the most careful consideration of the physician — 
the circumstances of the patient, the stage and character of his disease, his tastes, 
etc., being carefully weighed before a decision is reached.] 

Finally, the employment of hydrotherapy should be mentioned in the hygienic- 
treatment of tuberculosis. Although this can not exert any specific influ- 
ence on the disease, and therefore must not be prized too highly, yet it is 
often beneficial in the form of cold sponging, or brief cool douching and the 
like; and the stimulation of the skin has a favorable influence upon the general 
health. In severe febrile cases we may order sponging and rubbing in bed with 
cold water, brandy, vinegar, and the like. Also for the relief of symptoms (vide 
infra), such as pain, fever, and perspiration, we may often employ sponging, cold 
or warm compresses, and the wet pack. 

The symptomatic treatment of phthisis is directed in the first place against the 
pulmonary symptoms. We use much the same remedies to help the cough as in 
chronic bronchitis. We try inhalations with a solution of common salt, or of the 
alkaline carbonates, or, if there is much secretion, with solutions of tannin and 
the balsams, such as turpentine, or balsam of Peru. When there is severe, spas- 
modic cough, inhalations with narcotic solutions sometimes give some relief, such 
as cherry-laurel water, opium, or bromide of potassium. 

Morphine stands first among the drugs employed to check the cough. We 
should be cautious and sparing in its use at first, but it is an indispensable remedy 
in severe and hopeless cases. It relieves the irritation of coughing, the pain and 
the oppression in the chest, and at least gives the patient for a time the desired 
sleep. In chronic cases, with moderately severe symptoms, we may use for a long 
time the milder narcotics with advantage, particularly codeine (powders of gr. 
0.5-1.0, gramme 0.03-0.05) or phosphate of codeine; also the extracts of hyos- 
cyamus and of belladonna (extracti hyoscyami 1, aquas lauro-cerasi 20, fifteen to 
twenty drops every two hours). [Heroine is sometimes useful in doses of 
grain. — V.] It is important that the patient should learn to suppress his incli- 
nation to cough, at least up to a certain point. Sips of cold water often quiet 
the cough, as may also a " cough drop " held in the mouth, or a pastille contain- 
ing the salts found in Ems mineral water. 

If the patient complains of difficulty in loosening the expectoration, we pre- 
scribe expectorants, the action of which often fails to meet our desires, but which 
can not be dispensed with in practice. The expectorants most frequently used 
are carbonate of ammonia, ipecacuanha, apomorphine, and senega. We very often 
combine expectorants with narcotics, as in Dover's powder. 

If severe pain in the chest comes on, we often use local applications : mustard 
plasters, warm poultices and cold compresses, painting with iodine, or embro- 
cations of chloroform. Narcotics, such as morphine, are indispensable in severe 
dyspnoea, which usually occurs only in the last stages of the disease or as a result 
of pneumothorax. 

The treatment of haemoptysis is important. As a slight admixture of blood 
in the expectoration often precedes a severe haemoptysis, such an appearance 
always suggests caution. When there is any haemoptysis, absolute rest in bed is 
necessary. We should avoid any careful examination of the lungs, especially 
any severe percussion. We should lay a flat and not too heavy ice-bag over 
the lung on the side from which we suspect the haemorrhage ; the cold is usually 
well borne, but sometimes it aggravates the cough, and must then be omitted. 
We would also recommend swallowing bits of cracked ice. Narcotics, such as 



260 DISEASES OF THE RESPIRATORY ORGANS 



morphine, are the most suitable internal remedies, since they aid the cessation of 
the haemorrhage by suppressing the attacks of coughing. The more troublesome 
the cough the more necessary is it, therefore, to administer morphine in solu- 
tion, by the mouth or even subcutaneously. Of remedies to check the blood we 
should name, first, extract of ergot or ergotine, which may be given by the mouth, 
or, still better, subcutaneously, in doses of 2 to 8 grains (grammes 0.1-0.5) 
several times a day. As to sphacelotoxine, and other special preparations of ergo- 
tine, there has been as yet no extended experience. We may also try the fluid 
extract of hydrastis, with equal parts of an elixir, giving thirty to forty drops 
of the mixture several times a day; also, acetate of lead and atropine. The in- 
fluence of these remedies, particularly those last named, is, however, quite uncer- 
tain. The inhalation of a one- to two-per-cent. solution of perchloride of iron 
usually excites cough, and is therefore more harmful than beneficial. A very 
popular remedy among the laity, and one almost always at hand, is common salt, 
of which several teaspoonfuls may be given in water. When the haemorrhage 
recurs frequently, it is also advisable to " tie off " the limbs — that is, to apply 
bandages rather firmly around the middle of the upper arms and the thighs. 
This causes venous congestion, and hinders the return of blood to the lungs. 
When pulmonary hemorrhage has occurred, the diet should consist at first of 
nothing but cold milk, eggs, and similar food. Hot food, alcohol, and large 
amounts of meat are to be forbidden. It is a good thing to give acids, such as 
lemonade, or aromatic sulphuric acid, well diluted. 

Even when the bleeding has ceased we must keep the patient several days in 
bed, and for a longer time be extremely cautious, since the haemorrhage is apt 
to be repeated. 

The hectic fever of consumption is remarkably little influenced by antipyretic 
drugs. It often is entirely useless, or even, on account of its evil effect upon the 
stomach, actually harmful to give to feverish consumptives, for long periods of 
time, large doses of such drugs as quinine, antipyrine, and antifebrine, particu 
larly as the fever often of itself has deep morning remissions. The prescription 
of antipyretics is only justified when they make the patient feel better. On the 
other hand, it is very appropriate to give a cold sponging and rubbing to the 
whole body or chest, with water or alcohol, especially in the evening when the 
fever is high. The sponging is almost always well borne, and makes the patient 
feel brighter and easier. The cold pack may also be tried occasionally. 

Cold sponging often diminishes the troublesome sweats in phthisis, but if this 
does not check them, we may often prescribe atropine to advantage, grain T ^ to 
■ffV (gramme 0.0005-0.001) at night, but its action does not usually last very long. 
Lately agaricine in T V to -|-grain pills (gramme 0.005-0.01) has been recom- 
mended for the night-sweats in phthisis; also picrotoxine, of which grain | to i 
(gramme 0.008-0.01) is given in pill or solution at bed-time, and lately camphoric 
acid, grains 20-30 (grammes 1.5-2.0) in wafers. Dusting the body with a powder 
of five parts of salicylic acid to ninety-five of French chalk is also good. Sage 
tea is a favorite remedy for night-sweats — two or three cups of it cold at night — 
and so are milk and cognac. 

If there is loss of appetite, small doses of quinine, compound tincture of cin- 
chona, wine of cinchona, and other bitter remedies, such as tinctura amara 
(P. G.), are sometimes of service. It is also frequently a good thing to prescribe 
a little muriatic acid, five to ten drops of the dilute acid, with the meals. It is 
often very hard to check diarrhoea in phthisis. Opium, combined with tannin or 
acetate of lead, is most effective. This subject will be discussed more fully in the 
chapter on intestinal tuberculosis. 

We often prescribe preparations of iron, combined sometimes with quinine or 
arsenic (vide supra), in the beginning of the disease to improve the general con- 



ACUTE GENERAL MILIAEY TUBERCULOSIS 



261 



dition and the ansemia, but, as experience shows, iron is contra-indicated in 
patients who are feverish or who have a tendency to haemoptysis. 

The treatment of the diseases complicating phthisis is to be found in the appro- 
priate chapters. 



CHAPTER VII 
ACUTE GENERAL MILIARY TUBERCULOSIS 

etiology. — Acute miliary tuberculosis is a form of tuberculosis which we are 
justified in describing particularly because of its anatomical relations and its 
peculiar clinical history. The disease is characterized anatomically by the ex- 
tremely abundant development of miliary tubercles in a comparatively short 
time in many organs of the body. We can not liken this process to anything 
but an overwhelming of the body with tubercle bacilli, which in some way reach 
the different organs simultaneously, and in them give rise to the eruption of 
tubercles. Buhl advanced the hypothesis a long time ago, that a cheesy focus 
could be found somewhere in the body in every case of acute miliary tuberculosis, 
and that the general infection of the body resulted from the absorption of these 
cheesy masses by the blood. Later investigations, however, have given us a much 
more definite explanation of the nature and manner of this general infection. 
Ponfick found, in some cases of acute miliary tuberculosis, an extensive tubercu- 
losis of the thoracic duct with breaking down of the tubercular new growth. It 
is easy to see how, in this way, a large amount of tubercular material could be 
brought directly into the circulation, from the free communication of the lymph- 
duct with the subclavian vein, and thus be " disseminated " through the different 
organs in a short time. Still more frequently, however, the tuberculosis of the 
large venous trunks, discovered by Weigert, especially the pulmonary veins, 
seems to be the starting-point for an acute general miliary tuberculosis. Usually 
there are tubercular lymph-glands, or sometimes other foci of tubercular disease, 
which involve the wall of a neighboring vein, gradually break through it, and 
project into its lumen. If caseation and ulceration result in this spot, the infec- 
tious material is of course constantly washed off by the blood-current and carried 
away, and thus it reaches the other organs. 

Since such a tubercular focus — e. g., a tubercular bronchial gland — may remain 
for a long time entirely without symptoms, we can understand how miliary tuber- 
culosis may break out in an acute form in persons who previously seemed per- 
fectly well. In other cases the patient has already suffered from some tubercular 
affection, and suddenly the conditions occur somewhere in the body which lead 
to the development of miliary tuberculosis. Thus we sometimes see it break out 
in a patient who has ordinary phthisis, but acute miliary tuberculosis is one of 
the rarities in advanced phthisis. If we find, at the autopsy of a case of acute 
general miliary tuberculosis, old phthisical changes in the lungs, which is by no 
means very common, they consist of old, partly cicatrized foci, pigment indura- 
tions, etc. We see miliary tuberculosis rather frequently as a sequel to pleuritic 
effusion. We have already previously called attention to the fact that in such 
cases the pleurisy itself is a tubercular disease. Miliary tuberculosis is also seen 
in persons with old tubercular affections of the bones and joints, such as coxitis 
and vertebral caries, with tubercular swellings of the lymph-glands, as in the 
neck and the axillae, or with tuberculosis of the genito-urinary organs. In such 
cases, of course, the tubercular affection which is discovered during life, is not 
always the source of the general miliary tuberculosis, but the discovery of the 



262 



DISEASES OF THE EESPTKATOEY ORGANS 



existence of such an affection is of the greatest significance in diagnosis, as in this 
way our attention is strongly directed to the possibility of a general tubercular 
affection. 

In some cases an outbreak of miliary tuberculosis has been seen to follow other 
acute diseases, such as typhoid, or measles. 

Pathological Anatomy. — Except for the presence of an old tubercular affec- 
tion in some organ, and except for the tuberculosis of a vein or of the thoracic 
duct, which are as a rule apparent, and which have been described above, the 
anatomical lesion in acute miliary tuberculosis consists in the dissemination of 
miliary tubercles through a large number of the organs of the body. The lungs, 
the liver, and the spleen are constantly affected; almost as constantly the kid- 
neys, the thyroid gland, the marrow of the bones, the heart, and the choroid; less 
constantly, but still quite frequently, the serous membranes and the meninges. 
The miliary nodules may be found in large numbers in all the organs mentioned. 
They may in part be easily recognized by the naked eye, and in the lungs they 
may be very plainly perceived by the touch. In many organs, however, especially 
in the liver and often in the spleen, they are hard to recognize with the naked eye. 
but they are easily discovered by the microscope. In regard to the histological 
structure of miliary tubercles, and the discovery of tubercle bacilli in them, we 
must refer to what has been said in the chapter on pulmonary tuberculosis, but 
we must also mention that, in some of the more chronic cases, some of the nodules 
may grow to be large tubercular foci, from the size of a lentil to that of a pea. 
Less developed cases of miliary tuberculosis are also found, in which only a lim- 
ited number of organs are attacked, and these with less severity. 

Clinical History. — The clinical symptoms of miliary tuberculosis depend upon 
two factors, the first being the general infection of the body, and the second the 
local tubercular affection of certain organs. Although in many organs miliary 
tuberculosis is entirely without symptoms, as in the liver, the kidneys, the heart, 
and the marrow of the bones, in two organs — the lungs, and more especially the 
brain — it leads to the most marked local symptoms. The miliary tuberculosis of 
the choroid, discovered by Cohnheim and Manz, is also without symptoms, but it 
can be made out with the ophthalmoscope, and it is therefore of great diagnostic 
value. 

Miliary tuberculosis affords quite different pictures, according to the predom- 
inance of one or the other of the groups of symptoms mentioned. We distinguish 
the four following forms : 

1. Miliary Tuberculosis, with Predominant Symptoms of General Infection: 
the so-called Typhoidal Form. — This form may in part greatly resemble typhoid 
fever. The patient, who previously seemed quite well, or in whom some local 
manifestation of tuberculosis was suspected, falls ill with gradually increasing 
general symptoms, dullness, loss of appetite, headache, and fever. Since there is 
no local affection to be discovered to explain the symptoms, the disease at first 
may well be taken for typhoid. The general condition grows worse constantly, 
the fever is high and continually rises, and cerebral symptoms appear. In some 
cases an exanthematous eruption, like roseola", may increase the resemblance to 
typhoid. With careful observation, however, symptoms are almost always de- 
tected later in the disease which are, to a certain degree, characteristic of miliary 
tuberculosis, and are due to the existence of that disease either in the lungs or in 
the brain. The patient's complexion assumes a peculiar pallor, and with it a defi- 
nite cyanotic hue. The respiration becomes remarkably deep, and there is dysp- 
noea; or signs of a tubercular meningitis arise, such as rigidity of the neck, loss 
of consciousness, disturbances in the innervation of the ocular muscles, etc., and 
death follows with these symptoms. These cases last from ten days to three 
weeks, reckoning from the beginning of the severe symptoms. 



ACUTE GENEKAL MILIARY TUBERCULOSIS 



263 



2. Miliary Tuberculosis, with Predominant Pulmonary Symptoms. — These 
cases, too, may begin quite suddenly, almost like an acute croupous pneumonia, 
or they may develop gradually with quite a long prodromal stage. Erom the 
onset the symptoms point especially to disease of the lungs or the pleura. The 
patient complains of a stitch in the side, cough, and dyspnoea. The expectora- 
tion may bear a decided resemblance to that of pneumonia. Such cases, espe- 
cially if they begin abruptly, are at first often erroneously regarded as croupous 
pneumonia, particularly if we find fine rales almost like crepitant rales over cer- 
tain portions of the lungs. But the expected crisis does not occur: the fever 
continues; the dyspnoea, general weakness, and anaemia of the patient increase; 
the physical signs of pulmonary disease (diffuse bronchitic rales) become more 
and more extensive. The patient's face is pale, cyanotic, and anxious. Death 
ensues with all the signs of impaired respiration. The course is usually some- 
what more protracted than in the typhoidal form, lasting for three or four weeks 
and more. 

3. Miliary Tuberculosis, with Predominant Cerebral Symptoms, due to Tuber- 
cular Meningitis. — Tuberculosis of the meninges does not belong among the reg- 
ular lesions of general miliary tuberculosis. It develops in about half the cases, 
according to our estimation ; but where it occurs it almost always gives the whole 
case the characteristic imprint of tubercular meningitis, by which the other symp- 
toms are entirely concealed. The predominant symptoms are headache, fever, 
stupor increasing to deep coma, rigidity of the back and neck, and disturbances 
in the innervation of the ocular muscles. In such cases the tuberculous menin- 
gitis may alone be diagnosticated, and not the universal miliary tuberculosis. 
In fact, all the other signs of general miliary tuberculosis are not infrequently 
obscured by meningeal symptoms, and yet we have repeatedly observed, even in 
the deepest coma of the patient, a peculiarly deep and hurried respiration, which 
was the only noticeable sign referable to the miliary tuberculosis in the lungs. 

The symptoms of tubercular meningitis ir. many cases predominate in this 
type of the disease from the onset, but in other cases they come on during the 
attack and form its final period. The duration of the disease varies accord- 
ingly. 

4. Miliary Tuberculosis with a Protracted Course and Indefinite Symptoms 
for a Long Time — Intermitting Form. — Besides the forms already mentioned, 
cases occur which usually take quite a protracted course, lasting for eight or ten 
weeks, and having such indefinite symptoms that an absolute diagnosis is for a 
long time, or even throughout the disease, quite impossible. The patient com- 
plains of a number of general symptoms, such as headache and dullness, and also 
of thoracic symptoms, for which, however, we can find on examination no suffi- 
cient basis. There is almost always fever, usually not very high, and with a very 
irregular course ; but we have seen a regular daily rise of temperature for a time 
in some cases, and attacks of fever with quite a severe chill, so that at first we 
thought of an irregular malarial intermittent fever — the intermitting form. 
Later on the symptoms gradually increase. The apparently inexplicable loss of 
strength, and the patient's anaemia and emaciation, are marked, and they are 
important in diagnosis. Finally, either severe pulmonary symptoms or the signs 
of tubercular meningitis set in, and to these the patient succmnbs. 

TVe must mention particularly that the four forms of miliary tuberculosis just 
described are only the types of the disease. In individual cases we often meet 
with variations and transitional forms between these types. 

Single Symptoms. — 1. General Symptoms. — In all cases of acute miliary tu- 
berculosis the general condition of the patient is very serious. Most patients 
have a subjective feeling of severe illness, although they make little special com- 
plaint of it from the painless character of the disease. As the disease increases, 



264 



DISEASES OF THE RESPIRATORY ORGAXS 



there is often a marked feeling of anxiety and oppression besides the dyspnoea. 
There is, especially in the face, quite a peculiar pallor, characteristic of the 
disease, and associated with a marked cyanosis of the lips and cheeks. 

2. Fever. — Acute miliary tuberculosis almost always runs its course with a 
more or less high fever, a course without fever having been observed in only a 
few instances. It often happens, in more protracted cases, that the temperature 
may be nearly normal for a time, or only slightly elevated. There is nothing 
characteristic or typical in the course of the fever. In the cases with typhoidai 
symptoms the fever is usually quite high, between 103° and 105° (39.5°-40.5° C), 
so that the temperature-curve may be exactly like that of typhoid. In other cases 
the fever is irregular and is broken by many remissions, remitting or intermit- 
ting quite regularly for some time. Death ensues with a moderately high tem- 
perature or in collapse. In cases with tubercular meningitis there is also a 
marked rise of temperature at the close, up to 108° (42° C.) and over. 

3. Respiratory Apparatus. — It goes without saying that physical examination 
of the lungs may give no definite results. Almost all positive evidence is often 
wanting, and the contrast between the labored breathing and dyspnoea and 
the insignificance of the physical signs in the lungs is an important feature in 
diagnosis. Auscultation, as a rule, gives the signs of an intense bronchial ca- 
tarrh; we hear rhonchi or numerous fine and medium moist rales all over both 
lungs. The respiratory murmur itself is usually higher in pitch than normal, 
and in many cases it is obscure, rough, or harsh. In one of our cases there was 
heard, over a circumscribed area of the lung, a wholly peculiar, sharp, " lapping " 
sound on inspiration, which we have never heard under any other circumstances. 
Jiirgensen describes a soft friction sound, due to miliary tuberculosis of the 
pleura. Percussion usually gives no objective changes. At times the resonance 
is rather tympanitic, or slightly dull in some places. 

In some cases circumscribed pneumonic infiltration has been observed in the 
lungs in acute miliary tuberculosis, which, as we have said, may give rise to a 
confusion between miliary tuberculosis and croupous pneumonia, from the pres- 
ence of marked dullness, crepitant rales, and bronchial respiration. 

We must mention, finally, that in some of the cases physical examination of 
the lungs shows old changes in them, a phthisical affection of the apex, a former 
pleurisy, and the like. Positive evidence of such old tubercular affections may 
be of great diagnostic value in doubtful cases. 

Dyspnoea has been repeatedly mentioned among the pulmonary symptoms. 
The respiration is usually very much accelerated, especially during the more 
advanced stage of the disease, so that we see in adults forty, sixty, and even 
seventy respirations a minute. The respiration is also very deep, and is some- 
times noisy. As a rule there is cough, but it is usually troublesome only in the 
cases with severe bronchitis. It is often very slight. The expectoration is usu- 
ally scanty, and it is not characteristic. Special mention must be made of the 
fact that tubercle bacilli are absent in it, unless old ulcerated tubercular foci are 
present at the same time in the lungs. 

4. Circulatory Apparatus. — The pulse is frequent, about 100 to 120 a minute, 
often weak and small, and sometimes irregular, especially if tubercular menin- 
gitis co-exists. The miliary tubercles, which post mortem are almost always to 
be found in the heart, especially in the endocardium, cause no symptoms. In 
uncomplicated, acute, miliary tuberculosis there is little if any increase in the 
number of white corpuscles in the blood. The presence of tubercle bacilli in the 
blood will be mentioned below. 

5. Digestive Apparatus. — Vomiting is frequent at the onset of the disease. 
The bowels are usually constipated, but in many cases there is a moderate diar- 
rhoea. The loss of appetite, the thirst, and the dry tongue are due to the general 



ACUTE GEXEKAL MTLTAKY TUBEECULOSIS 



265 



disease and the fever. The spleen is usually somewhat, but not very much, 
enlarged. 

6. Nervous System. — In many cases in which the pulmonary symptoms pre- 
dominate the intellect remains quite clear until the last, but in other cases cere- 
bral symptoms, such as headache, dizziness, stupor, and delirium, come on quite 
early, and are a part of the general infection. As has already been said, the 
nervous symptoms in the cases combined with tubercular meningitis become 
quite prominent, but in individual instances it may be hard to decide whether 
they are due to such a complication, or are merely severe general symptoms. 

7. Eyes. — The ophthalmoscopic examination of the retina is of special diag- 
nostic importance, since the diagnosis may be made absolutely certain by finding 
miliary tubercles in the choroid. A negative result, however, is never decisive 
against the diagnosis, since the tubercles are sometimes absent, or at least are 
very few in number. Their discovery is almost always difficult, and demands 
much practice in the method of examination. In cases with tubercular menin- 
gitis we sometimes find an optic neuritis. 

Diagnosis. — The diagnosis of acute general miliary tuberculosis is ordinarily 
and justly considered very difficult. It quite often happens that at the autopsy a 
miliary tuberculosis is found which was not even suspected during life. It must 
be confessed that frequently, in such cases, we might very well have thought of 
acute tuberculosis. If, therefore, the possibility of acute miliary tuberculosis is 
brought to our attention during the patient's life, we can occasionally make an 
absolute diagnosis. 

The severe general condition, usually associated with fever, is most important, 
and for this no local cause can be found. Then come the pulmonary symptoms, 
especially the peculiar dyspnoea, for which there is also no adequate corresponding 
physical change to be discovered. It gives decided support to our suspicion if we 
can make out a distinct predisposition to tuberculosis, either hereditary or consti- 
tutional, or the history of a previous tubercular affection, especially pleurisy, and 
also chronic affections of the bones. The peculiar cyanotic pallor of the patient 
is very characteristic. 

On these factors rests the differential diagnosis between the " typhoidal " 
form of miliary tuberculosis and typhoid fever. ^larked roseola and considerable 
enlargement of the spleen are distinct arguments for typhoid, although they 
sometimes occur in miliary tuberculosis, and so are the intestinal symptoms 
of typhoid, such as meteorism, the characteristic, loose yellow stools, and possi- 
bly intestinal hemorrhage ; but we must not forget that both the roseola and the 
intestinal symptoms may be absent in typhoid. The course of the fever must 
always be considered in the differential diagnosis. It is much more frequently 
irregular and atypical in tuberculosis than in typhoid. Of course, the tempera- 
ture-curve is not an absolutely decisive factor. The blood does not afford any 
indubitable signs of distinction between the two, since in neither disease is there 
a decided leucocytosis. If the number of leucocytes is conspicuously small, 
5,000 or less, typhoid is strongly suggested. The Widal serum-reaction with 
typhoid bacilli (see page 22) is very important, and, when it turns out positively, 
decisive. On the other hand, of course, the absolute demonstration of miliary 
tuberculosis in the choroid is unequivocal evidence in favor of miliary tuber- 
culosis. 

In many cases the onset of meningeal symptoms may aid the diagnosis. Of 
course, if the patient is not seen until the last stages of meningitis, especially 
when there is an incomplete history, the diagnosis is next to impossible. In this 
case, if the fluid obtained by lumbar puncture is found to contain tubercle bacilli, 
the diagnosis may be settled (compare the chapter on tubercular meningitis). 

Acute tuberculosis is often confounded with severe bronchitis, especially in old 



266 



DISEASES OE THE RESPIRATORY ORGAXS 



persons who are considered emphysematous. The very severe general condition, 
the pallor, the rapid loss of strength, and the fever, are the only things here which 
call our attention to acute tuberculosis, and render the diagnosis possible. We 
have already indicated the possibility of confusion at the onset between miliary 
tuberculosis and croupous pneumonia. 

Of decisive diagnostic value in all cases is the demonstration of tubercle 
bacilli in the blood, which is indeed a difficult matter, but it has already been ac- 
complished more than once (Weichselbaum and others). 

Prognosis. — The cases described in literature as " cured miliary tuberculosis " 
are so uncertain in their diagnosis that they can not be regarded as convincing. 
We must therefore consider the prognosis as absolutely fatal. The differences in 
the course of the disease have been already mentioned. 

Treatment. — Although drugs are absolutely powerless, still the case in hand 
must always receive treatment, especially if the diagnosis can not be made with 
absolute certainty. Our prescriptions are purely symptomatic. The cases with 
a typhoidal course are to be treated just like typhoid, with baths, stimulants, 
etc. Tepid baths, and also local applications to the chest, expectorants, and nar- 
cotics, are indicated when the thoracic symptoms predominate. If meningeal 
symptoms set in, we may try ice, perhaps local blood-letting, iodoform salve, or 
mercurial ointment externally, and iodide of potassium internally. 



CHAPTER YIII 
GANGRENE OE THE LUNGS 

Etiology. — The sole cause of pulmonary gangrene — that is, the death and 
putrid decomposition of the lung-tissue — is the entrance of the bacteria of putre- 
faction into the lungs. The opportunity for inhaling them is certainly very 
great, but the normal organism apparently possesses the property of nullifying 
them and making them powerless. Under certain conditions, however, they take 
root in the lung and cause the death of the pulmonary parenchyma, which then, 
as a result of the presence of these specific bacteria of putrefaction, succumbs to 
that peculiar form of putrid decomposition known as " moist gangrene." 

The factor which most frequently gives rise to the development of pulmonary 
gangrene is the entrance of organic foreign substances, especially bits of food, into 
the lungs. The bacteria of putrefaction either enter the lungs with the foreign 
substance, or they settle there later and set up a putrid decomposition, first in that 
portion of the lungs, and then in the neighboring lung-tissue. The entrance of 
organic foreign substances into the lungs occurs in different ways. It often hap- 
pens from swallowing the wrong way, or from an accidental inhalation. In this 
way pulmonary gangrene may arise in previously healthy people, but it occurs 
especially in patients who are very low, very stupid, and soporose, and also in the 
insane, in patients who can not swallow or cough well, and in patients with paral- 
ysis of deglutition, as in bulbar paralysis. Bits of food may also reach the lungs 
from eructations and vomiting. Thus are explained the cases of pulmonary gan- 
grene which occur in patients with cancer of the stomach, and, still more fre- 
quently, with cancer of the oesophagus. Putrid organic material may also reach 
the lungs from ulcerative and ichorous processes in the mouth, the pharynx, and 
the larynx. In cancer of the tongue, the pharynx, and the larynx, in other ulcer- 
ative processes, and in injuries or wounds from operations in the mouth and phar- 
ynx that have become septic, pulmonary gangrene may develop quite readily. 



GAXGBEXE OF THE LUXGS 



267 



Finally, septic foci in the vicinity may extend to the lungs or perforate into a 
bronchus. In this way pulmonary gangrene may arise from the perforation 
through the pleura into the lungs of an ulcerated cancer of the stomach or a 
gastric ulcer, or in rare cases from vertebral caries, or from sanious lymph-glands. 

In some cases the cause of the pulmonary gangrene can not be made out, since 
the entrance of a foreign substance has perhaps been wholly unnoticed, as may 
happen in children, or during sleep. We had a grown-up young woman under 
observation for a long time with pulmonary gangrene, and one day she coughed 
up several fragments of chicken-bones, but she could give no account of how they 
entered the lungs. 

Experience teaches us that pulmonary gangrene is more apt to develop in 
persons with impaired nutrition, in old, marantic individuals and drunkards, than 
in those who are healthy. The tendency of patients with diabetes mellitus to 
pulmonary gangrene is remarkable. 

Pulmonary gangrene often develops secondarily to some other pulmonary 
affection. We have already spoken of the relations between it and foetid bron- 
chitis. Foetid bronchitis, on the one hand, often leads to pulmonary gangrene 
through an extension of the process to the alveoli ; and, on the other hand, when 
there is a gangrenous focus in the lungs, the bronchi are often infected to a wide 
extent by the putrid secretion coming from it, and then there arises foetid bron- 
chitis. Both diseases often run into each other without any sharp boundary; but 
gangrene may develop secondarily in other affections of the lungs. A new infec- 
tion with putrid material, however, is always requisite, and the affection of the 
lungs that already exists furnishes merely a favorable soil. This is the only 
explanation of the process when croupous pneumonia " runs into gangrene," or 
when gangrene develops in catarrhal pneumonia, in bronchiectasis, or in phthisis. 

Although the agents of putrefaction enter the lungs through the bronchi in 
most of the modes of origin of pulmonary gangrene that have been mentioned, 
they may also be transported into the lungs by the blood-current. We call these 
forms embolic gangrene. We find such gangrenous nodules in the lungs in 
connection with extensive gangrenous bed-sores, puerperal processes, suppurative 
caries of the bones, etc. In these cases the putrid material enters a vein from the 
seat of the primary process and is brought to the lungs, and here we find, as a 
result of the putrid character of the embolus, not a simple infarction, but an 
embolic gangrene. 

Pathological Anatomy. — We more frequently find pulmonary gangrene in the 
lower lobes than in the upper, corresponding to its mode of origin. Either both 
lungs are affected or only one, and the right somewhat more frequently than the 
left. We distinguish a diffuse and a circumscribed form, according to the extent 
of the gangrene. Embolic gangrene belongs to the latter form, and its nodules, 
by preference, lie near the pleural surface. 

We can easily recognize the anatomical changes in gangrene. The lung-tissue 
is changed to a discolored, dirty, greenish-gray mass, which gradually and pro- 
gressively becomes dissolved, forming a most foul-smelling ichor. We find, left 
in it, necrotic fragments of tissue and vessels. Gangrene cavities, with irregular, 
ragged walls, are formed from the partial expectoration of the softened gangre- 
nous nodule. The lung-tissue in the vicinity of the gangrenous spot is to a greater 
or less extent inflamed, partly in the form of catarrhal pneumonia, partly in the 
form of circumscribed croupous pneumonia. The inflamed parts in the vicinity 
are gradually involved in the gangrene, so long as the process extends, but finally 
a suppurating line of demarkation may be formed about the gangrene, the whole 
gangrenous fragment is in a measure sequestrated, encapsuled, and gradually 
expelled, and so healing becomes possible. We have already stated that foetid 
bronchitis may arise from a gangrenous nodule. 



268 



DISEASES OF THE EE S PIE AT OK Y OEGANS 



Whenever a gangrenous nodule reaches the pleura, a purulent and usually a 
sanious pleurisy follows from direct infection. Pneumothorax may arise from 
perforation of a gangrenous cavity. 

Clinical History. — The symptoms of gangrene depend for the most part upon 
the local affection in the lung. The condition of the expectoration is characteris- 
tic, and it alone may decide the diagnosis. 

In many ways the expectoration greatly resembles that of foetid bronchitis, 
and indeed a great part of it does not come directly from the gangrenous nodule, 
but is the secretion of the diseased bronchi. The penetrating stench of the 
sputum, a most repulsive, putrid odor, is very striking. The patient's breath 
and cough also have this stench, which infects the whole vicinity. The amount 
of the sputum is usually large ; it may reach ten or twenty ounces (200-500 cubic 
centimetres) in twenty-four hours. If the sputum is collected in a glass it forms 
three layers, like the sputum of foetid bronchitis — an upper layer, muco-purulent, 
greasy, consisting in part of nummular sputa, and covered with much froth; a 
middle serous layer, in which some firm masses from the upper layer float; and 
a lower layer, almost wholly of pus, but greasy and greenish-yellow, which usually 
contains many large and small plugs and shreds of tissue. We find in these 
plugs, on microscopic examination, beautifully twisted needles of the fat acids 
(see Fig. 24, page 168) imbedded in countless bacteria, fat-drops, and detritus, 
and often collected in large bundles ; but besides these we find in the sputum the 
constituents of the parenchyma of the lungs, and this alone is the decisive factor 
in distinguishing between pulmonary gangrene and simple foetid bronchitis. 

Traube's statement that in pulmonary gangrene the expectoration contains 
few, if any, elastic fibers, because the elastic tissue itself is destroyed by gan- 
grene, is not correct; or, at any rate, it is too sweeping. We have almost invariably 
found in the expectoration an abundance of elastic tissue, as well as other frag- 
ments of the parenchyma, pigment granules, and the like. Yet there is a prob- 
ability, no doubt, that in pulmonary gangrene the elastic tissue is for the most 
part destroyed. Filehne succeeded in extracting from the sputum of pulmonary 
gangrene, by means of glycerine, a ferment which in alkaline solution completely 
dissolved elastic tissue in a few days. The sputum always contains in enormous 
numbers bacteria of various kinds, both cocci and bacilli. Which of these are 
the special cause of the gangrene has not yet been definitely settled. The chem- 
ical examination of the sputum shows the presence of those substances which may 
always be found in the putrefaction of organic matter — tyrosine, leucine, am- 
monia, sulphuretted hydrogen, butyric acid, valerianic acid, caprylic acid, etc. 
The fresh sputum usually has an alkaline reaction, but on standing it becomes 
acid. 

Many cases of gangrene lead to erosion of the vessels and severe hsemoptysis. 
Slight admixtures of blood in the sputum are not infrequent. 

The other symptoms on the part of the lungs are not especially characteristic 
of gangrene. Most patients complain of cough, pain in the side, and more or less 
severe dyspnoea. Physical examination, as a rule, permits us to make out the seat 
of the nodule, but not always, since the physical signs, of course, depend upon the 
situation and extent of the gangrene. Small nodules, situated centrally, often 
give no objective evidence of their presence. Every extensive infiltration, how- 
ever, must cause dullness on percussion. Over the area of dullness we hear bron- 
chial respiration, and usually quite numerous moist rales. If a gangrenous cavity 
is formed, the physical examination may show plain symptoms of a cavity — tym- 
panitic resonance on percussion, amphoric respiration, coarse moist rales, etc. 

The physical signs are sometimes due to the accompanying pleurisy ; the dull- 
ness is more complete, the respiratory murmur and the vocal fremitus are dimin- 
ished, and the adjacent organs are displaced by the abundant effusion; but an 



GANGRENE OF THE LUNGS 



269 



absolute diagnosis of an accompanying pleurisy is often to be made only by an 
exploratory puncture. We have already . spoken of the occasional development 
of pneumothorax. 

In many cases there is fever, of quite an irregular character and of very vary- 
ing intensity. In the cases in which the gangrenous nodule is sequestrated, and 
the secretion can be freely emptied through the bronchi, so that there is no ab- 
sorption of septic material into the blood, fever may be entirely absent. 

We often see gastric and intestinal symptoms in jmlmonary gangrene, the dis- 
turbance being without doubt due to swallowing some of the foetid sputum. Many 
patients complain of loss of appetite, and sometimes of vomiting or diarrhoea. 
In severe acute cases there is sometimes a well-marked typhoidal state, with such 
symptoms as stupor, delirium, and great cardiac weakness. This condition is 
probably caused by the absorption of septic material into the blood. Rheumatic 
pains in the muscles and joints are seen in this disease, just as in foetid bronchitis. 
Finally, it should be remarked that the appearance of secondary abscesses in the 
brain (see page 1107) has been repeatedly observed in pulmonary gangrene. This 
fact must be borne in mind when, in the course of pulmonary gangrene, marked 
brain symptoms are developed, especially if we have not only such general symp- 
toms as coma, but also such local symptoms as hemplegia and other forms of 
paralysis, and convulsions. 

The general course of the disease shows very great variations. In all cases 
in which the pulmonary gangrene is secondary to some other affection, the course 
and the general type of the disease depend very largely upon the primary attack, 
but the cases of idiopathic gangrene also present great variations. The onset is 
either quite gradual and slow, or quite acute, and associated with fever and tho- 
racic symptoms. The stinking expectoration and the bad odor from the patient's 
mouth first direct the attention to the existence of putrid processes in the lungs. 
The disease is usually very chronic, lasting for months or even years. Many 
remissions and intermissions occur. With proper care and treatment we may see 
a decided improvement, and often apparently a complete cessation of the disease. 
The bad odor ceases, the expectoration diminishes or disappears entirely, and the 
patient's strength and nutrition become almost normal; but relapses may occur 
after long intervals. When the affection is of slight extent we may even see a 
complete recovery. 

Pulmonary gangrene always takes a worse course in previously weak and 
marantic persons, and an unfavorable termination may follow in a comparatively 
short time. Death ensues either from a general loss of strength, as a result of the 
disease, or from complications, such as pulmonary hgemorrhage, ichorous pleurisy, 
pneumothorax, or abscess of the brain. Rupture of an ichorous empyema out- 
wardly, or into the peritoneum, or into other cavities, is rare. 

Special mention must be made of the fact that the symptoms of pulmonary 
gangrene are not always so very pronounced. In persons who are weak and run 
down we often see pulmonary gangrene at the autopsy, although during life there 
have been no marked symptoms, not even offensive sputum or foetor from the 
mouth. 

Diagnosis. — The diagnosis can not be made with certainty unless the charac- 
teristic sputum is present. We can decide whether the sputum comes from a 
foetid bronchitis or from the foetid contents of a bronchiectasis, or from actual 
gangrene, only by finding under the microscope the remains of lung-tissue in the 
expectoration. Physical examination in gangrene, at least in part of the cases, 
also gives the signs of infiltration or of cavity-formation in the lungs. 

Prognosis. — The prognosis depends first upon the nature of the underlying 
disease, and then upon the extent of the affection, the strength of the patient, and 
the possibility of sufficient care and proper treatment. If the process in the lung 



270 DISEASES OF THE EESPIEATOEY OEGANS 



becomes sequestrated, marked improvement may follow, even in the severest con- 
ditions; but we must always remember that a relapse is possible. Complete re- 
covery from pulmonary gangrene is certainly extremely rare, if it ever occurs. 
We have already mentioned the dangers which may cause a fatal termination in 
pulmonary gangrene. 

Treatment. — Prophylaxis plays an important part in those cases in which 
there is danger of the entrance of bits of food into the air-passages from de- 
fective deglutition. We must think of the possibility of this with all patients 
who show great stupor, and also with patients who have pharyngeal paralysis, in 
order to watch them while taking food, and eventually to try artificial feeding 
with the oesophageal tube. 

The treatment of already existing pulmonary gangrene has, as its chief aim, to 
check the putrid processes of decomposition in the lungs. Unfortunately, the 
remedies at our command are not in all cases sufficient for this. The different 
disinfecting inhalations are the most effective. They are used in the same way as 
in foetid bronchitis (vide supra). Turpentine deserves the most confidence, and 
it may also be given internally with good results. According to Lepine, however, 
terpine acts even better than turpentine. We may also call attention to inhala- 
tions with carbolic acid, Curschmann's carbolic mask, inhalations with salicylic 
and boracic acids (4 parts of salicylic and 20 of boracic acid to 1,200 of distilled 
water), bromine (bromine and bromide of potassium, 2 parts of each to 1,000 of 
water), and similar substances. 

Besides oil of turpentine, other internal remedies are recommended: half a 
grain to a grain (gramme 0.03-0.06) of acetate of lead every two hours, creasote, 
carbolic acid, etc. Their action is uncertain. Of late, myrtol has been greatly 
extolled. It is given in capsules containing gr. ijss. (grm. 0.15), of which two or 
three are to be taken every two hours. 

The general treatment of the patient is very important — he should have good 
food, and live in as good air as possible. We must treat the pain in the chest and 
the cough symptomatic ally, local applications and morphine being most useful. 
The fever seldom gives occasion for direct interference. We may try to relieve 
the gastric and intestinal symptoms by giving antiseptics internally, especially 
by small doses of muriatic acid, salicylic acid, or creasote, as well as by the ordi- 
nary remedies, such as bitters and opium. 

If a secondary ichorous pleurisy develops, with or without pneumothorax, 
removal of the fluid by operation is necessary, if the patient has sufficient strength 
to bear it. 

In some few cases trial has been made of opening up the foci of gangrene by 
surgical means. As yet, it must be confessed, the results have not been very 
encouraging. 



CHAPTEE IX 

DISEASES FROM THE INHALATION" OF DUST 

( Pneumonoconiosis) 

Although there are a number of important contrivances in the respiratory 
apparatus to prevent the entrance of foreign substances into the lungs, still, if a 
person remains in a dusty atmosphere, so many particles of dust may be inhaled 
that they are not without effect on the lung-tissue. The diseases arising from 
the inhalation of dust are usually purely professional diseases, which occur espe- 
cially in workmen whose occupation involves the continual inhalation of some 



DISEASES EKOM THE INHALATION" OF DUST 



271 



kind of dust. In earlier chapters of this book, particularly while considering 
chronic bronchitis, we have already emphasized the harmful influence of the 
inhalation of dust. We have seen how the habitual respiration of organic dust 
in particular (from grain, wool, wood, and tobacco) is very apt to lead to severe 
forms of bronchitis and bronchiolitis. We must now draw attention to certain 
specific diseases similarly caused. 

We must first mention, however, a condition of the lungs which can scarcely 
be regarded as pathological, although it has its origin in the constant inhalation 
of dust, especially of coal-dust — the ordinary black pigmentation of the lungs. 
There can now no longer be any doubt, although there was once a long dispute 
about it, that the black pigment in the lung comes, in large part at least, from the 
inhalation of carbon. The particles of carbon pass into the lungs themselves, and 
thence into the bronchial glands by means of the lymphatics. A certain part of 
the coal-dust inhaled is removed with the expectoration, and it may easily be 
found in it microscopically, and often by the naked eye, as we see it in the well- 
known black expectoration which we often have in the morning, if we have spent 
the previous evening in a room filled with smoke. In Germany, Traube was the 
first to discover the particles of carbon in the expectoration of a charcoal-burner. 
In the man's lungs, aftei 
death, the vegetable origin of 
these particles could be rec- 
ognized, and Traube gave the 
correct explanation of them. 
In workmen who inhale large 
amounts of charcoal-dust, an- 
thracite coal-dust, soot, or 
graphite, the " normal " pig- 
mentation of the lung passes 
into a pathological condi- 
tion, anthracosis pulmonum. 
With this is usually associated 
an extensive chronic bron- 
chitis. In the expectoration of such patients are found many cells, filled with 
black particles of coal, even long after they have left the dusty atmosphere. The 
pigmented cells are leucocytes, or perhaps some of them epithelial cells (see 
Fig. 35). 

Zenker first discussed comprehensively the fact of the entrance of the different 
sorts of dust into the lungs and the consequent results. Besides the anthracosis 
already mentioned, the pulmonary disease from inhaling the dust of flint and 
other stones is of especial importance, the so-called stone-cutter's lung — chalicosis 
pulmonum — and also that from inhaling metallic dust, especially oxide of iron — 
siderosis pulmonum. The " stone-lungs " have been observed in workmen in the 
stamping-rooms of glass-factories, in mill-stone cutters, stone-polishers, stone- 
hammerers, plasterers, workers in porcelain, masons, slate-quarrymen, potters, 
etc. " Metal-dust lungs " occur in file-cutters, iron-workers, mirror-polishers, and 
especially in grinders, who inhale a mixture of stone- and iron-dust. The first 
case of a " red iron lung " was observed by Zenker, in a girl who had inhaled a 
thick dust of iron for ten or twelve hours a day. Her work was to color blotting- 
paper with a powder of red oxide of iron. During the inhalation of all these 
and similar kinds of dust, a portion of the inspired particles of dust are taken 
up by the leucocytes, and perhaps also by the epithelial cells, finally reaching the 
lymph-channels of the lungs. Some of the particles of dust remain in the inter- 
stitial connective tissue of the lungs. Others find their way to the bronchial and 
retro-bronchial lymph-glands. 




Fig. 35.— Expectoration of a man who worked on graphite. 
Numerous cells filled with particles of carbon. (Erlangen 
medical clinique.) 



272 



DISEASES OF THE KESPIKATOKY OKGANS 



If the inlialation of dust is long continued, it causes not only this abnormal 
pigmentation of the lungs, but also macroscopic anatomical lesions. These con- 
sist, partly, in a more or less severe and extensive chronic bronchitis, and partly 
in an interstitial inflammation which is due to the chronic irritation of the for- 
eign matter (e.g., flinty particles), and leads to the formation of connective 
tissue. The lungs are studded with nodules, which feel hard to the touch, and 
grate on section with a knife. All of these nodules consist of firm connective 
tissue, in which the particles of stone or iron are encapsuled. By the union 
of single nodules we may get more extensive induration and cicatricial forma- 
tion. Chemical examination of such lungs gives, as might be supposed, a large 
amount of silicic acid, iron, etc. 

In most of the cases which come to autopsy we find further changes in the 
lungs, which are not the immediate result of the inhalation of dust, but consist of 
sequelae and complications. Chronic diffuse bronchitis in the worker in dust, 
like any other chronic bronchitis, may give rise to pulmonary emphysema, and 
later to cardiac hypertrophy, etc. We very often find in the lungs co-existing 
and pronounced tubercular changes. It need hardly be emphasized that these 
changes are not the direct result of the inhalation of dust, but that the changes in 
the lungs set up by such an inhalation furnish merely a favorable soil for infec- 
tion with tuberculosis. In most cases, the " dust-lungs " acquire a marked clinical 
significance chiefly from the sequelae mentioned — namely, emphysema and tuber- 
culosis. The circumscribed nodules of interstitial pneumonia have no very 
marked symptoms following them. In all cases in which there is a fatal termina- 
tion, with pulmonary symptoms, we should regard the immediate action of the 
dust as much less the cause of death than are the secondary diseases. 

The actual points to be considered in judging of the clinical symptoms of the 
diseases from inhaling dust are contained in what has been said. The symptoms 
are those of chronic bronchitis, pulmonary emphysema, or chronic phthisis, 
and attention to the injurious influences associated with the patient's calling is 
the only possible way of making a diagnosis, but in individual cases it may always 
be a matter of doubt how far other accidental causes of disease may come into 
play. 

The prognosis depends, in the first place, upon whether the patient can be 
removed from the action of these injurious influences or not, but we must also 
mention the fact, which has been often observed, that many individuals get some- 
what used to the dust. After they have once recovered from the initial bron- 
chitis, such persons can live in an atmosphere of dust for a long time without 
any noticeable injury. 

The prophylaxis of diseases from inhaling dust forms an extended chapter in 
the hygiene of occupations, which we can not dwell upon here. The workman 
must be taught the danger to which he is exposed, and the danger itself must be 
diminished as much as possible by sufficient ventilation of the work-rooms, by 
cleanliness, and, under some circumstances, by a change in the technicalities of 
the business. , 

We need not give any special directions regarding the treatment of diseases 
from inhaling dust. It is founded on the same principles as the treatment of 
chronic bronchitis, emphysema, and chronic pulmonary tuberculosis. 



EMBOLIC PEOCESSES IN THE LUNGS 



273 



CHAPTER X 

EMBOLIC PROCESSES IN THE LUNGS 

{Hazmorrliagic Infarction of the Lungs) 

^Etiology. — The sources from which the material for an embolic plugging of 
branches of the pulmonary artery comes lie either in the right side of the heart or 
in the veins of the body. Pathological anatomy teaches us how often thrombi are 
formed in the veins, especially in the veins of the lower extremities and in the 
pelvic veins, and in the right side of the heart, in the recesses between the tra- 
becule, in the auricles, on the valves and the chordae tendinse, and at the apex of 
the ventricle. The particles, torn loose from thrombi so situated, are carried on 
by the blood-current, reach the lungs, plug a larger or a smaller branch of the 
pulmonary artery, according to the size of the particles, and thus cause further 
changes in the lung-tissue. Since the branches of the pulmonary artery are " ter- 
minal arteries," and since thus the vascular territory belonging to each branch 
can not be supplied, or can be supplied only to a small amount, with blood by 
collateral circulation from other vessels, the closure of a branch of the artery 
shuts the territory supplied by it out of the circulation. The pressure, in the part 
of the vessel lying peripherally to the point of plugging, becomes almost nil, and, 
as a result, there is a collateral or backward current into the region shut off, flow- 
ing from the capillaries in the vicinity, and probably even from the veins belong- 
ing to it. Yet the blood which flows in is under so slight a pressure that it does 
not flow through, but stagnates in the affected area. The walls of the capillaries 
and veins, in which the normal blood-current has ceased, lose their natural con- 
sistency as a result of this. The vascular walls become abnormally pervious. 
The fluid of the blood, the white blood-corpuscles, and also very many red blood- 
corpuscles, penetrate through the walls of the vessel into the surrounding tissue, 
and change it into the so-called hemorrhagic infarction. 

Every embolic closure of a branch of the pulmonary artery does not necessarily 
result in the formation of an infarction. Upon the sudden plugging of a main 
trunk, or of several large branches of the pulmonary artery, death may ensue at 
once, so that naturally all further changes in the lung-tissue cease. We also find 
quite frequently, especially in central portions of the lung, embolism of single 
branches of the pulmonary artery without the formation of an infarction. In 
such cases there must necessarily be a little circulation in the vascular territory 
which has been shut off, either by anastomoses between the territory of the pul- 
monary artery and that of the bronchial or mediastinal artery, or by the neigh- 
boring capillaries, whose arteries of supply remain open. 

The changes thus far described are the result of a purely mechanical closure of 
a pulmonary artery. We have noticed this especially when simple fibrinous 
plugs have given the occasion for the embolic process. Pulmonary infarctions 
are most frequent in chronic heart disease, in all forms of primary and secondary 
dilatation of the heart, but especially in disease of the mitral orifice, most often 
mitral stenosis. Thrombus formation is frequent in the dilated right side of the 
heart, and furnishes material for pulmonary emboli ; but these emboli are seen in 
all other possible conditions of disease, in which thrombosis in the right side of 
the heart or in the veins may occur. 

The changes in the lungs assume quite a different appearance if the embolic 
material is not simple fibrine, but if it contains at the same time some specific 
infectious matter. If emboli reach the lungs from an acute malignant endocar- 
ditis in the right side of the heart, or, as is most frequently the case, from a puru- 
lent (septic) phlebitis anywhere in the body, giving rise to a puriform, liquefying 
18 



274 DISEASES OF THE KESPIRATOEY OKGANS 



thrombus, the specific factors in inflammation — that is, bacteria — get into the 
lungs. Thus arise embolic abscesses and embolic gangrenous nodules in the lungs. 
We have already spoken of the latter, and the former are among the most constant 
lesions in every typical case of pyaemia. 

The fundamental facts as to the occurrence and significance of embolic pro- 
cesses in general, and those located in the lungs in particular, were discovered by 
Virchow. Eor a fuller understanding of the results of embolic closure of the 
vessels we must thank chiefly Cohnheim. 

Pathological Anatomy. — Hemorrhagic infarctions may involve one or more 
lobules, or almost a whole lobe of the lung, according to the situation of the 
embolus. Most infarctions are situated at the periphery of the lung, and have 
approximately a conical shape, corresponding to the extent of the region of the 
vessel. The base of the cone lies against the surface of the pleura. It generally 
projects a little above that surface, and its dark color can usually be plainly rec- 
ognized through it. The pleura itself is the seat of a fibrinous inflammation at 
the point to which the infarction reaches, and sometimes for a large space around 
it. The conical shape of the infarction is plainly recognized on section. The 
lung-tissue is changed to a firm, fragile, uniformly black-red tissue, devoid of air. 
The embolus can usually be readily found in the branch of the pulmonary artery 
leading to the infarction. Under the microscope we see a diffuse infiltration of 
tissue, with red blood-corpuscles in the infarcted portion. The alveoli and finer 
bronchi are also filled with coagulated blood. Under favorable circumstances, in 
cases of longer standing, the blood may be reabsorbed in part ; so that the lung 
again contains air, but it remains much pigmented in that place, and more or 
less indurated from the development of interstitial connective tissue. In excep- 
tional cases there is complete destruction of the pulmonary tissue where the in- 
farction is situated. This broken-down material is either discharged or absorbed ; 
then cicatrization with contraction takes place. 

Hemorrhagic infarctions are usually situated in the lower lobes, and more 
frequently on the right side than on the left. 

The smaller embolic abscesses are sometimes very numerous, and are dissemi- 
nated over the whole lung. In larger abscesses the conical shape may often be 
plainly recognized. When an abscess extends to the pleura, a purulent pleurisy 
arises from direct infection. Combinations and transitional forms between the 
ordinary hemorrhagic infarction and embolic abscesses are occasionally found in 
the lungs. 

Symptoms. — We often find at the autopsy embolism of single branches of the 
pulmonary artery, with or without infarction, which has caused no symptoms at 
all during life. 

Embolism of the main trunk, or of a large branch of the pulmonary artery, 
may cause sudden death, as has been repeatedly observed in patients with heart 
disease, or with venous thrombosis. If death be not immediate, sudden severe 
dyspnoea and oppression arise. The diagnosis may at least be suspected in such a 
case if we know of a possible source for an embolus. In some instances, when an 
embolus is situated in a large branch of the pulmonary artery, but has not com- 
pletely filled it, we can hear a systolic vascular murmur over the affected spot, as 
has been observed by Litten. The diagnosis, however, becomes certain if the 
further signs of infarction appear later. 

The most characteristic symptom of infarction in the lungs is the bloody 
expectoration. If we see quite suddenly bloody sputum in a patient with mitral 
stenosis, we are usually right in assuming a hsemorrhagic infarction of the lung. 
Either the sputum consists almost entirely of dark blood, or the blood is mixed 
with more or less mucus ; but there is never much air in it. The bloody expecto- 
ration often lasts for several days. 



BEOWN DTOUKATION OE THE LUNGS 



275 



We try to learn more of the size and situation of the' lesion by a physical ex- 
amination of the lungs. Of course this often gives a negative, or at least a doubt- 
ful, result. It goes without saying that small infarctions, and also those which 
are central, can not be made out by physical examination. Large peripheral 
infarctions may give rise in many cases to dullness on percussion, crepitant rales, 
and harsh or bronchial respiration, but it is often hard to decide in an individual 
case whether the physical signs which we meet with are not due to other patho- 
logical changes in the lungs, such as bronchitis or hydrothorax. We sometimes 
hear a pleuritic friction-sound in some part of the chest a few days after we sus- 
pect that an infarction has occurred, by which the diagnosis gains additional cer- 
tainty. We have already mentioned the subjective symptoms in embolism of a 
large pulmonary vessel — sudden dyspnoea and oppression. Small nodules often 
cause no special symptoms, but in other cases the patient feels a severe pleuritic 
pain, due to irritation of the pleura. 

Fever may be wholly absent, though we sometimes see a moderate rise of tem- 
perature at the onset. 

The embolic abscesses in the lungs hardly ever give rise directly to clinical 
symptoms. They form a part of the general picture of pyaemia and similar gen- 
eral infectious processes. Marked symptoms on the part of the respiratory appa- 
ratus are seen only when the abscesses are present in very large number. If an 
empyema develops from a focus which extends to the pleura, it sometimes occa- 
sions definite physical signs. 

It follows from all that has been said, that in the diagnosis of embolic pro- 
cesses the chief stress must always be laid on the presence of an astrological 
factor. We must regard the bloody sputum as the main direct symptom in 
hsemorhagic infarction. Embolic abscesses in the lungs may often be suspected 
in pysemic diseases, but they can hardly ever be diagnosticated with certainty. 

The prognosis is entirely dependent upon the underlying disease. In heart 
disease the occurrence of a hemorrhagic infarction is usually on the whole an 
unfavorable sign, since it points to weakness of the right ventricle, and hence to 
the formation of a thrombus in it ; yet it often happens that the symptoms of a 
pulmonary infarction may pass away entirely. 

We need not give special directions for treatment. It is in part purely symp- 
tomatic, and in part coincident with treatment of the underlying affection. As 
regards prophylaxis, we must bear in mind the absolute necessity of as perfect rest 
as possible for those patients in whom the presence of venous thrombi — e. g., in 
the femoral veins, suggests the possibility of pulmonary embolism. 



CHAPTEE XI 

BROWN INDURATION OF THE LUNGS 

(Lungs of Heart Disease) 

In heart disease, especially in mitral stenosis, we often find a peculiar change 
in the lungs, whose origin must be sought in the long-persisting engorgement of 
the pulmonary circulation. The lungs are hard and dense, and show on a fresh 
section an abnormal brownish-yellow color. In the larger pulmonary vessels, both 
arteries and veins, there is a thickening and cloudiness of the intima as a result of 
the stasis. We see here and there on the surface of the section, and beneath the 
pleura, little dark spots of pigment and fresh haemorrhages. We term this condi- 
tion brown induration of the lungs. 



276 



DISEASES OE THE EESPIEATOEY OEGAXS 



Microscopic examination shows that the capillaries are evidently dilated and 
twisted as a result of the persistent stasis. They even extend a good way into the 
alveoli, whose lumen is thus actually diminished. The interstitial connective tis- 
sue seems somewhat thickened, and we find in it many brown pigment-granules, 
the remains of the extravasated and decomposed red blood-corpuscles. The pig- 
ment-granules are some of them free, and some contained in cells (escaped leuco- 
cytes). In the intima of the larger vessels we often find fatty degeneration of the 
endothelium. 

With regard to the clinical importance of the pulmonary changes due to heart 
disease, we should say that it is very probable that the dyspnoea of such patients 
is aggravated by the diminution of the alveolar spaces throughout the lungs, as a 
result of their being crowded with desquamated pulmonary epithelium. Clin- 
ically, however, we can not well distinguish this factor from the other causes of 
dyspnoea. 

We have no positive factors by which to diagnosticate brown induration of 
the lungs during life. The anatomical lesions, too, show a certain variation, not 

always to be explained, in that, under 
apparently the same conditions, the 
brown induration is often very 
marked, and often extremely slight. 
In cases in which we find this in- 
duration in the cadaver we have re- 
peatedly heard, during the patient's 
life, a very sharp, puerile respiratory 
murmur, which seems to be character- 
istic of many cases of the " heart-dis- 
ease lung." We might lay still more 
stress upon the presence of large, 
characteristic cells in the expectora- 
tion, which are thickly filled with 
large and small yellow or brown 
pigment - granules (see Eig. 36). 
These large pigmented cells (" cells 
of heart disease") are especially 
abundant in the expectoration of 
patients with extreme mitral stenosis. 
They are identical with the above- 
mentioned pigment-cells which are found in the lymph of the alveoli after death. 
Many investigators regard them as alveolar epithelium, while we are more in- 
clined to regard them as mainly leucocytes which have taken up the pigment of 
the disintegrated red blood-corpuscles. Besides these pigment-cells we also^ fre- 
quently see the still intact red blood-corpuscles in the expectoration of patients 
with heart disease. 

The prognosis and treatment coincide with those of the underlying cardiac 
disease. 




Fig 



. 36.— Sputum of a patient with mitral stenosis, 
containing the so-called "cells of heart disease." 
(Personal observation.) 



CHAPTER XII 

TUMORS OF THE LUNGS. CANCER OF THE LUNGS. ECEINOCOCCUS 
OF THE LUNGS. PULMONARY SYPHILIS 

1. New Growths in the Lungs. Cancer of the Lungs. — Most of the new 
growths which are met with in the lungs are of a secondary nature. Secondary 
cancers are sometimes found in the lungs, with carcinoma of other organs, whose 



TUMORS OE THE LUXGS— PULMOXAEY SYPHILIS 



origin may always be explained by supposing a growth of the primary tumor into 
a vein, and the consequent carriage of the germs of the growth to the lungs. 
These secondary nodules in the lungs usually cause, no special clinical symptoms, 
unless they are very numerous and extensive, when they give rise to dyspnoea, 
and physical signs. There once came to the clinique in Leipsic a case of sec- 
ondary, and very extensive, miliary carcinosis of the lungs, which ran a brief and 
fatal course, simulating acute miliary tuberculosis with predominant pulmonary 
symptoms. 

Other secondary new growths deserving mention are enchondroma and sar- 
coma. We have seen an extensive development of secondary pulmonary sarcoma, 
following primary sarcoma of the bronchial lymph-glands, and also following 
lympho-sarcoma of the lymph-glands of the neck, which grew into the jugular 
vein. vVe have also seen secondary deposits of sarcoma repeatedly in connection 
with primary congenital sarcoma of the kidney (see page 644), 

Enchondroma, sarcoma, and endothelioma appear, also, as primary new 
growths in the lung. Pulmonary cancer is. however, the only primary tumor 
which has any great clinical importance. In its clinical relations we can also 
rank with it certain malignant, metastatic forms of alveolar sarcoma. The 
typical cancer of the lungs is always a cylindrical-celled carcinoma, which un- 
doubtedly arises from the bronchial epithelium. It is especially common in 
elderly persons, over forty, and seems to be found somewhat more frequently in 
the right lung than in the left, and in the upper lobes than in the lower. By its 
diffusion the lung-tissue in the parts affected by cancer is changed to a yellow- 
ish-gray and quite soft and crumbling mass, devoid of air. YTe can usually 
scrape away from the section the characteristic cancer-juice, in which the micro- 
scope shows the typical cancerous elements. The pleura is very often involved. 
The new growth has either extended directly into it. or single, and more circum- 
scribed, secondary nodules have formed in it. The lymph-glands are almost 
invariably affected, especially the bronchial glands, and also the axillary and 
cervical glands. Secondary carcinoma of other organs is rare, but it is found 
in some cases in the other lung, the liver, the brain, and elsewhere. 

It is almost always difficult to interpret correctly the clinical symptoms of 
cancer of the lungs at the beginning of the disease. They are referred to some 
other, more common chronic pulmonary disease, such as chronic bronchitis, phthi- 
sis, or pleurisy, but in the further course of the disease we succeed, at least in a 
number of cases, in making a correct diagnosis. In other cases, especially in old 
people, the growth may remain latent. 

The general pulmonary symptoms have little that is characteristic. The 
patient complains of gradually increasing difficulty in respiration, and of pressure 
and distress in the chest, which may finally increase to the most intense dyspnoea. 
]\fost patients suffer very much from the labored, frequent, and spasmodic cough. 
The expectoration in some cases has no peculiarity, but it often assumes, at least 
for a time, a characteristic consistency which is extremely important for diagno- 
sis. It contains blood, and also has a peculiar " currant-jelly-like " appearance. 
Under the microscope we can sometimes make out the characteristic elements of 
the tumor in it. Severe haemoptysis is also seen in cancer of the lungs. 

Physical examination of the lungs gives positive results in many cases, such 
as dullness, bronchial respiration, diminished respiration, rales, and sometimes 
pleuritic friction-sounds, none of which has anything characteristic in itself, 
although these signs may be of distinct significance in making out the seat and 
the extent of the new growth. Yet sometimes the area and peculiar limitations of 
the dullness — for example, if confined to the sternum — are so different from usual 
that from these factors alone suspicion of a new growth is excited. The sense of 
resistance upon percussion is quite considerable ; the respiratory murmur over the 



278 



DISEASES OF THE RESPIRATORY ORGANS 



tumor is often inaudible or concealed by the stridor due to encroachment on the 
lumen of the larger bronchi. Finally should be noted the not infrequent appear- 
ance of a diffuse swelling, and sometimes of a slight oedema of the skin over the 
affected spot. 

The occurrence of certain sequelae is of great diagnostic significance. The 
chief one is swelling of the lymph-glands in the neck or axilla, and also certain 
symptoms of compression, which either are produced directly by the new growth, 
or are due to the secondary enlargement of the lymph-glands. Pressure on the 
superior vena cava, or a large branch of it, causes oedema in the face, neck, over 
the wall of the chest, or in one arm. The subcutaneous veins in the regions 
named appear dilated and tortuous. Pressure on the oesophagus causes diffi- 
culty in deglutition; pressure on the brachial plexus, intense neuralgic pains 
and paresis of one arm; pressure on the recurrent nerve, paralysis of the vocal 
cords and hoarseness; pressure on the trachea or a primary bronchus, the 
symptoms of tracheal or bronchial stenosis. The pleura is . often involved so 
that the signs of a pleuritic effusion associate themselves with the other symp- 
toms. It is of diagnostic importance that in such cases the exudation is not 
infrequently hemorrhagic (vide infra, new growths of the pleura). Besides the 
symptoms already mentioned we must consider the general symptoms. As in 
carcinoma in general, so in pulmonary carcinoma, the well-known cancerous 
cachexia gradually develops. The patient grows dull, loses his appetite more and 
more, disturbances of digestion and sometimes moderate elevations of tempera- 
ture develop, until he finally succumbs to general marasmus. 

The whole duration of the disease is from six months to two years. The prog- 
nosis is fatal. The treatment can be only symptomatic, and we employ the same 
remedies as in other pulmonary affections. 

We must still briefly consider a new growth in the lungs which is extremely 
interesting from a theoretical point of view. In workmen in the cobalt mines of 
Schneeberg, in the Saxon Yoigtland, the development of malignant lympho- 
sarcomata in the lungs, with the occasional formation of metastases in the glands, 
the liver, the spleen, etc., is of frequent occurrence. The disease runs its course 
under the type of a chronic pulmonary affection, and almost always ends fatally. 
The endemic occurrence seems to point to an infectious origin for the tumor. 

2. Echinococcus of the Lungs. — Primary echinococcus of the lungs is very 
rare. In most cases the echinococci are brought to the lungs secondarily from 
other organs, either by way of the blood-current, or, as is far oftener the case, by 
perforation of an echinococcus of the liver through the diaphragm. 

The symptoms of echinococcus of the lungs are manifold. The parasite some- 
times remains entirely concealed. In other cases a more or less severe, and often 
febrile, affection of the lungs, is developed, with pain in the chest, cough, and 
sometimes bloody expectoration, and dyspnoea. Physical examination of the 
lungs gives in some cases dullness, absence of respiratory murmur, and diminished 
vocal fremitus, while after the expectoration of the echinococcus (vide infra) 
symptoms of a cavity may ensue. A correct interpretation of all these symptoms 
is possible only when, as has often been observed, the echinococcus cysts are 
coughed up, or at least when parts of them, like the membranes or the hooklets, 
are found in the expectoration. 

The termination of the disease may be favorable if the echinococci are expec- 
torated, or if we succeed in removing them by operative means. We can hardly 
hope to be able to kill the parasite by inhalations of turpentine or benzine. Some- 
times the echinococcus cyst becomes gangrenous, or suppurates. Rupture into the 
pleura, into the peritoneum, into the pericardium, and externally, has also been 
observed. This last termination is the most favorable, since otherwise, if the 
affection progresses, a fatal result may be caused by the sequelae, or rarely by the 



PLEUKISY 



279 



occurrence of suffocation. The details of the natural history of the echinococcus 
are given in the chapter on echinococcus of the liver. 

3. Pulmonary Syphilis. — This would also be the place to speak of syphilitic 
new growths in the lungs, but, in our opinion, in spite of the quite abundant lit- 
erature of this subject in recent times, no definite clinical description of pulmo- 
nary syphilis can be made. Those physicians who are disposed to consider every 
pulmonary disease in a previously syphilitic subject to be of a syphilitic nature, 
certainly regard many things as pulmonary syphilis which have nothing at all to 
do with syphilis. At least, we have found that all those cases which at first sug- 
gested a diagnosis of pulmonary syphilis, finally, upon more accurate examina- 
tion and after longer observation, have turned out to be something else, usually 
tuberculosis. There are a few indubitable cases of chronic indurative contrac- 
tion of the lungs following primary syphilitic infiltration. The clinical picture 
here does not differ in any characteristic manner from that of ordinary chronic 
interstitial pneumonia. A probable diagnosis may be made from the knowledge 
of the syphilitic taint, the simultaneous existence of other syphilitic lesions — 
e. g., of the liver — the physical signs of chronic pulmonary disease, and the fail- 
ure to find tubercle bacilli in the sputum on repeated examinations. It is also 
well established that there may be syphilis of the larger and medium-sized 
bronchi, which is recognized at the autopsy by extensive radiating cicatrices in 
the bronchial mucous membrane, which sometimes lead to stenosis. Single gum- 
matous nodules in the lungs are of the greatest rarity. We sometimes find in 
the pleura peculiar radiating cicatrices, which probably are of syphilitic origin. 
The pulmonary syphilis of the new-born, which occurs in the form of single nod- 
ules or as a diffuse syphilitic infiltration, the so-called pneumonia alba, has only 
a pathological interest. 

If the existence of a syphilitic disease of the lungs is suspected, of course 
specific treatment should be employed. Iodide of potassium must be adminis- 
tered and perhaps also a course of mercurial inunctions. The results are not apt 
to be brilliant, however, because it is of course impossible to restore the portions 
which have been cicatrized. 



SECTION V 
Diseases of the Pleura 

CHAPTER I 
PLEURISY 

(Pleuritis) 

JEtiology. — Pleurisy is divided into primary and secondary. In a strict sense, 
the only cases of pleurisy which can be termed primary are those in which the 
pathogenic organisms penetrate into a healthy body, and become localized in the 
pleura without any previous organic lesion elsewhere. !N"o doubt many a case of 
pleurisy seems primary from a clinical standpoint, which is really not so. The 
disease antecedent to the pleurisy may be so slight as to present no symptoms and 
attract no attention. The pleurisy appears as an apparently independent dis- 
ease, and is the first thing which attracts attention to the previously existing 
affection. 

Exclusive of traumatic pleurisy, resulting from such injuries as a penetrating 



280 



DISEASES OE THE RESPIRATORY ORGAXS 



thoracic wound, we know positively of only one form of pleurisy — viz., the rheu- 
matic — which is primary. This is, from an etiological point of view, most 
closely allied with acute articular rheumatism (Eiedler). In polyarthritis (see 
page 680) it is not very exceptional to have pleurisy develop secondarily. In 
many cases the rheumatic affection attacks the pleura at first, without any great 
involvement of the joints. Then often follow articular trouble, endocarditis, 
and the like, confirming, or for the first time disclosing, the aetiology of the 
attack. Whether still other pathogenic influences may produce primary pleurisy 
is not settled. Some cases of acute pleurisy, setting in with high fever, we have 
felt justified in referring to diplococcus infection, as suggested by the association 
of herpes and other symptoms. In such instances it is scarcely possible to ex- 
clude with certainty the presence of a small focus of pneumonia. In genuine 
primary pleurisy the pathogenic germs must first enter the circulation, and by 
that means reach the pleura. It is frequently impossible to find out any special 
exciting cause for the attack. Often it is ascribed to catching cold. 

Among those varieties of pleurisy which appear from a clinical standpoint as 
primary, while their existence is really referable to a previous lesion of the body, 
by far the most frequent and important is the tubercular. On this point it was 
only gradually and by means of long experience that physicians obtained a cor- 
rect conception of the truth. We believe it right to say that the great major- 
ity of all cases of apparently primary pleurisy are tubercular. The infection of 
the pleura is due to the invasion of it by germs from some tuberculous focus, 
situated near by. Either there are small tuberculous patches in the lungs which 
extend to the pleura, or, probably yet more frequently, bronchial or retro-bron- 
chial lymph-glands, being tubercular, break into the pleural cavity and promptly 
excite pleurisy. In many of these cases the further course of this disease clearly 
shows that the pleurisy was tuberculous at the start, and not infrequently the 
physican is justified, even at the very beginning of the illness, in expressing his 
suspicion of tuberculosis (vide infra, diagnosis). In many other cases of pleu- 
risy its secondary character is clear from the start. Most of these occur from 
the direct extension of the inflammatory process, from some neighboring organ, 
to the pleura. When considering pulmonary diseases, we had occasion to point 
out that the various pathological changes in the lungs, when they extend to the 
pleura, involve it in the disease. Thus we see pleurisy associated with croupous 
pneumonia, lobular catarrhal pneumonia, pulmonary gangrene, hsemorrhagic in- 
farction, embolic abscesses, and, most important of all, pulmonary tuberculosis. 
Many of the diseases just enumerated are frequent complications of the most 
diverse diseases. Hence, it is easy to understand that pleurisy is a not infre- 
quent phenomenon in all sorts of severe illnesses. 

Inflammation from other neighboring organs beside the lungs may extend to 
the pleura. Inflammation of the contiguous serous membranes may spread to the 
pleura by continuity; thus pleurisy complicates pericarditis and peritonitis. In- 
asmuch as the pleura and the outer surface of the pericardium lie in direct appo- 
sition and, furthermore, the pleural cavity and the peritoneal cavity are directly 
connected by the lymph-channels of the diaphragm, we can easily understand 
that not only serous and purulent, but also diplococcus, inflammation of the peri- 
cardium and peritoneum may have pleurisy for a sequel. 

Another variety of secondary pleurisy is due to the conveyance of the inflam- 
matory organisms not from the immediate neighborhood, but from other parts, 
by way of the circulation. Here should be mentioned pleurisy due to general 
sepsis, to polyarthritis, to nephritis (see page 632), and to genuine gout (which 
see). The factors which give rise to the inflammation are either organic or. in 
the case of gout and nephritis, chemical in their nature. The inflammation they 
excite in the pleura is most varied in its kind and degree. 



PLEUKISY 



281 



Of late years bacteriological investigations have been made by E. Levy, Prince 
Ludwig Ferdinand, and others, to obtain a more accurate knowledge as to the 
special variety of germs in the various forms of pleurisy, due to infection with 
organized material. It must not be forgotten, however, that these bacteriological 
investigations have been, for the most part, directed not to the diseased tissue, 
but to the inflammatory pleuritic exudation. This, however, in many cases con- 
tains no bacteria whatever. In particular, the exudation in most cases of tuber- 
culous pleurisy, whether serous or purulent, is absolutely sterile, and in the sec- 
ondary pleuritic exudations, in acute polyarthritis and nephritis, the search for 
bacteria has failed again and again. In other cases of pleurisy, however, staphy- 
lococci have been found in the exudate, and in empyema streptococci also. Meta- 
pneumonic pleurisy, whether serous or purulent, is often, though not always, 
characterized by the presence of genuine pneumococci. In general, the question 
with regard to the special cause of the disease will have to be whether the pleu- 
risy, in each case, is a part of the original primary disease — that is, whether we 
find tubercle bacilli in tuberculosis and diplococci in pneumonia, or whether the 
pleurisy is a secondary complication, so that, for example, we find streptococci 
in typhoid fever. Further investigations are needed for complete enlightenment 
with regard to all these matters. 

Pathological Anatomy. — The inflamed pleura is markedly injected, it has lost 
its normal luster, and instead has a dull surface. This dullness is due to the 
coagulated fibrinous exudation upon the pleura, the exudation, in mild cases, 
forming only a thin layer. In more advanced cases, however, the surface of the 
pleura is covered with thick, rough, and shaggy masses of fibrine. As long as the 
fluid in the pleura is little or not at all increased, we speak of a simple fibrinous 
or dry pleurisy (pleuritis fibrinosa vel sicca). 

In other cases, however, besides the layer of fibrine there is an abundant exu- 
dation of fluid from the capillaries of the pleura, forming a pleuritic effusion. 
This is ordinarily of a simple serous character — serous and sero-fibrinous effu- 
sions. The fluid collects between the surfaces of the pleura, or, if there is at the 
same time an abundant coating of fibrine, between the gaps and in the meshes of 
the fibrinous exudation. In such cases there are often many flakes of fibrine 
floating in the fluid. 

Upon microscopic examination there are invariably found a few leucocytes 
even in serous exudations, and also sometimes a very few blood-corpuscles and 
endothelial cells (often swollen or fatty-degenerated), and plates of choles- 
terin. 

If the number of pus-corpuscles in the exudation becomes much increased, we 
have a sero-purulent, or a purulent exudation. This is always due to the presence 
of a specific organized poison which excites the suppuration. The pleurisies 
which come from embolic abscesses, from gangrenous foci in the lungs, and from 
carious ribs, and those which arise from the rupture of tubercular cavities into 
the pleura, are almost always of a suppurative character. We call the purulent 
pleuritic effusion empyema. If putrefactive agencies enter the pleural cavity at 
the same time with the pus poison, as in the pleurisies which develop in pulmonary 
gangrene, the purulent exudation assumes an ichorous, putrid character — ichorous 
effusion. 

Under certain circumstances the effusion assumes a hemorrhagic character — 
hemorrhagic effusion — especially if haemorrhages occur from the old or newly 
formed capillaries dilated by the inflammation. They arise partly by diapedesis 
and partly from rupture of the walls of the vessels. The exact cause of the haem- 
orrhages is usually unknown. We know by experience that hsemorrhagic effu- 
sions are most frequent in tubercular pleurisy, a fact which is of diagnostic im- 
portance. The exudation may also be haemorrhagic in connection with new 



282 



DISEASES OF THE RESPIRATORY ORGANS 



growths of the pleura, after severe croupous pneumonia, in septic disease (e. g., 
puerperal fever), and finally when there is a general haemorrhagic diathesis, as 
seen in scurvy, purpura haemorrhagica, and leukaemia. In all these last-men- 
tioned cases it should, of course, be considered that we are not always dealing 
with a true inflammatory exudation, but merely with a haemorrhage into the 
pleural cavity. 

The amount of fluid collected in one pleural cavity is, in the majority of cases, 
somewhere between a pint and a quart (500-1,000 cubic centimetres), but it may 
reach three or four quarts. Every large effusion must influence the position of 
the yielding walls of the pleural cavity, the chest-wall, the lungs, the medias- 
tinum, and the diaphragm, through the consequent increase of pressure in the 
affected pleural cavity ; and the resultant symptoms of pressure on the neighbor- 
ing organs are of the greatest clinical significance. Attention is first called to 
the lungs themselves. Since the normal lung is expanded in the thorax beyond 
its elastic equilibrium, it will retract as soon as a part of the pleural cavity is 
occupied with fluid. Until it has reached its position of elastic equilibrium there 
can be no question of a positive pressure on the lung. The lung floats on the effu- 
sion, in a certain way, if there be no adhesions, but, as the amount of the fluid 
further increases, compression of the lung follows. With a very large effusion the 
lung is pushed wholly up and back against the vertebral column, and is changed 
to an almost bloodless, airless, flat mass. It is, however, possible that the atelec- 
tasis of the lung is not caused exclusively by compression from without, but that, 
after the normal respiratory movements have ceased, a part of the air in the lung 
may be absorbed by the vessels, or even by the effusion. 

We also see the results of the pressure exerted by the pleuritic effusion on the 
mediastinum and diaphragm, as well as on the lungs. Displacements of the heart 
arise from the lateral pressure on the mediastinum, which must take place if the 
pressure in the diseased pleural cavity is equal to that of the atmosphere, for a 
greater and positive pressure is unnecessary, since a negative pressure prevails on 
the healthy side. 

The downward pressure of the diaphragm, which usually affects both halves of 
it, although in unequal degree, makes itself manifest on the right by the low posi- 
tion of the liver, and on the left by the downward displacement of the stomach 
and large intestine. It must be particularly noticed, however, that adhesions 
may prevent all the pressure-displacements which we have mentioned, both of the 
lungs and of the neighboring organs. 

As regards the further changes and terminations of the pleuritic processes, 
they depend upon the amount and character of the effusion. Favorable cases may 
result in complete recovery and absorption of the effusion. The fluid contents 
are taken up directly by the lymphatics of the pleura, and the solid constituents, 
the fibrine and the white blood-corpuscles, are decomposed, dissolved, and ab- 
sorbed. Old fibrinous patches sometimes become impregnated with lime salts, 
so-called "pleuritic ossification." 

Whenever a case of extensive pleurisy, with an abundant fibrinous or fluid 
exudation, gets well, there is a marked cicatricial contraction of the pleura, 
in which the whole thoracic wall is involved. It requires months for the lungs 
and the thorax to regain their normal expansion, if they can ever do so. 

That recovery from large pleuritic exudation is so often incomplete, is ex- 
plained for the most part by the nature of the original disease. We often find 
that temporary improvement is followed by a fresh relapse of pleurisy, or by the, 
appearance of extensive and usually tuberculous disease of the lungs or other 
organs. 

In the case of purulent exudations, also, final absorption of the fluid is possi- 
ble. This is especially likely when the empyema is meta-pneumonic and benign, 



PLEURISY 



283 



but this demands much time, and thick, cheesy masses of pus are often left in the 
pleural sac. In most cases of empyema, if there is not timely operative interfer- 
ence, the pus seeks an outlet for itself. It may break through the visceral pleura 
into a bronchus, and be emptied externally, thus giving rise to a pyopneumo- 
thorax ; but in many cases the pleura seems to be destroyed only superficially, and 
the pus is pressed into the alveoli as into a sponge, especially by the movements 
of coughing, and thence reaches the bronchi, without letting the air enter the 
pleural cavity (Traube). In other cases the empyema breaks externally through 
the chest-wall — empyema necessitatis. The point of rupture is usually found in 
the vicinity of the sternum, where the chest-wall is thinnest. In very rare cases 
the empyema breaks into the deeper parts of the trunk, or into the abdominal 
cavity. 

Course of the Disease. — We will speak in what follows especially of the course 
and symptoms of ordinary, apparently primary {vide supra), fibrinous or sero- 
fibrinous pleurisy, the so-called simple pleuritic effusion. What is said of it 
obtains in large measure in the other form of pleurisy also. The physical signs, 
of course, are almost wholly independent of the character of the effusion. As far 
as the different forms of pleurisy differ clinically, we will mention their peculiari- 
ties below. 

Only rarely is the onset of pleurisy quite acute and sudden, beginning with a 
rigor. In such cases we must guard against confusing it with croupous pneu- 
monia. Pleurisy usually begins slowly and gradually. The symptoms, which 
the patient himself feels, are in many cases to be referred directly to the disease of 
the pleura. One of the most constant is the pleuritic pain, the stitch in the side. 
A more or less severe pain comes on in the side at every deep breath, and hence 
upon any physical exertion; also upon movements of the body, in stooping, 
coughing, or gaping. Shortness of breath soon appears, and constantly increases. 
There is often a frequent, dry cough. Sometimes there are scarcely any cough 
and expectoration. Such expectoration as there may be is usually simply mu- 
cous. Besides that, severe general symptoms almost always develop ; the patient 
feels dull, looks pale, and has no appetite. Patients who can endure a good deal 
often keep at work for a long time, until, after feeling miserable for three or four 
weeks, they are forced to stay at home and summon a physician. It is very impor- 
tant to know that in not a few cases the general symptoms are much more promi- 
nent, at the beginning of pleurisy, than the local ones. The patient comes to the 
physician complaining only of weakness, loss of appetite, or headache, and the 
physical examination is the first thing that shows the presence of perhaps a large 
pleuritic effusion. 

In most of the severe cases the further course is slow like the beginning, but 
sometimes the severest symptoms, most intense dyspnoea, marked cyanosis, etc., 
may come on in a short time, owing to a sudden increase of the effusion. On the 
other hand, in mild cases the symptoms may disappear again in a few weeks, but 
the objective signs in such cases are generally to be made out for a longer time. 
The disease ordinarily lasts for at least five or six weeks, and often much longer. 
Gradual recovery follows, or the onset of some new disease, usually tubercular 
{vide infra). 

Single Symptoms. — The pleuritic pain, the stitch in the side, is one of the 
most frequent subjective symptoms. We have previously mentioned that in pri- 
mary diseases of the lungs, too, as in croupous pneumonia, the stitch in the side 
is due to the accompanying pleurisy. It is remarkable that the intensity of the 
pain in no way corresponds to the apparent intensity of the disease. There is 
often the severest pain in the side when the physical examination shows almost 
nothing. On the other hand, we often hear a decided pleuritic rub without the 
patient's complaining of any special pain. Pressure on the chest-wall on the 



2S4 



DISEASES OF THE EESPIKATOEY OKGANS 



affected side is often very painful. With severe pain we may consider the possi- 
bility of an invasion of the intercostal nerves by the inflammation. We have 
never observed cases, like those described by some authors, of " crossed pleuritic 
pain " — that is, cases in which the pain is localized on the side not affected. 

Cough and Expectoration. — The cough is probably excited directly by the dis- 
ease of the pleura. We often find that the pain in the side and also the cough 
are brought on by a deep inspiration. Expectoration is entirely absent in uncom- 
plicated pleurisy, or it is scanty, and consists simply of mucus. Much expectora- 
tion always means a pulmonary complication. A large amount of purulent 
sputum is evacuated if a purulent effusion breaks into the lungs {vide supra). 

Dyspnoea. — The respiration is usually shallow, and consequently frequent, be- 
cause of the pleuritic pain. In every large effusion which prevents respiration 
in one lung the dyspnoea becomes more severe, and may, with a very extensive 
effusion, reach the highest degree of orthopncea. The stronger the patient was 
before the disease, and the more rapidly the effusion develops, the more severe, as 
a rule, is the dyspnoea. 

Fever. — Most severe pleurisies are associated with fever, but its height is not 
very great, so that it quite rarely reaches 104° (40° C). The fever has no typical 
course. In cases with an acute beginning it is sometimes quite continuous, or 
slightly remitting at first. If improvement takes place, the fever goes down in 
about two or three weeks by lysis, so that this part of the temperature-curve may 
be precisely like the period of defervescence in typhoid. 

In the more protracted cases the fever gradually becomes more remitting, vary- 
ing between 100° and 101° (38°-38.5° C), and it assumes more and more the 
form of hectic fever. The longer the evening rise of temperature lasts, the more 
we are justified in suspecting tuberculosis. In empyema we see a higher, irregu- 
lar fever, sometimes associated with severe chills. 

The pulse is constantly rapid, up to 100 and over. In all severe cases the 
strength and tension of the pulse are much diminished. Irregularity of the pulse 
is not infrequent. All these changes are probably due in great part to the pres- 
sure of the effusion on the heart and large vessels. Lichtheim has discovered 
experimentally that it is not the compression of the vessels in the compressed 
lung which lowers the arterial tension. 

General Symptoms. — Pleurisy is almost always associated with a pronounced 
general malaise, muscular weakness, and dullness. The patient is pale, and often 
markedly cyanotic in cases with much disturbance of respiration. There is 
great emaciation if the disease is of long duration. 

The appetite declines from the outset. There is often occasional vomiting, 
especially in the first period of the disease. The bowels are usually constipated. 
Many patients complain of headache. 

The condition of the urinary secretion is very important. In every pleuritic 
effusion the amount of urine is decidedly diminished so long as the effusion 
increases or remains at the same height. The daily amount is sometimes only 
eight or ten ounces (200-400 cubic centimetres). The urine is also concentrated, 
its specific gravity being about 1020-1028. Sediments of urates often fo" ^. 
This diminution of the excretion of water by the kidneys is largely the resuL of 
the diminished arterial pressure. An increase of the amount of urine is always a 
favorable symptom, often the first sign of beginning absorption of the effusion. 
If a large effusion is rapidly absorbed, the amount of urine may increase to 
eighty or a hundred ounces (2,500-3,000 cubic centimetres) daily. The urine, 
then, of course, is abnormally clear and of low specific gravity. 



PLEUKISY 



285 



Physical Signs 

1. Fibrinous Pleurisy — Pleuritis Sicca. — Simple fibrinous pleurisy sometimes 
gives rise to no physical signs at all. If it develops as a result of some pulmonary 
affection, the physical signs present are often dependent upon the latter alone. 

In many cases, however, dry pleurisy may cause marked objective signs. On 
inspection, we are struck by the impaired mobility of the affected side on respira- 
tion, which is due to the pain caused by breathing. Because of this same tender- 
ness the patient at first often lies on the sound side. Percussion gives no qualita- 
tive change of resonance as yet. With the beginning of exudation slight dullness 
appears, at first almost always in the posterior portion of the lungs. Sometimes 
the resonance becomes tympanitic as a result of retraction of the lung. We can 
almost constantly make out, especially in the back, that the lower edge of the 
lung moves less than usual on respiration. Auscultation gives a respiratory mur- 
mur that is either qualitatively unchanged or indefinite, but it is always dimin- 
ished. The peculiar pathognomonic sign of dry pleurisy, however, is the pleuritic 
friction-rub, that characteristic rubbing, grating, creaking sound, which arises 
from, the sliding of the rough pleural surfaces over each other, and is detected 
especially in the lateral portions of the thorax. We can hear it both on inspira- 
tion and on expiration. It is often jerky, one rub following another after a con- 
siderable interval. If we are sure we hear a pleuritic rub, it is direct evidence of 
the existence of a dry pleurisy, but its absence will not let us exclude pleurisy. 
The friction-sound must be absent if there are pleuritic adhesions. We can often 
feel a marked rub by laying the hand on the chest. Sometimes the patient feels 
it himself, but in other cases he has no sensation of it. We may confound a slight 
rub with fine crepitant rales. Repeated examinations before and after the 
patient has coughed usually confirm the diagnosis, since the rales are often 
changed by coughing. 

To be distinguished from the mild form of dry pleurisy just described is that 
variety in which there is an extensive and abundant fibrinous exudation, with 
scarcely any liquid. We have repeatedly seen severe cases following pneumonia, 
or even apparently primary cases, which displayed marked dullness and sense of 
resistance on percussion over the whole of one side of the chest, with diminished 
or absent respiration, and yet upon exploratory puncture only a few drops of 
serous exudation could be obtained. Evidently we had to do with the forma- 
tion of large amounts of coagulated fibrine. Attacks of this sort usually run a 
severe and tedious course, but they may, nevertheless, get well at last. 

2. Pleuritic Effusion. — Small amounts of fluid in a pleural cavity escape 
discovery. Physical signs first appear when the amount of effusion reaches eight 
or ten ounces (200-300 cubic centimetres). 

Inspection shows first the more or less marked impairment of motion on the 
affected side on respiration. If the amount of the effusion is large, there is an 
evident distention of the affected side in the lower posterior and lateral portions 
of the thorax. The intercostal spaces are flattened or even a little convex. The 
nipples and shoulder-blades are farther removed from the median line on the 
a. icted side than on the healthy side. The hypochondrium on the affected side 
is more prominent. In an extraordinarily large effusion on the left side we have 
seen and felt, in the left hypochondrium, the lower surface of the diaphragm, 
which was actually arched downward. By direct measurement in severe cases we 
can make out that the affected side is expanded several centimetres. 

With every large effusion there is marked dyspnoea and accelerated respira- 
tion. The slight excursions of the affected side on respiration are usually very 
striking, while the sound side moves so much the more. In this stage of pleurisy 
the patient often lies upon the affected side, in order to breathe with the healthy 



286 



DISEASES OE THE RESPIRATORY ORGANS 



lung with as little restraint as possible. "With large effusions complete orthopnoea 
may develop. 

The signs due to displacement of the neighboring organs, which are noticeable 
on inspection, will be mentioned below in the appropriate connection. 

Everywhere that a layer of fluid comes between the lung and the chest-wall 
there is a loss of clearness in the percussion-note. If the thickness of the layer 
of effusion is five or six centimetres, the resonance seems completely dull or flat. 
The pleuritic dullness is almost always made out first in the lower posterior por- 
tions of the thorax, more rarely in the lower lateral portions. With a slight 
effusion the height of the dullness is only a few centimetres, but, with much 
effusion, it rises higher in the back and the lateral portions of the thorax ; and on 
the right, resonance gradually grows dull anteriorly and inferiorly, above the 
liver. With very large effusions the dullness may begin in front at the second or 
third rib, or in rare cases even the whole half of the chest, front and back, may 
give a totally flat percussion-note. Pleuritic dullness is always attended with a 
marked feeling of resistance on percussion. 

With medium-sized effusions, when the dullness does not extend over the 
whole back, the upper boundary of the dullness usually forms an oblique t line, 
highest at the vertebral column and thence running obliquely downward to the 
side of the thorax. Exceptionally the line runs the other way. On the right it 
is not possible to distinguish by percussion the lower limit of the exudation from 
the liver. On the left we can often distinguish its lower limit from the tympa- 
nitic resonance of the stomach, and are thus aided in diagnosis (vide infra, dis- 
placement of organs). 

[In moderate effusion without adhesions or pneumonic complications, the line 
of flatness in the back, the patient being in the vertical position, is lowest near 
the spinal column, and rises in a curve like the letter S as it passes outward 
toward the axillary region. The experiments by Dr. Garland, of Boston, with 
reference to this point are well known. Before attempting to mark out this line 
the patient should be told to take several deep inspirations, in order to inflate the 
triangular portion of lung which dips down near the vertebraB.] 

The percussion-note above a pleuritic effusion deserves attention. The begin- 
ning of pleuritic dullness is almost always relative, gradually passing to an abso- 
lute flatness. The pulmonary resonance above the beginning of dullness is usu- 
ally tympanitic, from retraction of the lung-tissue. We find the tympanitic 
resonance beautifully distinct in large effusions in the first and second intercostal 
spaces in front. It is loud and deep, and remains unchanged with the mouth 
open — Skoda's resonance. With very large effusions, which cause an actual com- 
pression of the lung, we sometimes find, in the second intercostal space, a dull 
tympanitic resonance, which becomes higher on opening the mouth. This reso- 
nance arises from the vibrations of air in a large bronchus surrounded by com- 
pressed lung — " Williams's tracheal tone," With large effusions we sometimes 
heaT over the retracted lung, in the upper anterior intercostal spaces, a distinct 
buckram sound — the " cracked-pot sound." , 

Displacement of the neighboring organs, which is made out chiefly by percus- 
sion, forms one of the most important physical signs in pleurisy with effusion. 

In right-sided effusions the liver, especially the right lobe, is displaced down- 
ward. We find the lower border of the liver dullness extending several centi- 
metres below the ribs. In very large effusions the liver may be pushed down to 
the level of the umbilicus. The pushing of the mediastinum to the left in large 
effusions may be recognized upon percussing from the right toward the left, by 
dullness over the upper part of the sternum, reaching to or beyond the left border 
of the sternum. The displacement of the heart to the left in the majority of well- 
marked cases is associated with a displacement of the apex of the heart upward. 



PLEURISY 



287 



This is easily explained by considering the position of the heart and the direction 
of the pressure, which first acts from below. We recognize the displacement of the 
heart chiefly by the position of the apex-beat, which is seen and felt at or outside 
the left mammillary line in the fifth space, or often higher, as we have said — in 
the fourth. Percussion gives a corresponding displacement of the left boundary 
of the cardiac dullness to the left. 

In left-sided effusions the displacement of the heart to the right, which can 
usually be made out even in moderate effusions, is especially noticeable. Reso- 
nance over the lower part of the sternum is diminished, the heart's dullness 
extends to the right border of the sternum or several centimetres beyond it. In 
the most marked cases the heart is pushed to the right mammillary line. The 
displacement of the mediastinum is also to be made out over the upper part of the 
sternum, the dullness reaching to the right border of the sternum or beyond. 
The low position of the diaphragm is made out by a depression of the left, and in 
marked cases of the right, lobe of the liver. It is an especially important sign, 
however, that dullness occurs in the zone, about a hand-breadth wide, of normal 
tympanitic resonance above the left border of the ribs — the " semilunar space " 
of Traube. The normal tympanitic resonance here comes from the stomach or 
large intestine. As the diaphragm is pressed downward the pleuritic effusion 
presses on these organs. The semilunar space is therefore diminished, and finally, 
with large effusions, there is absolute dullness down to the edge of the ribs. 

Changes in dullness in pleuritic effusions may occur with a change of the 
patient's position, but they may often be absent on account of adhesions. As a 
rule the normal change in the position of the lower border of the lung corre- 
sponding with respiration is abolished. 

Auscultation always gives a diminished respiratory murmur over the pleuritic 
effusion. With a beginning effusion it may sound approximately vesicular, but 
later it becomes indefinite, harsh, and finally bronchial, if the larger bronchi re- 
main open for the respiratory current of air. The bronchial respiration sounds 
distant and low, and has the character of the sharp German ch, but in rare cases 
it also assumes a distinct amphoric tone, so that it sounds almost like a cavernous 
respiration. The respiratory murmur may finally disappear entirely over very 
large effusions. Above the upper boundary of the effusion the respiration almost 
always sounds harsh. Among the adventitious sounds we must mention the 
pleuritic friction sound, which of course can be heard only at the upper boundary 
of the effusion, where the two pleural surfaces meet. Moist rales and rhonchi 
signify a co-existing disease in the lungs. With slight effusions we often hear, 
on deep breathing, pure crepitant rales on inspiration, as the walls of the alve- 
oli and bronchioles in the atelectatic lung, which were stuck together, are torn 
apart. 

On auscultation of the voice we sometimes hear bronchophony, and sometimes 
that bleating, nasal sound known as segophony. Baccelli advanced the theory 
that auscultation of the whispered voice might be of service in diagnosticating 
the character of the effusion. With a serous effusion we can understand a whisper 
distinctly through the thorax, but not with a purulent effusion, since theoret- 
ically the cell-elements destroy the waves of resonance. This theory holds true in 
many cases, but by no means in all. 

On auscultation of the heart we notice, as a result of its displacement, an ab- 
normal extension of the region over which the heart-sounds are audible. If the 
inflammation spreads from the pleura to the outer surface of the pericardium, 
we can sometimes hear an extra-pericardial friction-rub, accompanying both the 
respiration and the action of the heart. 

The vocal fremitus is always diminished over the pleuritic effusion, and in 
marked cases is entirely absent. 



288 



DISEASES OF THE RESPIRATORY ORGAXS 



3. Absorption of the Effusion — Pleuritic Contraction. — The beginning ab- 
sorption of the effusion is usually first made evident by the percussion-note in the 
upper part of the dullness becoming clearer and sometimes tympanitic. The 
respiratory murmur is also plainer. Where it was bronchial it becomes in- 
definite and gradually vesicular again. The vocal fremitus is again to be felt. 
All these improvements take place gradually but slowly. It is usually a very long 
time before the percussion-note resumes its normal clearness. 

The changes in the form of the thorax are especially striking. Only in pleu- 
risies with slight effusion does the somewhat expanded thorax resume its old form 
without further change. After every severe pleurisy with large effusion there is, 
during its absorption, a marked contraction of the affected half of the chest. In 
cases of moderate intensity the contraction affects only the lower lateral portions 
of the thorax, in severe cases the upper and anterior portions as well. We find 
the most marked contractions in children and young persons with a yielding 
thorax. The circumference of the affected side is much less than that of the 
sound side. The ribs are pressed together and the intercostal spaces become 
very narrow. The fossae are deepened and the nipples and shoulder-blades are 
drawn nearer the vertebral column, which takes on an abnormal lateral curva- 
ture, in which its convexity is directed usually toward the affected side, but some- 
times to the sound side. Dullness and diminution of the respiratory murmur and 
vocal fremitus continue with the contraction of the pleura, but they no longer 
depend upon the presence of a fluid effusion, but are due to the pleuritic thick- 
ening. 

The process of marked contraction always lasts for months, or even longer. 
In favorable cases the contraction of the thorax may be readjusted very much 
later, often after years. The thickening is absorbed, and the lungs and thorax 
gradually expand, but in other cases there are extensive adhesions between the 
pleural surfaces, especially over the lower lobe, which result in a permanent dis- 
turbance of respiration. In almost all cases of pleurisy with contractions there 
arises a vicarious emphysema in the lung on the sound side. 

Complications. — Peculiar complications of pleurisy are rare. Where such 
occur they are due either to the primary disease which has led to the pleurisy, or 
to the simultaneous action of the same cause of disease, such as tuberculosis. 
Hence it happens that we speak of the frequent " complication " of pleurisy with 
chronic bronchitis or with tuberculosis of the lungs or other organs. It is impor- 
tant to bear in mind that, by a direct advance of the inflammation, the pleurisy 
may also invade the pericardium, and rarely the peritoneum, through the dia- 
phragm ; but we see this extension of the process almost solely in tubercular and 
purulent pleurisies. We must mention, finally, that we have seen several cases 
with a large serous effusion, in which an acute haemorrhagic nephritis occurred. 
For the paralysis of the arm on the corresponding side observed in some cases of 
empyema, compare what is said in regard to reflex paralyses on page 833. 

Various Forms of Pleurisy 1 

1. Primary Rheumatic Pleurisy. — As we have already pointed out, when con- 
sidering the aetiology of pleurisy, clinical observations have lately led to the 
belief that some of the cases of acute primary pleurisy are due to the same cause 
as acute articular rheumatism (which see). Although there are as yet no suffi- 
cient number of decisive bacteriological investigations, we are, nevertheless, 
strongly inclined, from our present experience, to acknowledge the correctness of 
this view, even if we do not estimate the frequency of rheumatic pleurisy nearly 
so high, as, e. g., does Fiedler, on the ground of his observations in Dresden. 

Rheumatic pleurisy usually develops rather suddenly in persons previously 
healthy. Sometimes it is preceded by mild rheumatic pains in the muscles or 



PLEURISY 



289 



some of the joints. The local discomforts, such as pain in the side, are often 
very severe, the fever is moderately high, though rarely over 104° (40° C.) ; 
and as the case progresses such rheumatic symptoms as swelling of the joints and 
endocarditis may associate themselves with the pleurisy, and confirm the diag- 
nosis. In general, however, the course of the disease is favorable. The fever 
lasts, as a rule, only a week or two, and even when there is a large exudation it 
finally undergoes complete absorption with recovery. 

2. Tubercular Pleurisy. — In an serological sense we must declare the larger 
part of the ordinary "pleuritic effusions," which clinically seem primary, to be 
tubercular. The further course of the cases, if we can watch them long enough, 
almost always permits us finally to recognize the tubercular nature of the dis- 
ease ; yet we can not say that some other tubercular disease, particularly phthisis, 
is always the immediate sequel of the pleurisy. 

In a comparatively small number of cases do the symptoms of acute tubercu- 
losis, or more frequently of chronic phthisis, appear as an immediate result of the 
pleurisy, which at that time is usually still present or in the contracting stage. 
The objective changes of phthisis are evident' either in the apex or in the lower 
lobe of the affected side. The fever continues, the pulmonary affection advances, 
the other lung is also attacked, and the disease takes a fatal course under the 
type of an ordinary phthisis, now more acute and now more chronic. 

In other cases acute tubercular affections arise sooner or later as a result 
of the pleurisy — tubercular meningitis, or general miliary tuberculosis. In other 
cases still the disease develops under the form of tuberculosis of the serous mem- 
branes, to which we will return again in the description of tubercular pericar- 
ditis and tubercular peritonitis. We often have to do with a double pleurisy 
with no evident complication in the lungs. In varying succession are added the 
symptoms of chronic tubercular peritonitis, with pain, swelling, and effusion of 
fluid into the abdomen, or the symptoms of tubercular pericarditis. Death finally 
ensues with persistent hectic fever and increasing general emaciation and weak- 
ness. The whole affection usually runs a chronic course, lasts for months, and 
often shows marked remissions and temporary improvements. 

In very many instances, on the other hand, the pleuritic effusion has through- 
out an apparently favorable course. After some weeks the fever ceases, the effu- 
sion is absorbed, the patient gets up, and is finally discharged as nearly well. 
Of course, some dullness and retarded motion often remain in the affected side, 
but even these may gradually disappear. These cases, too, very often turn out 
in the end to be tubercular. After a longer or shorter period of apparent health, 
sometimes after the lapse of years, a " new " disease appears — that is, either a 
return of the pleurisy, a pleurisy on the other side, or some other acute or chronic 
tubercular affection. In such cases, too, we must look upon the former pleurisy, in 
an serological sense, as tubercular. It is not impossible, however, for even a tuber- 
cular pleurisy to recover, and for the recovery to be permanent, if no other organ 
is at the same time affected by tuberculosis, especially if the lungs remain intact. 

Finally we must mention the cases in which a pleuritic effusion develops sec- 
ondarily to an already pronounced phthisis. Here too we almost always have to 
do with a tubercular pleurisy. 

The anatomical changes in tubercular pleurisy consist in the ordinary signs 
of inflammation, and also the presence of the specific nodules of tubercle. The 
number of tubercles differs very much in different cases. The pleura is in some 
cases completely studded with miliary nodules, and in others we find the tuber- 
cles, at least with the naked eye, only in single spots. The effusion is usually of 
a sero-fibrinous character. Sometimes it is hsemorrhagic, as the majority of cases 
of apparently primary " hsemorrhagic pleurisy " are generally of a tubercular 
nature. Empyema also (vide infra) occurs not infrequently in association with 
19 



290 



DISEASES OF THE RESPIRATORY ORGANS 



tuberculosis; and finally, in a few cases the exudation has been of a peculiar 
milky character, and has contained numerous oil-globules, probably originating 
from fatty-degenerated and disintegrated leucocytes and endothelium. 

3. Purulent Pleurisy — Empyema. — A purulent exudation is developed in the 
pleura when the inflammation of that organ is due to a specific cause which 
excites suppuration. So far as is yet known, the streptococcus pyogenes seems 
to be the most frequent factor in producing empyema. It is found in the pus 
of empyema, due to such causes as external injury, caries of the ribs, pulmonary 
tuberculosis, pneumonia, and pysemia. Less often empyema is excited by staphy- 
lococci. This is almost always a rather favorable form of the disease. Likewise 
comparatively benign is meta-pneumonic empyema, which in most instances is 
caused by the pneumococcus. The empyema of tuberculosis is, as has been 
already pointed out, in most cases devoid of bacteria (A. Frankel and others), 
and here we may have to do with the formation of chemical poisons capable of 
exciting suppuration. 

Empyema usually causes severe symptoms. The fever is higher than in the 
other forms of pleurisy, but it is irregularly intermittent, and is often associated 
with chills. There are severe general symptoms besides the fever, such as great 
languor, headache, a dry tongue, and a rapid pulse. We sometimes notice a slight 
oedema of the chest-wall on the affected side. Otherwise the local symptoms and 
disturbances are, of course, the same as in the other forms of pleurisy. If the 
pus is not evacuated artificially, the empyema may finally break externally or into 
the lungs (vide supra). In the latter case a very large expectoration of pus sud- 
denly occurs, and is usually followed by pneumothorax. 

Diagnosis. — Our chief attention in regard to diagnosis is directed to the dis- 
tinction between pleurisy and acute or chronic pneumonia, which is not very easy 
in all cases. We will briefly contrast the distinctive features as made out on 
physical examination. 

Inspection. — A marked distention of the affected side points to effusion; it 
does not occur in pneumonia. 

Percussion. — The dullness in pleurisy is complete, and the feeling of resistance 
on percussion is very marked; in pneumonia, however, the dullness is rarely so 
marked, and there is often a tympanitic sound. The discovery by percussion of 
signs of displacement of the neighboring organs is of especial weight, as these 
signs are always absent in uncomplicated pneumonia, while with few exceptions 
they can be easily demonstrated in every case of pleurisy when the exudation is 
at all considerable. 

Auscultation. — Diminished or suppressed respiratory murmur points to pleu- 
risy, loud bronchial breathing and rales to pneumonia; but we must not forget 
that in pneumonia auscultation may give the same signs as in pleurisy, if a 
bronchus is plugged. 

Vocal Fremitus. — Marked vocal fremitus over dullness is direct evidence of 
pneumonia, diminished or absent vocal fremitus of pleurisy; but the vocal fremi- 
tus may also be diminished in pneumonia if a bronchus is plugged. 

Besides the physical signs, other phenomena to be observed are the mode of 
commencement, the course of the disease, the fever, the expectoration, and the 
appearance of herpes. The most reliable means of deciding in all doubtful cases 
is exploratory puncture, although even then we may of course be left in doubt 
whether an infiltration of the corresponding portion of the lung may not exist, in 
addition to pleurisy. If the exudation is largely fibrinous, or if there is an 
abundant new growth of inflammatory connective tissue, the results of aspira- 
tion may be negative. Hence, in doubtful cases we should always make re- 
peated trials. 

If we have diagnosticated a pleuritic effusion, the next question is always as 



PLEURISY 



291 



to the character of the effusion, because the prognosis and treatment are to a large 
degree dependent upon this. Although certain well-known ^etiological circum- 
stances, and the severity of the fever and the general symptoms, often permit us 
to suspect the nature of the effusion, whether serous or purulent, the only certain 
information comes from an exploratory puncture with a hypodermic syringe. 
If the syringe is carefully disinfected, and the operation is cautiously conducted, 
this procedure is entirely devoid of danger, and we must urgently advise, its 
employment in all doubtful cases in order to settle the diagnosis. It is indeed of 
practical importance to know that there is a likelihood in empyema of obtaining 
no fluid by means of exploratory puncture (vide supra), even when, upon incision, 
pus is found. We have had this experience repeatedly. In doubtful and severe 
cases in which there is suspicion of empyema, it is therefore decidedly advisable, 
when life is threatened, to make an incision of the pleura, Besides a macro- 
scopic inspection, a careful microscopic examination of the fluid withdrawn is 
sometimes of importance. Besides the ordinary constituents — red and white 
blood-corpuscles, endothelial cells, and cholesterine crystals — we may sometimes 
find something of special diagnostic significance, such as bacteria in septic pleu- 
risy, carcinoma-cells in cancerous pleurisy, etc. 

We can not always judge from the beginning whether a pleurisy is tuber- 
cular or not; but we should never forget, as has already been affirmed, that in 
every case of pleurisy, even if it is apparently primary, there is a strong sus- 
picion of tuberculosis. We must observe in particular the general habit and 
the nutrition of the patient, and inquire into the hereditary predisposition and 
any previous illnesses. In the further course of the disease persistent hectic 
fever, slowly increasing emaciation and pallor, fresh relapses, and the onset of 
pulmonary symptoms, point to the tubercular character of the pleurisy. Every 
double pleurisy, and every pleurisy associated with pericardial symptoms, leads 
us most decidedly to suspect tuberculosis. A hemorrhagic effusion, as we have 
said, points strongly to tuberculosis. Tubercle bacilli are usually not present in 
the exudation of tuberculous pleurisy, because the tubercular nodules of the 
serous membrane scarcely ever ulcerate. On the other hand, we have often been 
able to demonstrate tubercle bacilli in the scanty expectoration of such patients, 
even when there were scarcely any pulmonary symptoms. The peculiarities of 
rheumatic pleurisy have been already detailed. 

Prognosis. — The prognosis, as regards the immediate danger of the disease, 
depends entirely upon the severity of the symptoms, and especially upon the 
dyspnoea. The prognosis, as regards the further course of the disease, depends 
chiefly upon the nature of the pleurisy. Many secondary and also many appar- 
ently primary pleurisies, although extensive, recover completely and permanently 
after weeks or months. Unfortunately, we only too frequently have to give a 
doubtful or an unfavorable prognosis, especially if the tubercular nature of the 
pleurisy be probable or certain. The prognosis of empyema depends partly upon 
the underlying disease, but especially upon judicious and timely operative inter- 
ference. In benign cases of empyema recovery is usually complete in a few weeks 
after operation, but sometimes months are required. The possibilities of a spon- 
taneous rupture of empyema, internally or externally, have been mentioned above. 
With incomplete healing, which leaves a pleural fistula, we must fear the appear- 
ance of general amyloid disease in various organs. 

In rare instances with large effusions sudden death occurs, an event which can 
not always be satisfactorily explained. Probably there are different factors in 
different cases, such as pulmonary embolism, cerebral embolism, sudden cerebral 
anaemia, weakness of the heart, or the onset of pulmonary oedema. 

Treatment. — In the beginning of the disease the treatment is purely symp- 
tomatic. We try to alleviate the patient's symptoms, the pain and dyspnoea, by 



292 



DISEASES OF THE RESPIRATORY ORGANS 



local applications, especially by mustard plasters, warm poultices, which are 
usually more grateful than cold applications, sometimes, too, by dry cups, also by 
embrocations with chloroform liniment, and, with severe symptoms, by mor- 
phine internally or subcutaneously. Unfortunately, we have but few remedies to 
check the inflammatory process in the pleura. If an ice-bag is well borne, it may 
be of service. The efficacy of the much-used painting with iodine is doubtful, but 
it may always be tried if there is a severe pleuritic pain. Perhaps more efficient 
is the application of iodized vasogen, or of iodoform ointment (1 to 15). 

If a large serous effusion has formed, it is the universal custom to prescribe 
diuretics. The idea is to cause, or at any rate promote, the absorption of the 
exudation by increasing the excretion of urine. It is, however, very difficult to 
obtain any real proof of the usefulness of diuretics in pleurisy with effusion. 
They often are of no use whatever, but again, the absorption of the fluid may 
follow the administration of a diuretic, so that it does not seem impossible that 
the latter has a therapeutic influence. With regard to a choice of the diuretics to 
be employed we would name, first, salicylate of sodium, 75 to 120 grains (grammes 
5 to 8) a day, because a specific influence has been ascribed to this drug in pleu- 
risy. This applies particularly to cases of supposed rheumatic origin (vide 
supra). Many good observers assert that primary pleuritic exudations often run 
a remarkably rapid and favorable course, when treated with salicylate of sodium. 
Moreover, the drug has a direct diuretic effect. Besides this, the acetates of potas- 
sium and of sodium are frequently prescribed, as well as squills, and, of late, diu- 
retine (sodio-salicylate of theobromine), given in doses of thirty grains (grammes 
2) two or three times a day. We have sometimes found this remedy apparently 
very efficient. If there are signs of cardiac weakness and diminished arterial 
tension, digitalis must be prescribed, alone or with a diuretic. Other internal 
remedies are at present seldom employed in pleurisy with effusion. The influence 
of iodide of potassium as an " absorbent " is extremely doubtful. Drastic purga- 
tives and such diaphoretic remedies as hot packs and pilocarpine usually affect 
the general condition unfavorably, and are of little use. Probably there are to- 
day few advocates of the so-called Schroth method of treatment, according to 
which the amount of fluid ingested is reduced to a minimum, so as to promote the 
absorption of the exudation. In many cases the operative treatment of pleu- 
risy (introduced by Trousseau) — the evacuation of the effusion by puncture — is 
of the greatest importance. Many cases of pleurisy with effusion run a favor- 
able course without it, and we consider it at least superfluous to puncture every 
effusion without sufficient grounds, but puncture is often one of the most service- 
able therapeutic influences at our command. The first and most important indi- 
cation for puncture is present when the effusion becomes so large as to be directly 
dangerous to life. As soon as the patient's dyspnoea reaches a dangerous degree, 
and the cyanosis becomes marked and the pulse weaker, a puncture must be 
made as a direct vital indication. When the exudation is of considerable size 
there may be a very sudden aggravation of the symptoms, so that in such cases 
one should not wait too long. It is much better to puncture too early than too 
late! Trousseau urged that tapping should invariably be performed when the 
dullness caused by the exudation involves not only the back, but also the whole 
or nearly all of the anterior wall of the thorax, a rule which the author almost 
always follows. The benefit of such a puncture is often pronounced. The sec- 
ond indication is a too protracted absorption of the effusion. Puncture is indi- 
cated if the effusion does not disappear after an apparent remission of the in- 
flammatory symptoms, especially after the fever has gone. We often see the 
further absorption stimulated by such a puncture. It has been said that, if pos- 
sible, tapping should be delayed until the fever has ceased, but to us this does 
not seem at all necessary. When the exudation was large, or the absorption was 



PLEURISY 



293 



delayed, we have repeatedly aspirated even when the patient was still feverish, 
and have not infrequently found that the fever diminished remarkably upon the 
removal of the exudation (see the temperature chart, Fig. 37). 



40.= 



39. 




mwm mmm 



Fig. 37.— Temperature-curve in pleurisy with effusion before and after tapping-. (Erlangen medical 

clinique.) 

[There is considerable danger in delaying interference with a large effusion, 
especially if it has come on pretty rapidly, however comfortable the patient may 
be. The liability to sudden and fatal dyspnoea under these circumstances is now 
well recognized.] 

As regards the performance of the puncture, we can not here go into all the 
numerous methods and forms of apparatus proposed. The distinctions are imma- 
terial. The simpler the method, the easier it is to perform, and hence the better 
it is. 

Every puncture must be preceded by an exploratory puncture in order to settle 
the diagnosis as to the presence and character of the exudation. A medium-sized 
trocar with a lateral opening, to which a rubber catheter can be fastened, serves to 
evacuate the fluid. Billroth's and Frantzel's trocars are useful. Aspiration 
can be performed still more conveniently with a hollow needle, and best of all, 
according to our experience, with that proposed by Eiedler, which is now exclu- 
sively employed in the author's wards, because the point of this needle is guarded 
so that it can not scratch the tissues, and also, if it becomes plugged with clots of 
fibrine, these can be pushed out." The instruments and the chest-wall at the 
point of puncture must be carefully disinfected. We usually choose a point for 
puncture, somewhere about the sixth intercostal space, in the middle or poste- 
rior axillary line. The patient sits up in bed, but is held and supported by 
another person, when it is possible. Before and during the puncture he takes 
a little strong wine, strophanthus, or similar stimulant. The pain of the opera- 
tion may be mitigated by previously injecting morphine [or still better, by caus- 
ing local ansesthesia with a half- to one-per-cent. solution of cocaine]. In the 
overwhelming majority of cases, and especially if the exudation is abundant, we 
can remove a large part of the fluid by simple puncture with siphonage. With 
few exceptions, the pleuritic exudation is under a positive pressure of 10 to 25 
millimetres of mercury. The evacuating tube of the trocar must be previously 
filled with carbolized water and conducted under a layer of the same into the 
vessel prepared to receive the effusion. The evacuation of the effusion should 
always be slow and gradual. !Many physicians advise stopping when 1,500 
cubic centimetres have been removed, but if the fluid is allowed to escape slowly 
and everything is going well, this quantity may often be exceeded with im- 

* r Fiedler"s instrument consists essentially of a sharp hollow needle, with an outer jacket, which can 
be moved so as to cover the sharp point after the chest-wall has been penetrated. If the lumen is 
stopped up. a pointed steel wire thrust directly through the attached rubber tubing displaces the 
obstruction. — Tbau&J 



294 



DISEASES OF THE EESPIEATOEY OBGAXS 



punity in the case of large exudations. While, as we have said, in most in- 
stances the exudation may be satisfactorily removed by simple puncture and 
siphonage, it will sometimes prove necessary to employ aspiration. Hence some 
physicians invariably do so, and to this there is no objection, even if it is unne- 
cessary. The forms of apparatus most used for this are those invented by 
Dieulafoy and Potain. In puncture with aspiration we proceed more slowly and 
cautiously. 

[The necessity for two punctures — one exploratory, the other distinctly opera- 
tive — does not seem clear. The two can be perfectly combined, a fair-sized trocar 
or needle being as easy of introduction and producing really no more pain than a 
veiy fine one, and being more sure to give results on which reliance can be placed. 
An ordinary Davidson's syringe makes a very satisfactory pump and can always 
be obtained.J . &w 

Unpleasant, incidents, which may cause a cessation of the process are rare. 
If the patient complains of dizziness or f aintness we must cease, or at any rate, 
pause. Usually everything goes well until the needle begins to rub against the 
pleura : then there is pain and generally a violent cough. It is well, then, to 
remove the needle at once. The cough can usually be promptly quieted by rest 
and a little morphine, but sometimes after aspiration there will develop a sort of 
pulmonary oedema, with the expectoration of a large amount of frothy serous 
sputum {expectoration albumineuse). This is perhaps due to the increased per- 
meability of the vascular wall, or to feebleness of the left ventricle. 

When the process is over, we close the little opening with a bit of sticking- 
plaster or with iodoform collodion. A regular surgical dressing is scarcely ever 
necessary. 

If the exploratory puncture has shown a purulent effusion, we can first evacu- 
ate the pus by puncture, if the vital indication exists; but a permanent cure 
from tapping is exceptional. The pus almost always reappears. Empyema is like 
an abscess, which can not be cured until a permanent, free exit for the pus has 
been provided. We must, therefore, not only remove the pus, but institute 
drainage of the pleural cavity. The best method, and the one which is almost 
exclusively practiced in the surgical wards in Erlangen, is by incision of the 
pleural cavity, preceded by resection of a portion of a rib for the purpose of com- 
pletely emptying out the pus, and obtaining a better final result. This compara- 
tively simple method gives results so good and so entirely satisfactory that, to be 
frank, we can not understand why there has been so much discussion over the 
treatment of empyema. We are perfectly willing to allow that good results are 
likewise obtained with other methods, and in particular with the drainage by 
siphon action, advocated by Biilau. Yet there is not, in our opinion, any satis- 
factory ground for abandoning the ordinary surgical principles, relating- to the 
treatment of internal suppuration, in the case of empyema. With regard to the 
minutiae of the operation, we must refer to text-books on surgery. 

In treating the chronic, contracted pleurisies with thickening, but without 
fluid effusion, methodical respiratory efforts, " lung-gymnastics,'"' are of use. Be- 
sides these we should strengthen the general condition as much as possible. We 
should advise the patient to breathe deeply, and prescribe cold sponging of the 
chest daily. Inspiration of compressed air by means of a pneumatic apparatus is 
often accompanied by good results. Well-to-do patients, who have had a severe 
pleurisy, should be sent to a suitable climatic health-resort. 



PERIPLEURITIS 



295 



CHAPTER II 
PERIPLEURITIS 

Under the name of " peripleuritis " Wunderlich was the first to describe a rare 
form of disease, which consists of an inflammation of the connective tissue 
between the costal pleura and the ribs, and which terminates in the formation of 
an abscess. Similar cases have since been repeatedly observed, and all were char- 
acterized by the lack of any discoverable aetiology. There is neither a previous 
injury, nor a primary disease of the ribs or the pleura. Nevertheless the cause 
must be sought in an invasion of micrococci, which excite the suppuration. A 
knowledge of the particulars, however, can only be gained from future investiga- 
tions. They will determine whether peripleuritis can be regarded as an inde- 
pendent disease or not. 

The disease occurs chiefly in men. It usually begins suddenly with a chill, 
and runs its course with quite a high fever. In pronounced cases the local symp- 
toms have the greatest similarity to those of an empyema, but the greater protru- 
sion of the chest-wall is striking. The ribs are crowded apart by the abscess, and 
there is often spontaneous rupture externally, scarcely ever into the pleura. Per- 
cussion gives no symptoms of displacement of the neighboring organs, a distin- 
guishing point from empyema. It is of diagnostic significance that we can often 
discover normal lung-tissue containing air below the abscess. The mobility of the 
lower border of the lung is also usually retained, contrary to what is the case in 
empyema. Another important sign was first brought to notice by Bartels: the 
wall of the abscess relaxes on inspiration and becomes tense on expiration. We 
may also mention that acute nephritis has often been observed among the com- 
plications. 

Erom these points we may be able to make the diagnosis during life, at least in 
many cases. The prognosis is quite unfavorable, but recovery does occur. The 
treatment can be only operative, and it is quite analogous to that for empyema. 



CHAPTER III 

PNEUMOTHORAX 

(Pyopneumothorax. Hydro-'pneumothorax) 

etiology. — Pneumothorax — that is, a collection of air or gas in the pleural 
cavity — arises, in an overwhelming majority of cases, from the penetration of air 
into the pleural cavity through an opening in the pleura. The opening may be 
in the external chest-wall from a penetrating wound of the chest or an empyema 
operation, or it may be in the pulmonary pleura. Pneumothorax is by far most 
frequently associated with phthisis, when a cavity lying beneath the pulmonary 
pleura perforates into the pleural cavity. This is more apt to happen in compara- 
tively acute phthisis than in very chronic forms, because the extensive adhesions 
and contractions in the latter hinder its development. It usually appears in 
quite far advanced cases, but it may sometimes arise with but slight changes in 
the lung. 

Pulmonary gangrene or abscess, as well as phthisis, may cause pneumothorax 
by perforation into the pleural cavity. It may also arise from the rupture of an 
empyema into the lung. In some cases a perforation of the oesophagus or stom- 



296 



DISEASES OF THE EES PIE AT OE Y OEGAXS 



ach into the pleura, as in gastric ulcer, has been observed, with the formation of 
pneumothorax. 

The development of this condition from severe injuries, as from laceration 
of the previously healthy lung, without injury to the chest-wall, is rare. Forced 
respiratory movements, associated with physical exertion, seem especially capable 
of exciting such a process. We have ourselves seen pneumothorax develop sud- 
denly in a previously healthy woman while hanging out her washing, and another 
time in a young man during very labored rowing. Both cases recovered rapidly 
and completely. 

All the last-named causes, however, are far less important than pulmonary 
tuberculosis. We should mention that in phthisis, too, there is sometimes a defi- 
nite exciting cause — severe coughing, vomiting, or muscular exertion — which 
may favor the development of the pneumothorax. 

Many authors maintain that, by decomposition of a putrid pleuritic effusion, 
gas may be produced, and thus we may have pneumothorax ; but such an event is 
extremely rare, if it ever happens. 

Pathological Anatomy. — On opening the pleural cavity a part of the air usu- 
ally rushes out, sometimes with an audible noise. We then look into a large 
cavity filled with air, and find, in total pneumothorax, the lung completely re^ 
tracted and lying compressed against the vertebral column. If, however, the air 
fills only a part of the pleural cavity, as a result of extensive adhesions of the 
pleura?, we speak of a circumscribed or sacculated pneumothorax. The amount 
of air contained in the pleural cavity may reach 2,000 cubic centimetres. The 
pressure which it is under is almost always positive — on an average five or ten 
centimetres of water. 

In the cases of pneumothorax arising from perforation of the pulmonary 
pleura we can usually make out the point of perforation in the lungs. This is 
more frequently situated in the upper lobe than in the lower. Sometimes it is 
already grown over or is covered by a layer of fibrine, and can no longer be found. 
The opening is usually quite small, but it may reach the size of a ten-cent piece. 
Left-sided pneumothorax seems to be somewhat more frequent than right-sided. 

The pleura itself is only rarely normal. Usually agents of inflammation have 
entered it with the air, and hence it is found in a state of inflammation. A part 
of the cavity is then filled with effusion. This is usually wholly purulent — pyo- 
pneumothorax — or sero-purulent, but it may even be serous or sero-nbrinous — 
sero-pneumothorax, or hydro-pneumothorax. 

The neighboring organs, especially the heart and liver, are found pushed out 
of their normal position, as in large pleuritic effusions. 

Symptoms and Course. — The onset of pneumothorax (we speak in what fol- 
lows especially of pneumothorax in connection with pulmonary tuberculosis) is 
quite often made known by a sudden pain, usually associated with an increase of 
the dyspnoea and of the general symptoms. There is sometimes collapse. The 
temperature sinks below normal, the pulse rises to 140 and over. The patient 
looks pale and cyanotic. He usually sits upright or is in a half -sitting position 
in bed, either more on the affected side, in order to use the normal lung as much 
as possible for breathing, or more on the sound side on account of the tenderness. 
If the pneumothorax has come on as a result of the rupture of an empyema into 
the lungs, there is at the same time a very abundant expectoration of pus. 

Although in many cases the symptoms mentioned lead to a suspicion of pneu- 
mothorax, yet a positive diagnosis can be made only after a physical exami- 
nation. 

Inspection gives a very marked distention of the affected side. The inter- 
costal spaces are stretched out, or even protruded. In some cases, as we have our- 
selves noticed, there is a marked elastic " air-cushion feeling " on palpating the 



PNEUMOTHORAX 



297 



intercostal spaces. On respiration, the affected side is almost entirely motionless, 
while the excursions of the other side are the more marked. The displacement of 
the heart is often evident from the risible displacement of the apex-beat. 

Percussion gives over the pneumothorax a remarkably loud, full note, abnor- 
mally deep, but usually not tympanitic, on account of the tension of the walls. 
It is especially important to note that this resonance extends beyond the normal 
limits of the lung on the right down to the seventh or eighth rib, and on the 
left to the fifth or sixth rib, and sometimes even to the edge of the thorax. The 
lower limit of this abnormally loud percussion resonance shows no change of 
position with respiration. 

The displacement of the neighboring organs can also be made out by percus- 
sion. With right-sided pneumothorax we find the lower border of the liver dull- 
ness abnormally low, and the left border of the cardiac dullness pushed over to 
the anterior axillary line. In left-sided pneumothorax the cardiac dullness is 
usually entirely absent from its normal place, and is found instead to the right of 
the sternum. The left lobe of the liver is pressed downward, and in the " semilu- 
nar space " we find, instead of the normal tympanitic resonance, the same deep, 
loud, and usually non-tympanitic note as in the upper parts of the thorax. 

Upon auscultation we are struck by the entire absence of respiratory murmur. 
This is in special contrast to the clear resonance on percussion. In other cases, 
however, we hear a number of metallic sounds, at least in many places and at 
many times, which are very characteristic of pneumothorax. Uirst among these 
is amphoric, metallic respiration. This arises in open pneumothorax (vide 
intra) from the direct passe ge of the air in and out. but in all other cases it is the 
ordinary respiratory murmur, which has acquired a metallic timbre from reso- 
nance in the pneumothorax. In an analogous way arise the metallic-sounding 
rales [" metallic tinkling "'], and the metallic resonance of the cough and voice. 
Heubner has devised a particularly beautiful and practically important method 
for demonstrating the metallic sound in pneumothorax. If we strike lightly on 
a pleximeter with a little rod, usually the handle of a percussion hammer, while 
we auscult near it — '"'rod percussion'" — we very often hear quite a distinct high 
metallic sound. 

The vocal fremitus over a pneumothorax is usually diminished, but it may be 
felt in spite of quite a large collection of air. 

A number of special physical signs are found if a purulent or serous effusion 
be added to the pneumothorax. In the first place, the resonance is thereby ren- 
dered dull, to a greater or less extent, in the lower parts of the chest. The bound- 
aries of the fluid by percussion show a very evident change with the patient's 
change of position, because the fluid in pneumothorax can move easily in all 
directions. Inasmuch as the shape of the remaining air space must change cor- 
respondingly, there is not infrequently a change in the pitch of any metallic 
sounds which may be produced, whether by percussion or respiration, varying 
with the posture of the patient (Biermer's change of note). In many cases, if 
the ear is applied to the chest-wall there is heard, on every motion of the fluid, 
produced, e. g., by gently shaking the patient, a metallic gurgling sound, so- 
called Hippocratic succussion. 

Forms of Pneumothorax. — According to the condition of the perforation dur- 
ing life, we distinguish three kinds of pneumothorax (Weil). We speak of an 
" open pneumothorax,''* if the point of perforation remains open, so that the air 
on respiration constantly passes in and out of the pleural cavity. If the perfora- 
tion is completely closed, we have a " closed pneumothorax.'' The third and most 
frequent form is the "valvular pneumothorax," in which air enters the pleural 
cavity at each inspiration, but on expiration there is a valve-like closure of the 
perforation, and thus the air can not escape again; but as soon as the pressure 



298 



DISEASES OF THE RESPIRATORY ORGANS 



in the pleural cavity increases so that no more air can enter it on inspiration, 
the valvular pneumothorax becomes closed. In open pneumothorax the pressure 
in the pleural cavity must be the same as the atmospheric pressure. A positive 
pressure in the pleural cavity can exist only in a closed or a valvular pneumo- 
thorax. 

A clinical diagnosis of the form of pneumothorax is not always possible, and 
has usually no great practical importance. The very loud, metallic, amphoric 
respiratory murmur, which may be heard in open pneumothorax, must be men- 
tioned, and Wintrich's change of pitch (see page 243) can sometimes be heard 
in this form. It is worthy of mention that symptoms of displacement of the 
neighboring organs must also arise in open pneumothorax. The predominant 
atmospheric pressure here is positive in contrast to the negative pressure in the 
other pleural cavity, and to the normal negative pressure which previously 
acted on the upper surface of the diaphragm. A very marked protrusion of the 
affected side, and great displacement of the heart and liver, however, speak most 
strongly against an open pneumothorax. Some authors have tried to find a point 
of distinction for the different forms of pneumothorax in the composition of the 
gas in the pleural cavity, but the results of chemical analysis are still contradic- 
tory. According to Ewald, we find in open pneumothorax not over five per cent, 
of carbonic acid and about twelve to eighteen per cent, of oxygen; in closed pneu- 
mothorax, however, fifteen to twenty per cent, of carbonic acid and ten per cent, 
at most of oxygen. If in an open pyo-pneumothorax or hydro-pneumothorax the 
point of perforation lies below the level of the fluid, there sometimes arise on 
every inspiration metallic sounds, since the bubbles of air drawn in rise and come 
up through the fluid — " the water-pipe sound," " metallic tinkling." A peculiar 
sipping and short snapping sound on inspiration, heard by us in one case, seems to 
point directly to the existence of a valvular pneumothorax. 

Course of the Disease. — In many cases the occurrence of pneumothorax causes 
such a high degree of respiratory disturbance that death ensues in a few hours or 
days. In other cases the patient improves, and may feel quite well for a long time 
in spite of the condition. We have ourselves frequently observed patients who 
passed the entire day out of bed with scarcely any inconvenience. Usually, how- 
ever, the disease which gives rise to the pneumothorax, most often pulmonary 
tuberculosis, leads in a shorter or longer time to death. Sometimes, again, the 
patient recovers. This almost always occurs in those rare cases above mentioned, 
when a healthy lung has been torn, but sometimes, also, in cases of pulmonary 
tuberculosis. The healing takes place in this way, that the air is first replaced by 
a fluid effusion, and then the latter is gradually absorbed, but the air may also be 
directly absorbed in whole or in part. It depends upon the origin of the lesion, 
then, and upon the intensity of the underlying disease, whether the recovery is 
permanent or not. 

Diagnosis. — The diagnosis of pneumothorax is usually easy with careful ex- 
amination, but the symptoms may sometimes be of so little prominence as to 
excuse overlooking it. It is very difficult and often quite impossible to make a 
differential diagnosis between very large cavities and a saccular pneumothorax, 
since both conditions must have in part precisely the same symptoms. We may 
mention as the chief points in distinction : A cavity is apt to be situated in the 
apex, pneumothorax in the lower part of the thorax ; over a cavity the chest-wall 
is often sunken in, over pneumothorax it is prominent ; the vocal fremitus is usu- 
ally marked over a cavity, weak over pneumothorax. Signs of the displacement 
of organs point to pneumothorax, as does distinct succussion, while a metallic 
respiratory sound and metallic resonance on rod percussion may also be heard 
over large cavities with smooth walls. Besides the above signs, we should also 
carefully regard the general course of the disease. On careful questioning we 



HYDEOTHOEAX. H^MATOTHOEAX 



299 



shall almost always find that the severe symptoms depending npon the develop- 
ment of a pneumothorax, set in with more or less suddenness. 

Treatment. — Whenever pneumothorax has developed we must seek to obtain 
perfect quiet for the patient, as well as diminution of his sufferings, by means of 
morphine given subcutaneously or internally. The results of the administration 
of this drug, in a sufficient though careful dosage, is often very satisfactory. 
We must also stimulate cardiac activity, if it is impaired, by means of stro- 
phantus or camphor. It is exceptional to find operative interference necessary 
because of the danger to life in the first days of the attack; and even later on we 
should usually wait to see how much spontaneous improvement of the condition 
may take place. If the symptoms remain severe and the displacement of organs 
is great, we should try to remove by aspiration as much air as possible from the 
pleural cavity. Likewise if there is an abundant exudation it is always useful 
to puncture and remove the fluid, repeating the operation if necessary. If the 
exudation is purulent, the treatment is precisely the same as for empyema, ex- 
cept that in hopeless cases of far-advanced tuberculosis we may limit our efforts 
to purely symptomatic treatment, or to the simple evacuation of the pus by 
puncture. 



CHAP TEE IV 
HYDEOTHOEAX. HJEMATOTHOBAX 

1. Hydrothorax. — We term the occurrence of a serous transudation into the 
pleural cavity, independent of an inflammation of the pleura, hydrothorax, or 
thoracic dropsy. ' The cause of hydrothorax is in rare cases a local hindrance to 
the outflow of venous blood or lymph from the thorax, as in compression of the 
veins or of the thoracic duct by tumors; but in the great majority of cases the 
hydrothorax is part of a general dropsy, occurring especially in cardiac or renal 
disease. Hydrothorax is often first developed after marked oedema of the sub- 
cutaneous cellular tissue and ascites, but it may sometimes be one of the first 
symptoms of dropsy, particularly in renal cases. It is usually bilateral, but it is 
often unilateral, or at least much greater on one side than on the other. The 
pleura itself is normal or else cedematous. We often find it traversed with a net- 
work of dilated lymphatics. The serous fluid in hydrothorax is distinguished 
from an inflammatory serous effusion by the smaller amount of albumen in it, 
and a correspondingly low specific gravity (usually below 1018), by the scanty 
number of cell-elements, and by the absence of or the slight tendency to spon- 
taneous coagulation. 

The clinical importance of hydrothorax lies in the hindrance to respiration 
which it causes. As a result of this the hydrothorax may be regarded in many 
cases, especially in renal disease, as the chief cause of death. The objective evi- 
dence of it comes from the physical examination, which must, in general, give 
dullness, diminished vocal resonance, and dislocation of neighboring- organs, the 
same as in pleuritic effusion. We desire to emphasize also the bronchial res- 
piration from compression in hydrothorax, which is often very loud, although 
at the same time usually high and sharp, and which may even given rise to 
a confusion with pneumonic infiltration in the lungs. This very loud respira- 
tory murmur, contrasting with that of pleuritic effusion, is explained by the nor- 
mal condition of the lungs and the absence of all adhesions. For the same rea- 
son, too, the change in the boundary of the dullness, as a result of the patient's 
change of position, is usually more marked in hydrothorax than in pleuritic 



300 



DISEASES OF THE RESPIRATORY ORGANS 



effusion. We often hear a few fine crepitant rales over the hydrothorax, which 
arise in the retracted and partly atelectatic lung. The main factor, however, in 
distinguishing hydrothorax from a pleuritic exudation is, in every case, the con- 
sideration of the primary disease. It should also be noticed that hydrothorax 
is usually bilateral, while pleuritic exudation is usually unilateral. 

Treatment is directed, first of all, to the primary disease. If we succeed in 
strengthening and regulating the action of the heart, or in restoring the secre- 
tion of urine, the hydrothorax often disappears with the other dropsical symptoms. 
If the dyspnoea caused by it reaches a dangerous degree, we often see great relief 
from aspirating the fluid. The nature of the underlying condition, of course, 
renders the benefit in many cases only transitory. 

2. Haematothorax. — Effusions of blood into the pleural cavity (hsemato- 
thorax) arise most frequently from traumatic lacerations of blood-vessels, rarely 
from the bursting of an aneurism of the aorta into the pleural cavity, from ero- 
sion of an intercostal artery in caries of the ribs, from the rupture of a cavity into 
the pleura in phthisis, if it simultaneously opens a blood-vessel, etc. In many 
such cases a typical exudative pleurisy follows the effusion of blood. The physical 
signs are the same as in other pleural effusions. Severe dyspnoea may demand 
the removal of the blood by puncture, or even by an incision. 



CHAPTER Y 
NEW GROWTHS OF THE PLEURA 

The majority of new growths occurring in the pleura are of a secondary na- 
ture. We sometimes find single metastatic nodules of cancer in the pleura after 
primary carcinoma of other organs, especially of the mammary gland and the 
lungs, but most carcinomata of the pleura arise from primary carcinomata of the 
lungs and are due to a direct invasion of the pleura by the new growth. 

Of the primary new growths in the pleura, only one is of great importance — 
the endothelial carcinoma, first described by E. Wagner. This develops de novo, 
in a diffuse manner, from a proliferation of the endothelial cells of the lymphatics 
and the connective tissue. Metastases occur in the lungs, in the lymph-glands, in 
the liver, in the muscles, etc. 

Single secondary nodules of cancer in the pleura cause no special clinical 
symptoms, but the cases of diffuse cancer of the pleura as a result of primary can- 
cer of the lungs are important, inasmuch as the symptoms of disease of the pleura 
often quite predominate over the pulmonary disease. The dullness is intense, the 
respiratory murmur and the vocal fremitus diminished. In one such case we saw 
a proliferation of the cancer upon the ribs in front so that there was externally a 
very marked circumscribed swelling. The character of the sputum is the only 
thing that can give us definite information as to the origin of the new growth 
in the lungs (see the chapter on cancer of the lungs). 

Primary endothelial carcinoma of the pleura runs a course similar to chronic 
pleurisy. As we sometimes find a co-existing fluid effusion in the pleural cavity, 
displacement of the neighboring organs may occur. The affection goes on for a 
long time without fever, or with slight and irregular elevations of temperature. 
Most cancers of the pleura are associated with severe pain. 

The diagnosis of new growths in the pleura can usually be made, if at all, only 
in the more advanced stages of the disease. At first almost all the cases are 
regarded as simple or tubercular chronic pleurisy. The diagnosis is founded less 



MEDIASTINAL TUMOKS 



801 



upon the physical signs than upon the general course of the disease, the habit of 
the patient, and the evidence of metastases in the glands and other organs. In 
some cases characteristic elements of the new growth can be found by the micro- 
scope in the cloudy fluid obtained by an exploratory puncture. 

The prognosis is absolutely unfavorable, the treatment purely symptomatic. 
In endothelial carcinoma we might perhaps try the long-continued use of arsenic. 



CHAPTER VI 
MEDIASTINAL TUMORS 

In the anterior mediastinum, in quite rare cases, extensive new growths occur, 
which are of importance on account of their severe clinical symptoms. The 
point of origin for the tumor is either the mediastinal lymph-glands, or the 
connective tissue, or sometimes the remains of the thymus gland. In their 
anatomical character the tumors are almost always sarcomata, usually lympho- 
sarcoma, rarely alveolar sarcoma. They usually occur in youth or middle age, 
and are somewhat more frequent in men than in women. The special serological 
factors are unknown. In some cases an injury is stated to be the cause of their 
development. 

The first clinical symptoms are usually of a very indefinite nature. The 
patient complains of general languor, headache, pain in the chest, and slight diffi- 
culty in breathing, and only gradually do severe subjective and objective symp- 
toms develop in the chest. 

The symptoms are in part due directly to the tumor, but in larger part they 
are symptoms of compression from the gradually increasing pressure of the 
tumor on a number of neighboring organs. 

The pain in the chest, which is located chiefly in the sternal region, and is 
associated with a marked feeling of oppression, may be very severe. It sometimes 
shoots into the lateral portions of the chest and into the arms, showing pressure 
on the brachial plexus. 

The dyspnoea may finally increase to an extreme degree. A patient with 
lympho-sarcoma under our observation could, in the last days of her life, breathe 
only while standing. The dyspnoea is due to a compression of the heart and 
lungs, and sometimes to actual stenosis of the trachea or a primary bronchus. 
Paralysis of the dilators of the glottis may also occur from a pressure paralysis 
of the recurrent nerves. Paralysis of one vocal cord has been repeatedly observed. 
In the case mentioned above a marked goitre developed, as a result of vascular 
stasis, which further increased the dyspnoea by pressure on the trachea. A hydro- 
thorax from local venous stasis may also aid in increasing the dyspnoea. 

Pressure on the oesophagus, and disturbances of deglutition due to it, are rare. 
Pressure on the vagus nerve and the sympathetic sometimes causes anomalies in 
the rate of the pulse — either marked acceleration or slowing of the pulse. If 
the sympathetic is involved there is inequality of the pupils. In some cases, by 
pressing on the tumor, an artificial dilatation of the pupil can be excited at will. 
By pressure on the vessels, especially on the superior vena cava, the subcla- 
vian vein, etc., oedema and cyanosis may arise in the corresponding parts of the 
body. 

Objective examination of the chest gives a marked diffuse prominence of the 
sternal region in a part of the advanced cases; in other cases this swelling is 
absent. The discovery of an abnormal dullness in the anterior part of the chest 



302 



DISEASES OF THE KESPIKATOEY ORGANS 



is of diagnostic importance; this usually joins the cardiac dullness on the left, 
and on the right it extends a varying distance beyond the right border of the 
sternum. The heart is often pushed somewhat to the left. We heard over the 
pulmonary artery in our case a marked systolic murmur, caused by compression 
of the vessel. A dissimilarity of the pulse on the two sides is not infrequent. 

The diagnosis of a mediastinal tumor is usually possible in cases with well- 
marked symptoms, but in other cases it is difficult and uncertain. The differential 
diagnosis between mediastinal tumors and aneurism of the aorta (q. v.) causes 
especially great difficulty. Tumors may also be confounded with abscesses in the 
anterior mediastinum. 

The prognosis is in all cases absolutely unfavorable. The disease terminates 
fatally, sometimes after a duration of six months or a year. 

The treatment can be merely symptomatic. Internally we may try iodide of 
potassium or arsenic. In the last stages of the disease we must try to alleviate 
the patient's great distress by narcotics. 



CHAPTER YII 
ACTINOMYCOSIS OF THE THORACIC CAVITY 

Bollinger and others have described a peculiar tumor affecting the jaw-bones 
of cattle, and occasioned by the presence of a special form of fungus, known as the 

actinomyces or ray-fungus. More recently 
a class of diseases has been studied in 
human beings, occasioned by the same 
fungus (Ponfick, Israel, and others). 
These diseases may, as in cattle, affect the 
jaws, the floor of the mouth, and the 
neck; but in these cases they are mainly 
of surgical interest. The actinomycotic 
diseases of the internal organs, however, 
possess a great clinical importance; and, 
inasmuch as the lungs and pleura are the 
most frequently affected organs, it will 
be well to present briefly here the most 
important facts which have as yet been 
learned with regard to actinomycosis. 
The botanical position of actinomyces has 
not yet been definitely settled. Cohn and 
O. Israel regard it as a mould fungus. 
Bostrom, on the other hand, classes it with 
the alga?, and namely with the variety 
cladothrix. In its growth, the fungus 
forms small or moderate-sized gray or sul- 
phur-yellow nodules which may be dis- 
tinguished with the naked eye in the pus 
of the diseased tissue (see below), and which upon microscopic examination re- 
solve themselves into a tangle of mycelium. It is an especial characteristic that 
many of these mycelia bear on their ends a club-shaped swelling. These are 
placed for the most part like radii on the periphery of a nodule, and so surround 
the entire mass like a circlet of rays (see Eig. 38). In nature actinomyces seems 




ACTINOMYCOSIS OF THE THOEACIC CAVITY 303 



to appear especially upon plants, for example npon the beard of spikes of wheat. 
Thus is explained the frequency of infection in the plant-eating cattle, and a 
similar direct infection seems occasionally to be possible in man. It is worthy 
of note that the fungus seems to locate itself often in carious teeth. Thus appar- 
ently arises the above-mentioned disease in the buccal cavity ; while on the other 
hand, the fungus may be carried from its nidus in the mouth by inspiration into 
the respiratory tract, or by swallowing into the prima? vice. Of course it may 
also be directly swallowed or inhaled. 

Wherever the fungus fastens itself in the body it occasions first a new growth 
of granulation-tissue, which h?,s a tendency to break down into a whitish or 
brownish pasty mass. The brown color is occasioned by the hemorrhage which 
frequently occurs. Very often actinomycosis goes on to suppuration; still, this 
probably depends upon the influence of pathogenic germs which have secondarily 
infected the part. Of especial importance is the tendency of the disease to extend 
from the lungs to the pleura and from the pleura to the peripleuritic connective 
tissue, and still further to the wall of the thorax. Thus arise not only extensive 
abscesses and wide-branching fistulous tracts, but also a very characteristic, 
extremely tough cicatricial infiltration of the affected part. ~Noi infrequently 
there is at last a perforation reaching the outer surface of the body. 

The entire process, as a rule, is slow and insidious, but constantly progressive. 
The symptoms consist at first in slight thoracic discomfort, pain, cough, and ex- 
pectoration. Physical examination will often detect changes in the lungs, but the 
correct interpretation of the signs found is of course at first difficult, if not impos- 
sible. The more the disease spreads the greater is the distress. Usually there is 
hectic fever, which may assume a pysemic character if there is extensive suppura- 
tion. The patient gradually loses flesh, and in repeated instances amyloid degen- 
eration of the liver, spleen, and kidneys has been observed. If a focus breaks into 
a pulmonary vein, the disease may be developed by metastasis in other internal 
viscera. Moreover, there may be a direct extension of the disease to the pericar- 
dium, or through the diaphragm into the peritoneal cavity. 

The diagnosis of actinomycosis is at first difficult. It is established when the 
characteristic fungus is found in the sputum, but this has occurred in only a few 
cases as yet. If very extensive peripleuritic and pericostal suppuration has taken 
place, and the process has spontaneously broken outward or been laid open by 
surgical means, the demonstration above described in reference to the fungus 
is easy. 

The treatment can be only symptomatic, unless the diseased spot can be 
reached by operation, and then the treatment becomes surgical. Permanent cure 
has so far been attained in but rare instances. [Iodide of potassium has proved 
curative in a considerable number of cases, and it should certainly be tried, in 
doses of forty to sixty grains a day. — V.] 



DISEASES OP THE CIRCULATORY ORGANS 



SECTION I 
Diseases oe the He aft 

CHAPTER I 

ACUTE ENDOCARDITIS 

(Endocarditis verrucosa. Endocarditis ulcerosa) 

etiology. — Organized excitants of inflammation of different sorts, which cir- 
culate in the blood, may settle on the endocardium, especially on the valves of the 
heart, and there give rise to an acute endocarditis. Endocarditis, therefore, in 
its astiological relations, is not to be regarded as a single disease. Pathogenic 
micro-organisms have been injected into the blood (the streptococcus pyogenes, 
staphylococcus aureus, and others), and in this way an artificial endocarditis has 
been set up in animals. The experiments are more apt to succeed if the valves 
or the inner coat of the vessels have been subjected to some slight injury before 
the injection, thus promoting the settling of the germs upon them (Orth and 
Wyssokowitsch, Ribbert). Most cases of endocarditis in man, both the vegeta- 
tive and ulcerative forms, appear to be caused by the staphylococcus pyogenes 
aureus. Streptococci are much less frequent than staphylococci, and it is only 
in rare cases that endocarditis is occasioned by the pneumococcus, gonococcus, and 
perhaps the diphtheria bacillus. 

In accord with these statements is the fact that in human beings acute articu- 
lar rheumatism, which is probably to be regarded as a staphylococcus infection, is 
that one of the infectious diseases which is especially apt to have acute endocar- 
ditis as a frequent and important complication. The staphylococcus infection 
need not appear, however, in the first place, as a typical acute polyarthritis. 
An acute endocarditis may appear as a sequel of many cases of apparently pri- 
mary pleurisy, tonsillitis, or other disease. Indeed, it is sometimes impossible 
to determine the gate of entry of the infection, and the whole disease takes the 
shape of an apparently primary endocarditis. In such cases the nature of the 
disease is made evident by the later appearance of multiple articular swellings. 
We also regard as allied to polyarthritis certain forms of infection called the 
"acute hemorrhagic diseases" (e.g., purpura rheumatica), and also chorea 
(which see). It is therefore not surprising that acute endocarditis is not infre- 
quently observed in association with these affections. 

There are other acute infectious diseases with which acute endocarditis may 
be associated. Probably in these it is usually the result of a secondary mixed 
infection, generally with the staphylococcus. This explains the appearance of 
acute endocarditis in scarlet fever, small-pox, diphtheria, measles, and typhoid. 
Not infrequently mild cases of acute endocarditis, without clinical significance, 
are found in association with primary tuberculosis and ulcerating carcinoma. 
Again, acute and chronic nephritis may sometimes occasion a development of 
304 



ACUTE ENDOCARDITIS 



305 



endocarditis. An especially important role in producing endocarditis is dis- 
played by grave septic and pyaemic conditions (vide supra). In these cases the 
acute endocarditis appears as one symptom, but it is often so prominent that the 
whole attack is called endecarditis (vide infra). In such severe diseases we have 
often to do with a streptococcus disease, although it may be a staphylococcus in- 
fection of especial virulence. The aetiology of gonorrhoeal endocarditis is not 
yet fully determined. Endocarditis as a sequel of gonorrhoea is fortunately very 
rare. It often seems to be an actual gonococcus infection, but in other instances 
is occasioned by some secondary germ. 

Finally, we have still to mention the important fact that acute endocarditis 
quite frequently develops on the soil of an already existing chronic endocarditis — 
the so-called acute recurrent endocarditis. In women, pregnancy and the puer- 
peral state sometimes seem to give the occasion for a recrudescence of the endo- 
carditis. 

Pathological Anatomy. — We usually distinguish an endocarditis verrucosa, 
with the formation of large or small papillary nodules on the endocardium, and 
an endocarditis ulcerosa (endocarditis diphtheritica), with ulcerations as a result 
of the destruction and wasting away of the superficially necrosed tissue. The 
malignant, invariably fatal form of severe septic endocarditis is chiefly ulcerative 
endocarditis. Endocarditis verrucosa is the milder form, which is seen especially 
in acute polyarthritis and allied diseases, but we can not draw either a sharp ana- 
tomical or a sharp clinical distinction between the two, since malignant cases of 
endocarditis verrucosa are also observed. 

The endocardial growths are usually situated on the valves, especially on their 
edges of closure. More rarely we find them on the chordae tendinese and on the 
endocardium of the ventricle and auricle. In the mildest cases they are scarcely 
as large as the head of a pin, but in severe cases they may increase to quite large 
warty and glandular masses. Microscopically, the base of the nodule consists of 
a newly formed vascular tissue, infiltrated with small cells, which on its surface 
changes to a granular, coagulated mass. This last is formed partly of coagulated 
albumen, dead cells, and fibrine deposited from the blood, and partly of micrococci 
(vide supra). The micrococci are found without exception in all cases of ulcera- 
tive endocarditis — having been first discovered by Eberth. The endocardial ulcers 
arise from the destruction of the superficially necrosed nodules. If the thin 
valve in any place yields to the blood-pressure, we have the so-called acute val- 
vular aneurism. Complete perforation of a valve, and tearing off of fragments 
of a valve and of the chordae tendineae, are also seen. 

The great majority of cases of acute endocarditis are confined to the valves of 
the left side of the heart — the mitral and aortic valves. Endocarditis on the tri- 
cuspid valve is seldom seen except as a secondary affection in old cases of heart 
disease. In a case of acute ulcerative endocarditis in a grown man seen by us, the 
process was confined exclusively to the tricuspid valve, and there were very many 
embolic abscesses in the lungs. This may be considered a great rarity. In con- 
trast to the ordinary localization of endocarditis we find foetal endocarditis most 
frequently in the right side of the heart. 

Many other organs may be affected by the endocarditis, through embolism. In 
the benign endocarditis verrucosa, the masses of fibrine deposited on the irregu- 
larities of the valve furnish the embolic material. They cause large or small in- 
farctions in the kidneys and spleen, embolic softening of the brain, etc. In the 
malignant, ulcerative forms, however, large numbers of bacteria get into the cir- 
culation at the same time with the necrotic masses of tissue which have been torn 
off. Here, then, we have to do not merely with simple mechanical obstruction but 
with infectious emboli. The emboli in ulcerative endocarditis, therefore, either 
give rise to embolic abscesses in the cardiac muscles, the kidneys, the spleen, the 
20 



306 



DISEASES OF THE CIRCULATORY ORGANS 



lungs, the retina, etc., or they result in haemorrhages, especially into the skin, but 
also into the kidneys, the brain, the retina, and the serous membranes. It is not 
yet known why in some cases abscesses are more frequent and in others hiemor- 
rhages. The two, however, may be combined. In general, we may suppose that 
the development of abscesses is everywhere connected with the presence of bac- 
teria, while haemorrhages may also arise from toxic influences ; but again changes 
in the vascular walls caused by bacteria might give rise to haemorrhages. Em- 
bolic abscesses belong almost exclusively to the severe form of septic endocarditis. 
Haemorrhages are seen in this form, and also — without co-existing abscesses — in 
certain severe forms of endocarditis occurring in the course of acute rheumatism 
and allied diseases. 

Clinical History. — Since acute endocarditis is not aetiologically a distinct dis- 
ease, and since its clinical course is very different in different cases, it seems ad- 
visable to us to describe, in what follows, the most important varieties separately ; 
but it must be expressly noted that the separate classes can by no means be sharply 
defined, and that there are many intermediate forms. 

1. Slight endocarditis verrucosa is quite frequently found in the cadaver, 
without the slightest signs of any affection of the heart during life. The little 
papillary excrescences on the valves of the heart in phthisis, and carcinoma, whose 
aetiology has been explained above, are to be classed under this head. 

2. The typical form of benign acute endocarditis is most frequent, clinically, 
in the course of acute articular rheumatism. It is much rarer in other infectious 
diseases (vide supra). In a few cases it is also seen as an apparently primary 
disease. Here there is a constitutional rheumatic infection which has taken 
place in some way, and which settles directly on the valves of the heart instead of 
in the joints (so-called primary rheumatic endocarditis). Careful questioning 
will sometimes reveal, or at least render probable, the place of infection (a mild 
case of tonsillitis or some slight external injury). Very often there will be later 
the symptoms of articular rheumatism. It is seldom that endocarditis as such is 
associated with special local disturbances, such as pain in the region of the heart, 
palpitation, and dyspnoea. Ordinarily the heart disease is discovered only by 
physical examination. The impulse of the heart in many cases is abnormally 
strong and diffuse; the pulse is accelerated, but strong, often somewhat jerky 
(pulsus celer), and usually regular, but sometimes a little irregular. Percussion 
at first shows no deviations from the limits of normal dullness. On auscultation, 
we hear at the apex, more rarely at the base, a loud blowing, systolic souffle. 
Diastolic murmurs are rare in acute endocarditis. The pulmonic second sound is 
often accentuated. The physical signs referable to the heart are only slightly 
marked in many cases of acute endocarditis. This is understood if we remember 
that the occurrence of a heart-murmur depends wholly on the localization of the 
endocarditis, on the development of some valvular insufficiency, etc. 

Besides the direct symptoms pointing to the cardiac affection, the onset of an 
acute endocarditis is often, but not always, associated with fever, or, if fever be 
already present, with an increase of it, and with a slight aggravation of the gen- 
eral disturbance. Embolic processes may occur in the brain, the spleen, the kid- 
neys, and the extremities, but they are comparatively rare. Sometimes a peri- 
carditis develops as a result of the endocarditis (vide infra). 

It is hard to make any accurate statements as to the duration of this form of 
endocarditis. The physical signs may last for days, or for several weeks. Com- 
plete recovery is possible, but in the majority of cases this variety passes into 
chronic valvular disease of the heart. 

3. Malignant, non-septic form of acute endocarditis (" rheumatoid endocar- 
ditis" of Litten). In many cases this form is perhaps only a quantitative in- 
crease of the preceding form, but in other cases it is probably distinct from it 



ACUTE ENDOCARDITIS 



307 



serologically. The severe general infection is usually quite prominent here, and 
the disease resembles in many particulars grave septic endocarditis. The ob- 
jective signs in the heart are the same as in the preceding form, but more intense 
and extensive. The subjective cardiac symptoms, such as palpitation and distress, 
may be quite pronounced, but they may also be almost wholly absent in this form. 
The general condition, however, is usually bad. There is sometimes high fever 
with an irregular or intermitting course, but in many cases the fever is remark- 
ably low in spite of quite severe constitutional symptoms. 

The constitutional infection is very often manifested in these cases by the 
appearance of small or large haemorrhages in the skin, sometimes in the mucous 
membranes, as in the conjunctiva and the soft palate, and rarely in the retina. 
Secondary articular swellings often develop; they are always of a serous charac- 
ter, and never purulent. Renal haemorrhages and acute hemorrhagic nephritis 
are quite frequent. Large emboli may also occur in the different organs in this 
as in every other form of endocarditis. 

The duration of the disease extends over many weeks. In severe cases death 
ensues with a gradual aggravation of the general condition, and often with severe 
cerebral symptoms, such as stupor and delirium. In milder cases, however, the 
patient may finally get well. 

Regarding the occurrence of this form, we see it most frequently in acute 
articular rehumatism; also, in rare cases, in gonorrhoea, when it comes on some 
three or four weeks after the beginning of the urethral affection; also in ne- 
phritis, chorea, peliosis rheumatica, etc. The apparently primary cases of this 
sort usually belong to the recurrent form of acute endocarditis. 

4. The recurrent form of acute endocarditis consists of an acute increase of 
the endocardial process, brought on by some exciting cause, in a patient already 
suffering from chronic endocarditis. The acute disease may show all the grada- 
tions from the mildest to the severest. The mild cases often run their course 
without any special symptoms. To this form we may frequently refer the more 
or less temporary elevations of temperature which we often see in patients 
with chronic valvular disease of the heart. In rarer cases the recurrent endo- 
carditis comes on quite suddenly in the form of a severe acute attack. This 
sometimes seems to be clinically a primary, independent disease, especially if the 
previous chronic heart disease has up to that time caused no special symptoms. 
The patient has general malaise, headache, chills, and fever. The last may be 
quite high — 104° (40° C.) and over — or moderate, varying between 100° and 102° 
(38°-39° C), or it may be entirely absent. In many cases it is intermittent, 
when the return of fever is often associated with a chill. The cardiac symp- 
toms may be quite pronounced, but in this form, too, they may be obscure and 
indefinite. In the further course of the disease we meet with cutaneous haemor- 
rhages, retinal haemorrhages, articular swellings, large renal haemorrhages, or 
typical haemorrhagic nephritis — in short, just the same general type of disease as 
in the other malignant forms of acute endocarditis. The course is rarely rapid, 
and often lasts for weeks. Severe cases almost always end fatally. 

5. The severe septic ulcerative endocarditis has already been described as a 
complication of a general septic state. We therefore refer to the appropriate 
chapter (see page 116) for all particulars. Septic endocarditis is probably en- 
tirely distinct aetiologically from the forms thus far described, and is manifested 
by quite a rapid fatal course, with severe typhoidal or pyaemic symptoms. It is 
characterized anatomically, apart from the cardiac affection, by the appearance 
of metastatic abscesses in the various organs, but in many cases, as we have said, 
abscesses and haemorrhages are combined. 

Diagnosis. — The diagnosis of an endocarditis, coming on secondarily in the 
course of articular rheumatism and other diseases, can be made only by a physical 



308 



DISEASES OF THE CIRCUL AT ORY ORGANS 



examination of the heart. We must therefore give constant attention to the con- 
dition of the heart in diseases which we know may give rise to endocarditis. 

The diagnosis of the malignant form of endocarditis often causes great diffi- 
culty, especially if the patient is not seen until the later stages. . It is confused 
with typhoid, meningitis, or acute miliary tuberculosis. Examination of the 
heart may furnish positive evidence, but sometimes, as we have said, there are 
no physical signs of cardiac disturbance, or the signs present are indefinite. Of 
other factors in diagnosis a special importance attaches to the secondary swelling 
of the joints, and also to the haemorrhages into the skin and retina, for these are 
much more infrequent in the diseases with which this form of endocarditis 
may be confounded. The acute hsemorrhagic nephritis, too, in connection with 
the other symptoms, is, at least to a certain degree, characteristic of malignant 
endocarditis. The course of the fever is of diagnostic value only when it is 
decidedly intermittent. A careful search for some serological factor is very 
important for diagnosis in all cases. Eor other points the reader is referred to 
the consideration of septic diseases (page 116). 

Prognosis.' — In the description of the course of the disease we have already 
mentioned the prognosis of the different forms. The severe cases of acute endo- 
carditis usually, and the cases of severe septic endocarditis always end fatally. 
Here, however, the cause of death is to be sought rather in the accompanying 
systemic infection than in the endocarditis itself. In mild cases recovery is pos- 
sible, but the process of repair is often so incomplete that chronic valvular disease 
of the heart develops from the acute endocarditis. 

Treatment. — The chief requisite in the treatment of every endocarditis is as 
complete rest as possible for the patient. If ice is well borne, the continuous 
application of an ice-bag to the cardiac region is of service. If there are signs 
<of cardiac weakness, such as a small, rapid, and irregular pulse, we must employ 
cardiac stimulants, strophanthus, camphor, and, above all, digitalis. It must be 
confessed that the effect of these is not very great. If there are marked sub- 
jective symptoms (such as dyspnoea) narcotics, particularly morphine, are indis- 
pensable. Effort is made to combat the systemic infection by salicylic acid, 
salicylate of sodium, and similar remedies, including phenacetine and salipyrine. 
Quinine is usually entirely without effect, even when the fever is of an inter- 
mittent character. Arsenic, however, seems to be useful, particularly in the more 
protracted cases. 

[Eor remarks upon the alkaline treatment of rheumatism, see page 680.] 



CHAPTER II 

VALVULAR DISEASE OF THE HEART 

{Chronic Endocarditis) , 

^Etiology. — A large number of cases of chronic valvular disease of the heart 
proceed from acute endocarditis. Hence the frequent statement in the history of 
chronic valvular disease that the patient has had articular rheumatism, once or 
many times. In a collection of 163 cases of undoubted valvular heart disease, we 
were able to ascribe 86 to a previous attack of acute articular rheumatism. Fol- 
lowing the acute valvular endocarditis, which is often associated with this dis- 
ease, marked thickening of the valves occurs, due to the growth of connective tis- 
sue. There are also changes in the way of contraction, adhesion, and finally often 
of considerable calcification. The unavoidable result of all these processes is that 



VALVULAE DISEASE OF THE HEAET 



309 



the altered valves are rendered incapable of fulfilling- their physiological function 
of regulating the circulation. Inasmuch as the mitral valve is most often 
attacked by endocarditis when associated with acute articular rheumatism, we 
find mitral disease predominating among rheumatic valvular troubles ; but lesions 
of the aortic valves, rheumatic in their origin, are by no means rare. 

If we find a valvular lesion in a patient who has never suffered from articular 
rheumatism we may, in some cases, be able to refer the origin of the valvular 
trouble to a previous attack of acute endocarditis, excited by one of the other 
causes above mentioned. Thus it is well known that acute endocarditis may 
occur in the course of scarlet fever, diphtheria, and typhoid fever, and eventuate 
in chronic disease, but this is, according to our experience, very rare. 

In quite a large number of cases of heart disease, however, we can not obtain 
a history of acute endocarditis. We have to do here with an endocarditis which 
is chronic from the start, which also leads gradually to thickening, contraction, 
adhesion, and calcification of the valves. 

The causes of this chronic fibrous endocarditis are probably the same as of 
acute articular rheumatism, but in such cases they act from the start in a 
chronic manner. Perhaps often there may have been an incipient acute endo- 
carditis, whose course was unperceived. We not infrequently learn from patients 
with chronic heart disease, who have never had an attack of acute articular rheu- 
matism, that in former years they did suffer repeatedly from mild rheumatic 
pains, to which they paid little attention. Furthermore, it is by no means excep- 
tional to observe that such patients with a well-developed cardiac valvular lesion 
later on undergo one or more attacks of acute polyarthritis. Heart disease is 
also rarely associated with genuine chronic arthritis deformans. In other cases 
of valvular disease we must consider the possibility of other lesions, some infec- 
tious, some perhaps of a chemical and mechanical nature. Here belong, in the 
first place, those cases of cardiac disease which are associated with general arterio- 
sclerosis (atheroma of the blood-vessels). Indeed, atheromatous degeneration of 
the aorta seems sometimes to extend directly to the aortic valves, and thus cause 
a valvular lesion. Every ^etiological factor favorable to general arterio-sclerosis 
is, therefore, important in the aetiology of valvular disease. This includes ad- 
vanced life, excessive physical labor, alcoholism, and genuine gout. Another 
important cause is syphilis. Of late years, since we have paid more attention to 
this last factor than formerly, we have observed many cases of valvular disease 
which were almost certainly of syphilitic origin. In particular, lesions of the 
aortic valves, when there is no evidence of other causation, must awaken our 
suspicion of syphilis. There remains to be mentioned the influence of chronic 
nephritis upon the development of cardiac valvular disease, although in the not 
infrequent cases in which chronic nephritis, particularly of the interstitial vari- 
ety, is associated with chronic endocarditis, it is not always easy to determine 
whether both conditions are related in the way of cause and effect, or whether 
they are both secondary, and both alike the result of some third unfavorable 
influence. . A hereditary predisposition to heart disease is not very frequent, but 
yet it can be made out with certainty in many cases. We have ourselves seen 
five members of the same family who have suffered from chronic heart disease, 
some from pure valvular disease and some from severe so-called idiopathic hyper- 
trophy. Perhaps the very frequent occurrence of heart disease in many families 
is also connected with a special family predisposition to rheumatic affections, the 
occurrence of which predisposition can not, in our opinion, be denied. Finally, 
a small number of cases of heart disease, especially in the right side of the heart, 
depend upon anomalies of development of the heart — congenital heart disease. 

Valvular disease of the heart occurs at every age of life. The time of origin 
of most cases, corresponding in part to the occurrence of acute articular rheuma- 



310 



DISEASES OF THE CIRCULATORY ORGAXS 



tism, falls in youth and middle age, somewhere between eighteen and forty; 
but severe valvular disease is not infrequent even in children ; while late in life 
the clinical picture of valvular disease is often confused by the simultaneous 
presence of general arterio-sclerosis, pulmonary emphysema, or kidney trouble. 
Heart disease is said to be rather more frequent in the female sex than in the 
male. Women with heart disease not infrequently date their symptoms from 
pregnancy and the puerperium. 

General Pathology of Valvular Disease of the Heart. — Every valve of the 
heart, in order to fulfill its physiological task, must, on the one hand, open per- 
fectly at the right time in order to furnish a free passage to the blood-current 
through the appropriate orifice, and must, on the other hand, close firmly and 
perfectly at the right time in order to make any abnormal backward flow of blood 
impossible. In both relations the function of the valves may be disturbed by 
chronic endocarditis, the disturbance being the result of their anatomical 
changes. If the tips of the valves are shortened on their free edges by contrac- 
tion, or if the complete unfolding of the auriculo -ventricular valves is hindered 
by a shortening of their chordae tendineas, the closure of the valve can not be 
complete. At the moment when the closure of the valve is necessary a fissure 
remains open between its apices. We call this condition an insufficiency of the 
valve. On the other hand, the valves may lose their capability of free and suffi- 
cient separation from one another, as a result of thickening and calcification of 
the connective tissue, and also as a result of adhesions of the points of the valves 
with one another. At the moment when the blood-current should pass freely 
through the open orifice, the valve remains a stiff, narrow ring, through which 
the blood must force its way — stenosis of the orifice. The changes in the valves 
are often of such a sort that they cause at the same time both an insufficiency of 
the valve and a stenosis of the orifice. The thickening and calcification of the 
valves in stenosis cause, as a rule, a valvular insufficiency at the same time; but 
an insufficiency, set up by a contraction of the edges of the valves, may occur 
without a coincident stenosis of the orifice. 

The abnormal and injurious effect of a valvular lesion upon the circulation 
in the heart is felt in two directions. Either the obstacles to the circulation are 
increased in certain places, or there is a greater diastolic distention of certain 
portions of the heart. Both circumstances of course demand greater cardiac 
effort. If the heart were to labor with only the same degree of energy as under 
normal conditions, in spite of the increased resistance, or in spite of the greater 
distention, there would speedily be an impairment of circulation, incompatible 
with the continuance of life; for, if the increased resistance were not overcome, 
or if the abnormally distended cavity were not properly emptied, there would at 
once be a rapidly increasing congestion behind the diseased valve, and beyond 
it a constantly diminishing pressure. We can speak of a circulation of the blood 
only when, in a given interval of time, exactly as much blood is driven out of the 
heart as flows into it. The slightest difference in this regard would, in a very 
brief period, produce such a congestion of blood in the veins and such a diminu- 
tion of blood in the arteries that the demand of the tissues for oxygen could no 
longer be satisfied, and death would be the necessary result. A normal circulation 
is maintained so long as the amount of arterial blood, which flows into the organs 
in a given interval of time, is sufficiently great and also capable of immediate 
increase, proportional to any temporary increase in the demands of the organs, 
as, for example, when there is bodily exertion. The amount of blood flowing 
through the organs in a given time depends upon the degree of distention, the 
frequency of contraction, and the complete emptying of the left side of the heart. 
This amount ("the size of the circulation"') may be diminished, and yet the 
circulation continue as such; but that the circulation can, in spite of the dis- 



VALVULAR DISEASE OF THE HEART 



311 



tnrbance occasioned by a valvular lesion, still be maintained in a satisfactory 
manner is due to the capability of the heart of overcoming the obstacles to the 
circulation by means of increased work. Ii is one of the wisest contrivances in 
our organism, that the heart has control of a reserve fund of strength, which 
comes into action, if need be, in a way to compensate as far as possible for any 
disturbance of the circulation. This explains why a man with valvular disease 
of the heart may be almost perfectly well for a long time, while the increased 
work of certain portions of his heart suffices to keep up an approximately normal 
circulation in spite of the existing valvular disease. We call a heart disease, in 
which there is at least no marked disturbance of circulation, a compensated heart 
disease. 

The abnormal increase in functional activity of certain portions of the heart, 
associated with every cardiac lesion, and referable in every case, as we have said, 
either to increased resistance or to increased distention, results in a hypertrophy 
of those particular portions of the heart, just as in the case of any other muscle. 
This hypertrophy does not consist of an increase in thickness of the individual 
muscular fibers, but chiefly of an increase in number. The total bulk of the 
cardiac muscle increases, and thus its capacity for work naturally becomes greater. 
It goes without saying that increased nutritive processes and a large supply of 
nourishment for the heart are necessary to bring about such a hypertrophy, by 
which alone a compensation of the heart disease is possible for any length of time. 
Hence we find the secondary hypertrophy of the heart absent, or at least only 
imperfectly developed, in feeble individuals, especially in those who have suffered 
from some other chronic wasting disease besides the heart disease, such as phthi- 
sis or carcinoma. 

Although the compensatory processes in the heart may prevent for a long time 
any marked disturbance of the circulation, the already overburdened heart can no 
longer completely satisfy any excessive demands upon it, even in a compensated 
heart disease. Hence patients with a compensated heart disease are free from sub- 
jective disturbance only when they remain at rest, while the signs of a disturbed 
circulation usually become quite apparent on slight physical exertion. 

The hypertrophied cardiac muscle can seldom supply permanently the ab- 
normally great drafts made upon it. There finally comes a condition of " fa- 
tigue,' ' of " cardiac insufficiency.'" The cause lies either in the increase of the 
valvular disease, so that the hindrance to the blood-current caused by it can no 
longer be completely overcome, or in the fact that the nervous and muscular ele- 
ments in the heart have their powers gradually impaired by a disturbance of 
circulation in the heart itself. In short, in every heart disease the moment may 
finally come when the capacity of the heart has reached its limit, and hence the 
compensation of the heart disease ceases. The results of stasis now appear with 
increasing severity in the different organs, as we shall learn to recognize later on, 
and the patient finally succumbs to them, unless some intercurrent event puts an 
end to life. 

After these general remarks, which will be understood better on reading what 
follows, we will pass on to the special description of the different forms of heart 
disease and their physical signs. 

1. Insufficiency of the Mitral Valve 

!Mitral insufficiency is one of the most frequent forms of heart disease. It 
develops in acute or chronic endocarditis of the mitral valve, from contraction of 
the free edges of the valve or from shortening of the chordae tendineae. In rare 
cases it comes on from partial adhesion of the valves to the walls of the ventricle. 

The closure of the mitral valve occurs normally at each systole of the left ven- 



312 



DISEASES OF THE CIRCULATOKY OKGANS 



tricle. It prevents the return of blood from the left ventricle to the left auricle. 
If the mitral valve is insufficient and its closure is incomplete, at every systole of 
the left ventricle a part of the blood is thrown back from it into the left auricle 
through the open space of the ostium venosum. This abnormal backward wave 
encounters the blood-current coming in an opposite direction into the left auri- 
cle from the pulmonary veins. The meeting of these two opposing currents, as 
well as the stream of regurgitant blood pressing through the open chink in the 
mitral valves, sets the blood in a whirl, and this impinging upon the tense edges 
of the valves produces a loud, blowing, systolic murmur. We hear this murmur 
loudest at the apex of the heart, corresponding to the laws of conduction in the 
thorax; yet it usually is propagated so far that it may often be heard at the other 
cardiac orifices, although not so distinctly. A loud systolic mitral murmur can 
also be heard sometimes in the back, on the left, and occasionally on the right. 
In some few cases the systolic murmur of mitral insufficiency is heard best in the 
second left intercostal space. This is probably because the murmur occasioned by 
the commotion in the left ventricle is conducted by the left auricular appendix to 
the anterior chest-wall (Naunyn). Curschmann has pointed out that this is par- 
ticularly apt to happen in cases of incipient mitral insufficiency; but, as a rule, 
even in these cases, the murmur is found at the apex of the heart. In most 
instances the systolic muscle-sound of the left ventricle, the so-called first sound 
of the heart, can also be heard besides the systolic murmur. It can be heard 
rather better if the ear is slightly removed from the ear-piece of the stethoscope 
[meaning the mon-aural instrument]. Exceptionally the sound may be com- 
pletely obscured by the murmur. The second sound is often not to be heard at 
the apex, probably because it is obscured by the relatively protracted murmur. 

Since the left auricle, at each systole of the ventricle, receives blood from two 
sides — its normal quantity from the pulmonary veins, and, besides that, the abnor- 
mal blood-wave from the left ventricle — it becomes much dilated. At the next 
diastole of the left ventricle the whole amount of blood collected in the auricle 
under increased pressure pours into the left ventricle through the mitral valve, 
which is now wide open (supposing a pure insufficiency of the valve without any 
stenosis). We see, then, that in pure mitral insufficiency the left ventricle must 
be filled beyond the normal amount during the diastole. The left ventricle must 
also expel in the following systole an abnormally large amount of blood. Al- 
though by this contraction only a part of the blood reaches the aorta in the 
direction of the normal blood-current while a part pours back into the auricle, 
the work of the left ventricle is of course excessive. Thus, in pure mitral insuffi- 
ciency, the left ventricle is dilated as a result of its increased filling in diastole, 
and is hypertrophied as a result of its increased labor. The general arterial 
tension remains approximately normal. It is not increased, since a part of the 
abnormal amount of blood, which pours out of the left ventricle at every systole, 
flows backward into the auricle. So long as the left ventricle is completely emp- 
tied by vigorous contractions, the aorta receives about the normal amount of 
blood, and the radial pulse remains, therefore, in cases of pure mitral insuffi- 
ciency, of about the normal strength and tension. 

The anomalies in the movements of the blood in mitral insufficiency produce 
still other effects. We have already seen that the left auricle is dilated from its 
overfilling.. It also becomes hypertrophied, so far as its weak muscular structure 
permits, but it is not in itself capable of compensating for the disturbance which 
the pulmonary circulation suffers from the mitral insufficiency, for the back cur- 
rent from the left ventricle, and the consequent high pressure in the left auricle, 
must plainly offer an abnormal hindrance to the flow of blood from the pulmo- 
nary veins. This stasis sets back through the pulmonary capillaries and arteries 
into the right ventricle. This may be recognized, on physical examination, by 



VALVULAR DISEASE OF THE HEART 



313 



the change in the pulmonic second sound, which is louder, more valvular, and 
" accentuated," since the closure of the semilunar valves in the pulmonary artery 
now takes place under the abnormally high pressure which prevails in the arteries 
of the lungs. The right ventricle has the task of overcoming this abnormal stasis 
in the pulmonary circulation. It can overcome the abnormal resistance in the 
pulmonary circulation by increased work, and as a result it becomes hyper- 
trophied. So long as the hypertrophy of the right ventricle suffices to maintain 
the normal pulmonary circulation, the stasis extends no farther backward, but in 
the later stages of heart disease we see the right ventricle becoming paralyzed, 
and more and more dilated as a result of stasis. The flow of venous blood from 
the body into the right auricle and ventricle is now rendered more difficult. The 
signs of venous stasis become manifest; the patient has a cyanotic hue, con- 
gestive oedema appears in the face and the extremities, symptoms of passive 
congestion of the liver, spleen, and kidneys appear, and, in short, there is devel- 
oped the picture of an uncompensated heart disease. 

If we now sum up the physical signs of mitral insufficiency, the different 
methods of investigation give the following results : 

Inspection. — The cardiac region often seems rather prominent, as a result of 
the hypertrophy of the heart. This protrusion is most marked in young persons 
with a yielding thorax. The apex-beat is, as a result of the dilatation and hyper- 
trophy of the left ventricle, displaced toward the left and sometimes downward 
into the sixth intercostal space. It is more extensive and stronger than normal 
("heaving"). The apex-beat is somewhat displaced toward the left as a result 
of the hypertrophy and dilatation of the left ventricle, and it is quite marked. 
Besides that, we often see a diffuse pulsation in the whole cardiac region. In 
the epigastrium we sometimes see an epigastric pulsation proceeding from the 
hypertrophied right ventricle. In cases which are no longer perfectly compen- 
sated the stasis in the veins of the body is rendered apparent by the general 
cyanotic appearance of the patient and the marked filling of the jugular veins in 
the neck. Undulatory or pulsating movements often occur in the latter (see tri- 
cuspid insufficiency, below). 

Palpation. — By palpation likewise we perceive the abnormal vigor and extent 
of the apex-beat, and the displacement of the same toward the left; and often, 
also, an extensive diffuse pulsation over the cardiac region, and in particular a 
distinct epigastric pulsation, due to the right ventricle. We often feel a systolic 
thrill at the apex of the heart — a " cat's purr " — by laying the hand flat on the 
chest. The same whirl of blood, which is audible as a murmur, may be per- 
ceived as a fine tremor of the chest-wall. 

The radial pulse is quite strong and usually regulai. The sphygmographic 
tracing of it shows nothing characteristic in mitral insufficiency. 

Percussion. — This usually gives at first only a moderate increase of the heart's 
dullness to the left, and a little upward dilatation of the left auricle and left 
ventricle, but in the later stages there is at the same time an increase of the 
heart's dullness to the right, caused by hypertrophy and dilatation of the right 
ventricle. The whole area of cardiac dullness may finally extend two fingers' 
breadth beyond the right edge of the sternum, and to the left it may reach the 
mammillary line, or even pass far beyond it. 

Auscultation. — At the apex of the heart we hear a loud, quite long, pure sys- 
tolic blowing murmur, limited to the systole, either replacing the first sound or 
accompanying it. The second sound is often obscure or inaudible at the apex, 
but the pulmonic second sound is increased and accentuated. Auscultation of the 
vessels gives nothing characteristic. 



3U DISEASES OF THE CIECULATOEY ORGANS 



2. Stenosis of the Mitral Orifice (Mitral Stenosis) 

Mitral stenosis often develops in chronic endocarditis of the mitral valve, as a 
sequel to a previous insufficiency. The valve constantly grows stifTer and more 
rigid, and the signs of stenosis gradually predominate over those of insufficiency. 
Hence we very often find stenosis and insufficiency of the mitral valve combined, 
but often the signs of stenosis are so much more prominent that we can properly 
speak of a pure mitral stenosis. 




Fig. 39.— Pulse curve in marked mitral stenosis. 



The disturbance which the circulation suffers in mitral stenosis is much 
greater than in mitral insufficiency. In mitral stenosis the orifice may finally 
become so narrow that it scarcely admits an ordinary lead-pencil. The influx of 
blood into the left ventricle is accordingly much impeded. During the diastole 
of the left ventricle the blood must force its way through the stiff and narrow 
ring of the mitral valve. In this way, again, are caused irregular whirling move- 
ments in the blood, and abnormal vibrations of the mitral valve, giving rise in 
most cases to an audible diastolic murmur. In mitral stenosis the left ventricle 
receives less than its normal amount of blood, and therefore it has no direct occa- 
sion for hypertrophy, and in fact it is sometimes found at the autopsy to be com- 
paratively small and to be crowded backward by the enormously dilated and 
hypertrophied right heart. Nevertheless, we do often find hypertrophy of the 
left ventricle in cases of mitral stenosis, and for this reason, that mitral stenosis 
usually develops gradually from a previous insufficiency of the valves. That is, 
the chronic endocarditis occasions, probably in every case, first, an insufficiency of 
the valve, which is later followed by stenosis as the change progresses. We have 
already seen that insufficiency of the mitral valve always leads to hypertrophy 
of the left ventricle, and so we find it to persist even at a time when stenosis 
has become the prominent lesion. In other cases of stenosis, hypertrophy of the 
left ventricle is due to certain associated conditions, such as arterio-sclerosis or 
chronic nephritis. And finally we should also consider Friedreich's theory, that 
severe venous congestion may extend into the capillaries, and thence finally 
occasion abnormal resistance to the arterial circulation. 

The radial pulse in mitral stenosis is approximately normal, as long as the 
ventricle is sufficiently filled with blood during diastole. In spite of the stenosis 
of the mitral valve, the left ventricle may be satisfactorily filled, and this is 
more likely if the action of the heart is slow, allowing a longer diastole; and if, 
also, the left auricle is still capable of vigorous contraction. If, however, the 
action of the heart is hurried, and the left ventricle is no longer sufficiently dis- 
tended with blood during the diastole, the radial pulse becomes small and of low 
tension. Marked arhythmia is very often present in mitral stenosis, probably 
because of the insufficient amount of arterial blood supplied to the myocardium 
and its ganglia. 

The hindrance to the flow into the left ventricle in mitral stenosis soon leads 
to a marked stasis, which extends to the right side of the heart through the left 
auricle, and the pulmonary veins, capillaries, and arteries. The left auricle is 
dilated first (often to an enormous extent), and its walls are hypertrophied, but it 
can overcome only a very small part of the resistance at the mitral orifice. The 
right ventricle can, by more work, so increase the pressure in the pulmonary ves- 



VALYULAK DISEASE OF THE HEART 



315 



sels that, in spite of the narrowed orifice, an approximately sufficient quantity 
of blood may pour into the left ventricle. Hence we find in mitral stenosis a 
very marked hypertrophy and dilatation of the right ventricle. The stasis in 
the pulmonary circulation, manifested objectively by the accentuation of the 
pulmonic second sound, has as a result a gradually developing ectasis of the 
pulmonary capillaries. Thickening of the intima of the pulmonary arteries 
and veins also usually develops. (See the chapter on brown induration of the 
lungs.) 

The results of physical examination are as follows : 

Inspection. — The whole cardiac region may seem slightly prominent, as a re- 
sult of the hypertrophy of the heart. This protuberance is most marked in chil- 
dren with their yielding thoracic walls. The heart's action is usually extended 
over a larger area, but in pure mitral stenosis the apex-beat is no stronger than 
usual, though often displaced to the left. We have frequently noticed a marked 
pulsation in the epigastrium, produced by the right side of the heart. The jugu- 
lar veins are apt to be prominent, and show the different forms of undulatory and 
pulsating movement. 

Palpation. — This also gives signs corresponding to the more extended action 
of the heart. We sometimes feel the pulsation of the dilated rig*ht ventricle even 
to the right of the sternum. In some cases we feel a diastolic thrill at the apex 
of the heart, which alone may almost establish the diagnosis of mitral stenosis. 
This thrill arises from the same vertiginous currents in the blood which form the 
basis of the diastolic murmur (vide infra). The radial pulse is small in every 
case of severe mitral stenosis, and is very often irregular. 

Percussion. — Percussion shows, in the first place, an extension of cardiac dull- 
ness toward the right, reaching to the right edge of the sternum, or far beyond. 
Dullness also extends as a rule further to the left than normal. This is in part 
due to the hypertrophy of the left ventricle (vide supra), in part to a dilatation 
of the right side of the heart, so great as to push the left ventricle backward and 
to the left. The great distention of the left auricle causes an enlargement of the 
cardiac dullness upward. We observed one case in which the left auricle was 
so enormously dilated that it extended behind and beyond the right auricle 
toward the right, and was one factor in the increase of cardiac dullness toward 
the right, as observed during life. 

Auscultation. — The characteristic auscultatory sign of mitral stenosis is the 
diastolic [pre-systolic] murmur at the apex. This is never so loud and blowing as 
the systolic murmur of insufficiency, but it usually sounds more rolling or rippling. 
It is loudest at the apex, and it is transmitted only slightly toward the base. 
Since, as has been said, the left ventricle in mitral stenosis is sometimes pushed 
to the left and backward by the very much enlarged right ventricle, in looking 
for the murmur we must often go far to the left, in order not to auscult the right 
ventricle only. 

The origin of the murmur is easily explained. In the diastole of the left 
ventricle the blood-current must force its way through the narrow mitral orifice, 
whence vertiginous movements arise in the blood, and produce the murmur. 
Since the blood flowing through the narrow orifice has a current of relatively 
slight intensity, the murmur produced by it can not be very loud. Indeed, in the 
most extreme cases of mitral stenosis, the murmur is particularly apt to be very 
faint, and when the heart's action is hurried and irregular, entirely inaudible. 
!Not infrequently the murmur is not heard until the second half of diastole. That 
is, when the contraction of the left auricle gives a fresh impulse to the current 
of blood streaming through the stenosed orifice. A murmur of this sort, which 
is audible only at the end of diastole, and passes with a distinct crescendo directly 
into the loud systolic sound and terminates with this, is called a pre-systolic 



316 DISEASES OF THE CIRCULATOKY OEGANS 



murmur. This murmur can often be plainly felt if the hand is laid upon the 
apex of the heart, as a pre-systolic thrill. 

It is not very exceptional to find no murmur audible in cases of extreme mitral 
stenosis. If such cases do not come under observation till the last stage of the 
disease, the mitral stenosis may readily be overlooked. We have ourselves re- 
peatedly found, in cases of mitral stenosis, that as the lesion grew worse the dis- 
tinct diastolic or pre-systolic murmur gradually and completely disappeared. 
This is explained by the fact that as the chink in the valve grows narrower and 
the weakness of the heart greater, the blood is not forced through the narrow 
orifice with sufficient vigor to cause audible vibrations of the thickened valves. 
If the left ventricle is wholly displaced backward by the enormous increase in 
size of the right ventricle, we have also less favorable conditions for the propa- 
gation of the waves of sound from the mitral valve to the ear. 

The first sound at the apex is maintained in pure mitral stenosis. Indeed, it 
is often noticeably loud and valvular. All the later observations confirm the 
view that the systolic sound is a muscle sound, and consequently it is probable 
that this vigorous first sound is due to the contraction of the left ventricle, which, 
as we have seen above (page 314), is often hypertrophied, and also, as a result of 
the stenosis, only imperfectly filled. The strength of the first ventricular sound 
in mitral stenosis affords, at any rate, a marked contrast to its weakness in aortic 
insufficiency (vide infra). We have a strong sound when the ventricle is ill- 
filled, diminution and dullness of sound when the ventricle is over-filled. If in- 
sufficiency of the valve co-exists, we may hear a systolic murmur with the first 
sound or instead of it. 

The very marked accentuation of the pulmonic second , sound, the result of 
the abnormally high tension in the pulmonary artery, is almost constant. It 
fails only in very anaemic, weak people, or in co-existing insufficiency of the 
tricuspid valve (vide infra). The second sound at the base is very often "di- 
vided " or reduplicated. The closure of the semilunar valves in diastole does not 
happen at the same time in the pulmonary artery and in the aorta, on account of 
the unequal tension in the two vessels, so that consequently the two sounds are 
heard, one shortly after the other. Although this division of the second sound is 
particularly frequent in mitral stenosis, it is by no means a pathognomonic sign 
of it, 

Mitral stenosis is one of the severest forms of heart disease. It almost always 
causes greater subjective disturbance than mitral insufficiency. Hypertrophy of 
the right ventricle may, indeed, maintain for a time an approximately complete 
compensation, but the signs of marked stasis in the pulmonary circulation, and 
further in the veins of the body, are apt to appear quite early. It must be 
admitted that the disturbances of compensation which occur in mitral stenosis 
are particularly susceptible of treatment, so that for many years there may be 
times of improvement, alternating with times of aggravation of the symptoms; 
but finally the time comes when it is impossible to regulate the circulation. The 
dyspnoea grows worse, and finally death occurs, usually preceded by dropsy. 

3. Insufficiency of the Semilunar Valves of the Aorta 

Insufficiency of the aortic valves is due most frequently to contraction of the 
free edges of the valves. Tears, perforations, or adhesions of the valve to the 
wall of the vessel more rarely lead to insufficiency. The cause of all these 
changes is either a valvular endocarditis, which is usually a sequel of articular 
rheumatism, or a general arterial atheroma, which extends gradually from the 
intima of the aorta to the valves. We have already referred to syphilis as a not 
very infrequent cause of aortic lesions. A question of practical importance is 



VALVTJLAK DISEASE OF THE HEAET 



317 



whether violent bodily exertion may suddenly occasion the partial laceration of 
an aortic valve. Many clinical observations, including a recent case of the 
author's, seem to show the possibility of this extremely rare occurrence. 

The function of the aortic valves is to close tightly at the time of diastole of 
the left ventricle, in order to prevent any return of blood from the aorta into the 
ventricle. If these valves are insufficient — that is, if they do not close perfectly 
at each diastole — there is a return current of blood from the aorta into the left 
ventricle. 

This regurgitant diastolic wave sets the tense edges of the valve in vibration 
as it passes over them. Furthermore, the two currents of blood impinging upon 
each other in the left ventricle, the one an abnormal regurgitation from the 
aorta, the other the normal stream from the left auricle, produce irregular whirl- 
ing motions in the blood. All these vibrations are propagated to the surround- 
ing structures, and produce the long-continued, blowing, diastolic, and remark- 
ably characteristic murmur of aortic insufficiency. 

Aortic insufficiency causes an immediate and great increase in the demands 
upon the left ventricle, because of its abnormal distention, for it receives, as we 
have already said, not merely its normal quantum of blood from the left ven- 
tricle, but also the blood which regurgitates through the leaking valves of the 
aorta. It is consequently overfilled at every diastole, and finally becomes per- 
manently distended. Dilatation of the left ventricle forms a constant anatom- 
ical lesion in every case of aortic insufficiency, and is shown not only in the dila- 
tation of the whole ventricular cavity, but also in the very characteristic flatten- 
ing of the trabeculge and of the papillary muscles. There is usually some fibrous 
thickening of the endocardium at the spot upon which the regurgitant blood-cur- 
rent is continally impinging. The left ventricle possesses sufficient reserve 
strength to discharge its contents completely for a long period by means of in- 
creased effort. This is indeed a task like that of Sisyphus, since the portion of 
the blood which is thrown into the aorta is constantly rolling back into the ven- 
tricle. The increased demands, however, lead necessarily at last to a hypertrophy 
of the left ventricle, often greater than is seen under any other conditions. 

From the facts enumerated we can easily understand the physical signs of 
insufficiency of the aortic valves. 

Inspection. — Great hypertrophy of the left ventricle often causes a marked 
protrusion of the whole cardiac region. The diffuse and very strong apex-beat, 
displaced downward and to the left, is especially striking. It may usually be 
seen in the sixth intercostal space, outside the left mammillary line, and some- 
times even at the anterior axillary line. Besides, we often see a marked diffuse 
tremor of the whole cardiac region. There is marked pulsation of the carotid 
arteries in the neck. The jugular veins show undulation and pulsation, when at 
last compensation begins to fail. 

Palpation. — We can appreciate the heart's action to a still greater extent by 
palpation than by inspection. The apex-beat is very resistant, massive, and 
plainly heaving — that is, the finger or stethoscope applied to the apex is lifted by 
the beat at every systole. In rare cases a diastolic thrill, corresponding to the 
diastolic murmur, can be felt over the base of the heart. In two such cases 
observed by us the murmur had a marked musical character (vide infra). The 
appearances in the arteries are given below. 

Percussion. — Percussion gives an extension of the cardiac dullness to the left, 
beyond the left mammillary line and even to the anterior axillary line, caused by 
the hypertrophy and dilatation of the left ventricle. The upper boundary of 
the cardiac dullness is normal, or it may extend up to the third rib. The right 
boundary is in its normal place at the left border of the sternum, but it may also 
be pushed farther to the right, either because the large left ventricle of itself 



318 DISEASES OF THE CIKCULATOKY OKGANS 



causes an extension of the whole heart to the right, or because the right ventricle 
is also hypertrophied. The latter change occurs in pure aortic insufficiency when 
the compensation is no longer complete, and the stasis extends backward from the 
left ventricle, through the pulmonary circulation, into the right side of the heart. 

It may also be remarked here that, in insufficiency of the aortic valves, the 
ascending aorta is often considerably dilated by the marked impulse from the 
amount of blood pouring into it. A moderate degree of dullness is found over 
the dilated aorta, which may sometimes be made out at the sternal end of the 
second right intercostal space. 

Auscultation. — Insufficiency of the aortic valves is characterized by a long- 
drawn, loud, blowing diastolic murmur, the origin of which has been explained 
above. The place in which the murmur is heard loudest is not the sternal end 
of the second right intercostal space, the ordinary point for auscultation of the 
aorta, but it almost always lies farther to the left. Corresponding to the back- 
ward current of blood toward the left ventricle, which begets the murmur, we 
hear the latter loudest over the upper part of the sternum or even at its left bor- 
der. In some cases the murmur assumes a marked " musical character " — that 
is, there is a definite high musical tone, which is due to a tendinous fiber arising 
from a wearing away of the valve, and set in vibration by the diastole, or to some 
similar cause. The diastolic murmur is often audible at the apex, but it is faint 
there. It is only in a few exceptional cases that there is no diastolic murmur 
in aortic insufficiency. Sometimes we hear not only the murmur, but also the 
diastolic sound of the closing valve. During systole we scarcely ever hear over 
the aorta a pure, loud, first sound, but almost always a short systolic murmur. 
This may, of course, be due to accompanying stenosis of the aortic valves, but 
yet is very common when there is insufficiency alone. It is explained by O. 
Eosenbach as being due to the fact that at the beginning of the systole of the left 
ventricle, the diastolic flow of blood has not yet completely ceased, so that the 
emerging blood-stream encounters this opposing current. This meeting of the 
two blood-currents in the root of the aorta during systole causes the vibrations 
which give rise to the short systolic murmur. It is to be noted that this circum- 
stance also may perhaps have some influence upon the development of the hyper- 
trophy of the left ventricle. 

It is very interesting and important that, as Traube pointed out, we find the 
first sound at the apex scarcely ever loud and pure, but often very indistinct and 
muffled; or else we hear a short systolic murmur instead of it. This veiling of 
the first sound at the apex of the heart has theoretic interest, because it has been 
employed as an argument against the view that the first mitral sound is a mus- 
cular sound; for it is not, in fact, at once apparent why the hypertrophied left 
ventricle should so often fail to produce a distinctly audible tone by its contrac- 
tion. But, as we have already pointed out (see page 316), the probable explana- 
tion lies in the previous over-distention of the left ventricle during diastole. 
This renders the systolic contraction difficult and somewhat slow, and may be the 
cause of the indistinctness of the muscle-sound. In later stages of the disease 
we may also adduce parenchymatous degeneration of the myocardium, as an ex- 
planation of its feebleness. The systolic murmur, often heard at the apex in 
aortic insufficiency, may depend upon a co-existing true mitral insufficiency, but 
it is probably often due to a relative insufficiency of the mitral, since the valves, 
which are normal in themselves, can no longer cause a perfect closure of the left 
mitral orifice now that the left ventricle is dilated. 

Symptoms in the Peripheral Arteries. — Such remarkable symptoms are 
found in the peripheral arteries in aortic insufficiency that they demand a brief 
special description. The first striking symptom is the strong pulsation not only 
of the larger but also of the smaller arteries, even those the pulsation of which is 



VALVULAK DISEASE OF THE HEAET 



319 



not generally visible. We see and feel not only a strong pulsation in the carotids, 
but also in the tortuous brachial artery, in the radial, ulnar, temporal, dorsalis 
pedis, etc. We sometimes feel an arterial pulse in the liver through the ab- 
dominal walls. 

The rapid decline of the pulse — the pulsus celer [Corrigan's pulse] — is most 
characteristic of aortic insufficiency, and is to be felt especially in the radial 
artery, but also in the femoral, dorsalis pedis, and other vessels. An abnormally 
large quantity of blood is thrown into the arteries from the hypertrophied and 
dilated left ventricle; hence the high ascent of the pulse; but since the distended 
artery quickly contracts again, and particularly as at the next diastole of the 
ventricle the blood escapes in two directions, into the capillaries and back into 
the ventricle, an abnormally rapid and deep decline of the pulse follows the 
high ascent of its wave — a condition which explains the " jumping," " springing " 
pulse (pulsus celer) of aortic insufficiency. The quality of the pulse may be 
plainly recognized also in the sphygmographic tracing (see Fig. 40). The abnor- 
mal backward wave 
may even be detected 
in the capillaries. We 
often see a marked 
pallor of the finger- 
nails at every diastole 
of the heart in pa- 
tients with aortic insuf- 
ficiency — Quincke's ca- 
pillary pulse. 

The auscultatory 
phenomena over the ar- 
teries are connected Fig. 40.— Pulse curve in aortic insufficiency, 
partly with the chang- 
ing conditions of tension of the arterial walls. We very often hear a short, 
rough, systolic murmur in the carotid. The second sound, which is well known 
to be the transmitted aortic second sound, is absent. Instead of it we sometimes 
hear faintly transmitted the aortic diastolic murmur. The sound of the medium- 
sized and smaller arteries is very characteristic. By applying the stethoscope 
lightly we hear over the femoral, the brachial, and often over the radial, the 
ulnar, the palmar arch, and the dorsalis pedis, a marked valvular sound, which 
is changed by pressure on the artery, especially in the larger arteries, to a loud 
stenotic murmur. The quicker the pulse, the more certain are we to hear these 
sounds in the arteries. In the most marked cases of Corrigan's pulse these vas- 
cular sounds are so loud that we may hear almost anywhere below the knee, by 
means of a stethoscope, a valvular sound. The double sound in the femoral 
(Traube's double sound) is quite a frequent phenomenon, about the origin and 
significance of which there has been much discussion. The double sounds either 
follow each other shortly, so that the first seems something like a preparatory 
blow for the second, or they are separated from each other by a longer interval, 
like the two sounds of the heart. Traube explained the origin of the first sound 
by the sudden tension of the vessel-wall, as in the simple femoral sound, and the 
second sound by the sudden relaxation of it. Friedreich has pointed out in regard 
to this that, in co-existing tricuspid insufficiency, a sound may also be produced 
in the femoral vein by tension of the venous valves. The double sound in the 
femoral may probably have different causes of origin. It is, of course, by far the 
most frequent in aortic insufficiency, but it has also been repeatedly observed in 
other forms of heart disease, as in mitral stenosis. The so-called Duroziez's double 
murmur in the femoral is more rare, and it is noticed almost exclusively in aortic 




320 



DISEASES OF THE CIRCULATORY ORGAKS 



insufficiency. This is when we hear, by pressing the stethoscope on the femoral, 
two murmurs plainly distinct from each other, of which the first comes from the 
passage of the systolic blood-wave, and the second from the passage of the abnor- 
mal backward wave coming from the periphery of the vascular system through 
the artificially contracted vessel. While the well-marked Corrigan's pulse and 
the arterial sounds associated with it are so characteristic, they do not appear 
with great distinctness in every case of aortic insufficiency, but only in many; 
while in other and apparently similar cases they are indistinct or quite absent. 
Probably this difference depends at least in part upon a difference in the elasticity 
of the arterial walls. At any rate, we have seen well-marked Corrigan's pulse and 
sounding arteries in youthful patients; while in elderly persons with accompany- 
ing arterio-sclerosis or similar changes, these phenomena are not apt to be striking. 

Aortic insufficiency is a comparatively favorable form of heart disease, since 
it may be almost perfectly compensated for years by hypertrophy of the left 
ventricle. Many patients with moderate aortic insufficiency feel perfectly well, 
and are even capable of quite hard work. They have not the slightly cyanotic 
hue which almost all patients with mitral disease exhibit, but they have a nor- 
mal or even a pale complexion. If, however, the signs of disturbed compensa- 
tion once appear in aortic insufficiency the severest sequelae may develop quite 
rapidly. In aortic insufficiency it is exceptional to see such repeated changes 
from bad to good, and good to bad, as are often observed, for instance, in mitral 
stenosis. If the left ventricle becomes enfeebled, it can no longer satisfy the 
excessive demands made upon it. Passive congestion ensues, extending back- 
ward through the pulmonary circuit into the systemic veins, even while the pulse 
may still seem to be powerful. The average arterial tension becomes subnormal, 
dyspnoea increases, and there are attacks of cardiac asthma. (Edema appears, 
and the patient dies with the symptoms of anasarca. We will speak more fully 
below of certain intercurrent events in aortic insufficiency, such as cerebral haem- 
orrhage and pericarditis. 

4. Stenosis of the Aortic Orifice 

Except for the mild forms of aortic stenosis, which often come on with aortic 
insufficiency, aortic stenosis is a rare disease. It arises from marked thick- 
enings and calcifications, and especially from adhesions of the aortic valves to 
one another. The stenosis may become so considerable that the orifice is finally' 
reduced to a mere fissure, through which the left ventricle must force the blood 
at its systole. The fluttering of the valves and the vertiginous movements in the 
blood thus arising produce a loud systolic murmur. The left ventricle is com- 
pelled to do greater work in consequence of the increased resistance of the aortic 
orifice, and hence becomes hypertrophied. In spite of the increased effort, how- 
ever, comparatively little blood reaches the arterial system, and consequently the 
radial pulse is small and the arteries contracted. 

Inspection and Palpation. — Upon physical examination of the heart we find, 
in the first place, the apex-beat displaced outward as a result of the hypertrophy 
of the left ventricle, and also often more powerful than normal. It may, how- 
ever, be noticeably feeble, perhaps because of the slowness of the systole. A 
former explanation of this feebleness was the diminution of the recoil of the 
apex (the Gutbrod-Skoda theory of the apex-beat). 

Percussion. — Percussion gives an extension of the heart's dullness to the left. 
The right ventricle is also dilated and hypertrophied to a moderate degree in the 
later stages, if the stasis extends backward through the pulmonary circulation. 

Auscultation. — On auscultation, we hear over the aorta a very loud " sawing," 
long-drawn, systolic murmur, which is usually transmitted to the right, corre- 



VALVULAE DISEASE OE THE HEAET 



321 



sponding to the course of the aorta, in distinction from the diastolic murmur of 
aortic insufficiency. It is usually to be heard loudest at the sternal end of the 
second right intercostal space, but it is audible to a lesser extent over almost the 
whole heart. It is usually quite loud over the carotids. The systolic sound at 
the apex is apt to be feeble. The second aortic sound is likewise faint or even 
inaudible. If there is co-existing insufficiency of the valve, the second aortic 
sound is replaced by a diastolic murmur. 

The pulse has been already described. It is small, and often surprises one by 
its contrast with the strength of the apex-beat. In well-compensated cases it is 
regular, and often moderately or even extremely slow. This slow pulse of aortic 
stenosis is often explained as a compensatory change in the heart's action, appro- 
priate to the existing- lesion — the systole being lengthened, an increased amount 
of blood can be driven through the narrow aortic orifice. But the slowing of the 
cardiac action is really, in main part, a prolongation of the diastole, and there- 
fore the slow pulse is probably due chiefly to the fact that the wall of the left ven- 
tricle is ill-supplied with blood, just as in the case of sclerosis of the coronary 




Fig. 41. — Pulse curve in stenosis of the aortic orifice. 



arteries. The sphygmographic tracing of the radial pulse (see Fig. 41) shows a 
low wave and a comparatively slow rise and fall. 

Aortic stenosis of slight or moderate degree may be tolerably well borne by 
the patient. We have even seen a man with well-marked aortic stenosis who 
for years did not have the slightest subjective symptoms of heart-disease, until 
he finally died with an acute recurrent endocarditis. When the stenosis is more 
complete we sometimes have a most peculiar clinical picture. The pulse is very 
infrequent, as low as thirty to twenty-four beats in a minute. From time to 
time there are attacks of vertigo or syncope, the patient often falls, and has epi- 
leptiform attacks. These seizures, which may be repeated for months or even for 
some years, are probably connected with a sudden anaemia of the heart and brain. 
We have observed this remarkable group of symptoms particularly in elderly per- 
sons with aortic stenosis, due to arterio-sclerosis. In other respects the course of 
aortic stenosis is similar to that of the acute valvular diseases, and in the same 
way terminates in general circulatory derangement with its results. 

5. Insufficiency of the Tricuspid Valve 

Insufficiency of the tricuspid valve is extremely rare as an independent dis- 
ease of the heart, but a secondary insufficiency of the tricuspid is quite fre- 
quent, and is therefore of practical interest, as it complicates other already-exist- 
ing valvular diseases in the left side of the heart. It arises either from a sec- 
ondary endocarditis, affecting the tricuspid, in quite an analogous manner with 
mitral insufficiency, or it is a so-called relative insufficiency. This name we give 
to that form of insufficiency which develops when the edges of the tricuspid valve, 
normal in themselves, at last fail to meet one another, from the increasing dilata- 
tion of the right ventricle, or at any rate from the inability of the enfeebled right 
ventricle properly to close the valve. 

The necessary result of tricuspid insufficiency is, that in every systole of the 
right ventricle a backward current passes through the open tricuspid orifice into 
the right auricle, and thence into the veins of the body. The tricuspid insuffi- 
ciency ensuing in other forms of heart disease must therefore increase the stasis 
21 



322 



DISEASES OF THE CIECULATOEY ORGANS 



in the veins of the body, and it is thus far an unfavorable complication. It has a 
compensatory significance only as it affords relief to the pulmonary circulation. 
Since a part of the blood passes back from the right ventricle into the veins, 
less blood than usual must reach the pulmonary arteries. The decrease in ten- 
sion thus produced in these arteries makes itself apparent on auscultation, since 
the accentuation of the pulmonic second sound in valvular disease of the mitral 
orifice diminishes when tricuspid insufficiency takes place. 

That tricuspid insufficiency must result in a hypertrophy of the right ven- 
tricle is explained in just the same way as the hypertrophy of the left ventricle 
in mitral insufficiency, from the increased influx of blood at increased tension 
into the right ventricle during diastole; but this effect of tricuspid insufficien- 
cy can rarely be made out in any individual case, since the right ventricle is usu- 
ally already hypertrophied as a result of the disease in the left side of the 
heart. 

The most important symptom from which we can diagnosticate tricuspid in- 
sufficiency is the venous pulse. The cause of this is the backward wave of blood 
produced at each systole of the right ventricle. So long as the venous valve 
above the bulbus jugularis is closed, we usually see only a " bulbar pulse," but 
very soon this valve also yields to the continued impulse of the blood, and then 
a strong, purely venous pulse is visible along the whole course of the jugular 
vein up to the vicinity of the mastoid process. The contraction of the right 
auricle very often causes a decidedly weaker elevation of the vein, which just 
precedes the marked pulsation caused by the ventricular systole (anadicrotic 
venous pulse) . On account of the straighter course of the right innominate vein, 
the jugular venous pulse is often stronger on the right side than on the left. We 
must state, however, that the jugular venous pulse is not an absolutely certain 
sign of tricuspid insufficiency, since it may arise in hypertrophy of the right side 
of the heart without any insufficiency of the tricuspid, from the closure of the 
valves. 

If there is pulsation in the bulb of the jugular vein and the jugular valve is 
still capable of closing, a low, audible, venous, valvular sound may be produced by 
its closure. A sound may also arise in tricuspid insufficiency, as has been already 
said, from the tension of the valves in the femoral vein. A visible pulsation in 
the larger veins of the extremities is very rare, but in tricuspid insufficiency we 
quite frequently feel a venous pulsation in the liver, which organ is usually en- 
larged by passive congestion. This may be quite apparent even in many cases 
in which the jugular venous pulse is absent, because the veins in the liver are 
without valves. [It is best appreciated by means of bimanual palpation. — V.] 

Auscultation over the right side of the heart gives a systolic murmur in insuffi- 
ciency of the tricuspid, arising from the regurgitating blood-current. This may 
be heard loudest over the lower part of the sternum, or at the sternal end of the 
right fifth rib. The significance of this murmur in diagnosis, however, is im- 
paired by the fact that it can not always be separated from the systolic mitral 
murmur that often co-exists. , 

6. Stenosis of the Tricuspid Orifice 

Stenosis of the tricuspid orifice is an extremely rare disease, and hence it is 
without practical significance. It has usually been observed, up to the present 
time, as a congenital form of heart disease, almost always combined with other 
anomalies of development in the heart. 

The physical signs of tricuspid stenosis can easily be constructed theoretically. 
The first result must be a marked dilatation of the right auricle, and the occur- 
rence of a diastolic or presystolic murmur over the right side of the heart. From 



VALVULAK DISEASE OF THE HEAKT 



323 



the rarity and complex character of the cases, however, we have so far seldom 
had an opportunity to confirm these theories at the bedside. 

The prognosis of this form of heart disease is very unfavorable, since a long- 
continued compensation by increased labor on the part of the right auricle is 
scarcely conceivable. 

[Seventy cases of tricuspid stenosis have been collected by Bedford Fenwick, 
whose analysis affords good grounds for thinking that the lesion is often ac- 
quired. In fifty per cent, of the cases there was a clear history of rheumatism, 
and nearly all of the patients were more than twenty years of age at the time of 
death. 

This lesion is never found alone, but invariably combined with mitral stenosis ; 
all but eight of the cases were in women. Fenwick thinks that the influence of 
sex lies in the less onerous nature of the work of women than of men, the granu- 
lating edges of the valves being kept more in apposition, thus healing with adhe- 
sion and causing obstructions at the orifice.] 

7. Insufficiency of the Pulmonary Valve 

Insufficiency of the pulmonary valve is also a very rare form of heart disease. 
It occurs as a congenital anomaly, often combined with other failures of develop- 
ment, or as a disease acquired after birth. The anatomical changes in the valve, 
which lead to insufficiency, are precisely analogous to those which cause insuffi- 
ciency of the aortic valve. 

The physical signs of this form of valvular disease consist chiefly of a marked 
dilatation and hypertrophy of the right ventricle, to be made out by percussion, 
and of a loud diastolic murmur over the pulmonary valve. These signs are 
explained in just the same way as the precisely analogous signs in the left ven- 
tricle in aortic insufficiency. 

In general, pulmonary insufficiency, like aortic insufficiency, seems to be com- 
pensated quite well for a long time by hypertrophy of the right ventricle. In 
many cases a co-existing patency of the foramen ovale also seems to be of favor- 
able influence, as it lessens the stasis in the right auricle and the veins of the 
body, while it renders easier the filling of the left ventricle. 

8. Stenosis of the Pulmonary Orifice (Pulmonary Stenosis) and the other 
Congenital Diseases of the Heart 

1. Congenital Pulmonary Stenosis. — While the stenosis of the pulmonary 
orifice acquired in later life is so rare that it has only slight practical signifi- 
cance, the congenital pulmonary stenosis is of far greater importance. It is, 
on the whole, the most frequent of the congenital forms of heart disease. Its 
origin is to be referred either to an endocarditis of the pulmonary valves during 
foetal life, or to anomalies in the development of the heart. The stenosis is often 
situated not merely at the pulmonary orifice itself, but farther back in the conus 
arteriosus, which seems to be narrowed by the formation of myocardial cicatrices. 
The pulmonary artery is often also narrowed as a whole. In the majority of 
cases we find, in addition, other anomalies of development in the heart, espe- 
cially patency of the foramen ovale, great defects in the ventricular septum, and. 
in about half the cases, patency of the ductus Botalli, etc. 

The symptoms of congenital pulmonary stenosis sometimes appear soon afte* 
the birth of the child. The first thing that strikes us is the marked cyanosis, 
which is constant, or else comes on with crying, or with movements of the body. 
Many children, however, reach a fair age, five or ten years, or even fifteen. In 
some cases the heart disease may be so perfectly compensated that the child may 



324 



DISEASES OE THE CIRCULATORY ORGAXS 



be comparatively well for a time, and severe disturbances may not appear for 
several years. 

As a rule, children with congenital pulmonary stenosis present a very strik- 
ing appearance. The cyanosis is especially noticeable in the face, the lips, the 
nose, and the hands and nails. The parts mentioned feel cool. The eyes are 
often somewhat prominent, and there is a slight cedematous swelling about them. 
The peculiar club-like thickening of the terminal phalanges of the fingers and 
toes, a result of stasis, as seen also in many cases of bronchiectasis, is very char- 
acteristic. The nails also present a characteristic claw-like curvature. 

The whole development of the child is remarkably retarded. It often seems 
several years younger than it is. The muscles and fatty layer are slight. The 
gums are sometimes very spongy and disposed to bleed. In severe cases the child 
suffers from faintness, vertigo, etc. 

On physical examination of the heart, we usually find the cardiac region 
rather prominent. Percussion gives an increase of the heart's dullness, especially 
toward the right. This extension of the dullness is due to the hypertrophy of the 
right ventricle, which must arise in the same way as hypertrophy of the left ven- 
tricle in aortic stenosis. On auscultation, we hear a loud systolic murmur, which 
is perceptible over the whole heart, but which has its greatest intensity at the 
sternal end of the second left intercostal space. The eddies of blood, which pro- 
duce the murmur, may also often be felt by the hand as a systolic thrill. In some 
cases, however, we miss the murmur in pulmonary stenosis, just as in mitral ste- 
nosis. The pulmonic second sound is weak or inaudible, or it is replaced by a 
murmur if there is also insufficiency of the valve. 

The course of congenital pulmonary stenosis is always unfavorable. As has 
been implied, few children get beyond the age of fifteen years. Death ensues, 
either with general disturbances of compensation evidenced by dyspnoea and 
dropsy, as in every other form of heart disease, or from complications. Among 
the latter, we may mention especially the very frequent development of phthisis. 

2. The Remaining Congenital Lesions of the Heart. — Inasmuch as other con- 
genital lesions than pulmonary stenosis have but slight clinical importance, we 
will limit ourselves here to a brief review of the same* 

(a) Patency of the foramen ovale is a comparatively frequent lesion, whether 
alone or combined with others. Physical signs are mostly absent. In a few 
cases a presystolic murmur has been heard. When mitral insufficiency co-exists 
with a patent foramen ovale, venous pulsation may be caused. 

(h) Defects in the septum between the ventricles. These are most frequently 
situated in the posterior section of the anterior septum, and they likewise are 
associated with other anomalies, such as abnormal distribution of the arteries, 
pulmonary stenosis, or defects in the septum between the auricles. Sometimes the 
patency of the septum gives rise to a systolic murmur, but a diagnosis of the con- 
dition during life is scarcely ever possible. 

(c) Persistence of the ductus Botalli. Inasmuch as this contributes blood 
from the aorta to the pulmonary circulation the pressure in the latter is raised, 
hence there is to be observed accentuation of the second pulmonic sound and 
hypertrophy of the right ventricle. There is sometimes also a loud systolic 
murmur. 

(d) We have already spoken of congenital stenosis of the tricuspid valve. 
Congenital narrowing of the mitral valve and of the aortic valves may also occur, 
but they are extremely rare. 



* A more extensive presentation of the subject can be found in the article by Kauchfuss in Ger- 
hardt's "Handbuch der Kinderkrankheiten," vol. iv, and in text- books on pathological anatomy— 
for example, Orth's. 



VALVULAR DISEASE OE THE HEART 



325 



9. Combined Valvular Diseases of the Heart 

Al though, in what has preceded we have dealt with the several forms of valvu- 
lar disease of the heart separately, in order to present them in a general way, 
yet in reality combinations of them often occur in great variety. We find 
especially, as has already been mentioned, stenosis of an orifice co-existing with 
insufficiency of the accompanying valve; but diseases of two or more different 
valves are not infrequent, combined in the most diverse manners. The physical 
signs of these " combined forms of heart disease " may, of course, be inferred from 
the signs of anomalies of single valves, but the phenomena are often so compli- 
cated that the diagnosis of combined heart disease is generally much harder than 
that of the simple forms. Sometimes the single forms neutralize one another in 
their action. Eor example, the left ventricle is usually small in pure mitral ste- 
nosis, but, if aortic insufficiency be also present, it is nevertheless found dilated, at 
least to a certain degree. The influence of an absolute or relative tricuspid insuf- 
ficiency on the action of mitral disease, especially the decrease in tension in the 
pulmonary vessels caused by it, and also the diminished accentuation of the pul- 
monic sound, have been mentioned above. 

In reference to the clinical symptoms of combined heart disease we may say, 
on the whole, that, in a large number of cases, the disease of one valve stands out 
as predominant in the whole picture of the disease. The other anomalies are only 
slightly noticeable, and often of later date. Hence, we may find at the autopsies 
of patients, who during life have shown the symptoms of disease of only one 
particular valve, unimportant changes on the other valves, which have been with- 
out clinical significance. 

General Comparison of the most Important Physical Signs in Valvular Disease 

of the Heart 



Form of 
Heart Disease 



1. Mitral in- 
sufficiency. 

2. Mitral 
stenosis. 



3. Aortic in- 
sufficiency. 



Inspection. 



4. Aortic 



Strong apex-beat, 
often somewhat 
displaced out- 
ward. 

Area of cardiac im- 
pulse enlarged, 
epigastric pulsa- 
tion. • 



Apex - beat very 
strong, displaced 
downward and to 
the left. Visible 
pulsation of the 
medium - sized 
and smaller ar- 
teries. 



Apex - beat dis- 
placed to the 
left. 



Palpation. 



Systolic thrill 
at the apex. 
Quite strong 
radial pulse. 

Diastolic thrill 
at the apex. 
Small and oft- 
en irregular 
pulse. 



Very strong, 
heaving apex- 
beat. Pulsus 
celer. 



Heart's action 
not very strong. 
Pulse small, in- 
frequent, some- 
times slow. 



Percussion. 



Hypertrophy of 
the left, later 
of the right 
ventricle. 

Hypertrophy of 
the right ven- 
tricle. 



Marked hyper- 
trophy of the 
left ventricle. 



Hypertrophy of 
the left ven- 
tricle. 



Auscultation. 



Loud systolic murmur 
at the apex. Pul- 
monic second sound 
accentuated. 

Diastolic or presys- 
tolic murmur at the 
apex. First sound 
sometimes loud. 
Pulmonic second, 
sound accentuated, 
and sometimes dou- 
ble. 

Loud diastolic aortic 
murmur, especially 
over the upper part 
of the sternum. 
Sounds in the ar- 
teries (femoral and 
brachial sounds, 
etc.). Sometimes a 
double sound or 
double murmur in 
the femoral. 

Loud systolic aortic 
murmur, transmitted 
to the right. 



326 



DISEASES OF THE CIRCULATOKY ORGANS 



[Bramwell reports that of 131 cases with macroscopic valvular lesion, the tri- 
cuspid was implicated in 33.58 per cent.; in all but 12 per cent, of these the 
changes were recent. Hence he thinks that tricuspid endocarditis is generally 
recovered from, and this he attributes to the relatively small strain to which that 
valve is subjected. The obvious therapeutic deduction is the importance of rest 
in mitral endocarditis.] 

General Sequels and Complications of Valvular Disease of the Heart 
After having discussed, in what precedes, the mechanism of the single forms of 
valvular disease, and the physical signs derived from it, we must now describe a 
number of symptoms and sequelae which may be present to a greater or less degree 
in all forms of valvular disease. With them we must also mention certain pecul- 
iarities of the individual forms. 

1. Subjective Symptoms. — Fully compensated heart disease may exist, at least 
for a long time, without any subjective symptoms. This is especially the case in 
aortic insufficiency, more rarely in mitral insufficiency. Stenosis of the mitral 
or of the aortic valves almost always causes subjective symptoms. These symp- 
toms often do not exist so long as the patient keeps perfectly quiet physically and 
mentally, but they develop under appropriate circumstances, especially upon bod- 
ily exertion. 

The existing subjective symptoms in heart disease are by no means always 
referred, in the first place, to the heart itself. It sometimes happens that the 
patient comes to the physician complaining of various digestive disturbances, or 
in other cases of headache, vertigo, etc. The physical examination alone leads us 
to recognize the heart disease. As a rule, the patient's first and chief complaint 
is directed toward his difficulty in breathing. The shortness of breath, which 
increases on any physical exertion, comes on quite early in many cases. In the 
later stages it is almost always the most distressing symptom. The causes of 
dyspnoea in heart disease are manifold. In the first place dyspnoea results from 
congestion of the pulmonary circuit, with consequent slowing of the circulation 
in the lungs, and limitation of the exchange of gases in those organs. In later 
stages the anatomical changes in the lungs contribute also to an increase of the 
dyspnoea (vide supra, the chapter on brown induration of the lungs). Basch 
ascribes special importance to the fact that the distended capillaries encroach 
upon the alveoli, as a result of the passive congestion. This broadens the alveoli 
("swelling of the lungs"), but at the same time impairs the mobility of the 
lungs (" rigidity of the lungs "), and thus embarrasses the exchange of gases in 
the lungs, just as in emphysema. Further investigations are necessary in order to 
determine the clinical importance of these conditions. 

The secondary bronchitis of heart disease is a very great factor in the dysp- 
noea. This bronchitis is a frequent result of the pulmonary stasis. Often the 
respiratory distress increases and decreases simultaneously with corresponding 
variations in the bronchitis. A purely mechanical cause of dyspnoea is the com- 
pression of the lower portion of the left lung by great cardiac hypertrophy. The 
highest grade of dyspnoea is reached when finally hydrothorax, hydropericardium, 
and pulmonary oedema are developed. From what has already been stated, it is 
easy to see why lesions of the mitral valve which directly impair the pulmonary 
circulation lead sooner to shortness of breath than do lesions of the aortic 
valves. Finally, it is self-evident that the condition of the heart has the great- 
est influence upon the degree of dyspnoea present, for all the phenomena of 
pulmonary congestion must increase or diminish, according to the functional 
integrity of the heart, and particularly of the left ventricle. If the contractile 
power of the left ventricle grows less, dyspnoea must at once increase. ~Not 
infrequently conditions of cardiac weakness develop with considerable sud- 



VALVULAK DISEASE OF THE HEAET 



327 



denness, and occasion attacks of dyspnoea which are .termed cardiac 
asthma. 

Palpitation is the first subjective symptom to be mentioned of those which 
are referred directly to the heart. It is not yet accurately determined under 
what circumstances the action of the heart is perceived by the patient himself. 
We sometimes see an uncommonly strong action of the heart, as in aortic insuffi- 
ciency, which is not perceived at all subjectively. In other cases, where objec- 
tively the heart is not especially active, palpitation forms the patient's chief 
complaint. It usually first appears when the heart disease ceases to be fully 
compensated. It is increased or first excited by physical exertion or mental 
excitement. In many patients attacks of palpitation occur without any discover- 
able external cause, due apparently to nervous disturbance. They are sometimes 
associated with a striking acceleration of the pulse, the so-called tachycardia. 

Pain in the cardiac region is only rarely present in heart disease. The patients 
more frequently complain of an indefinite feeling of pressure and oppression in 
the chest, but still there do occur, particularly in aortic insufficiency, attacks of 
violent pain in the front part of the chest and the region of the heart, radiating 
to the shoulders and arms, and associated with a general feeling of extreme anx- 
iety and weakness. Such conditions are termed angina pectoris, or attacks of 
stenocardia (vide infra). Pains in the epigastrium and abdomen, which some- 
times form the chief annoyance of the patient, usually depend upon passive con- 
gestion of the liver (vide infra), or upon the tension of the abdominal walls from 
ascites, oedema, etc. 

We must finally mention here the rheumatoid pains in the joints and muscles, 
from which many patients with heart disease suffer. 

The greatest subjective distress occurs in the last stages of heart disease, when 
general dropsy develops. The patient's helplessness usually culminates. All 
motions of the body are difficult, the dyspnoea and oppression in the chest ^con- 
stantly increase, until death finally releases the patient from his mournful' con- 
dition. 

2. Sequelae in the Heart Itself. — We have already discussed the most impor- 
tant sequelae of valvular disease in the heart itself, its hypertrophies and dilata- 
tions. It remains for us to describe the influence of the cardiac disease on the 
frequency and regularity of the heart's action, and also to discuss some secondary 
diseases of the cardiac muscle and of the pericardium. 

In every well-compensated heart disease the heart's action may for a long time 
be of approximately normal frequency and regularity. We often find a constant 
and moderate acceleration of the pulse, which is easily increased from temporary 
causes. Obviously this increase in the number of heart-beats is often compensa- 
tory. If the left ventricle receives during diastole less blood than normal — for 
example, in stenosis — there is such an increase in the frequency of the cardiac 
contractions that the same amount of blood reaches the various organs in a given 
interval of time as before. Diminution of the pulse-rate (bradycardia) is ex- 
ceptional in valvular heart disease, except when it is artificially caused by large 
doses of digitalis. It is most frequent in aortic stenosis, and here perhaps it 
has a compensatory effect (vide supra). Marked changes in the rate of the pulse 
are due to severe disturbances of the nervous apparatus of the heart, and hence 
they are often associated with arhythmia. Under such circumstances, the pulse- 
rate may be as high as 120-140 beats per minute. A rare but interesting symptom 
is the sudden onset of attacks of enormous rapidity of the pulse, up to 160-200 
beats and more (tachycardia). This is especially connected with mitral lesions. 
In the intervals the action of the heart is quiet, with approximately complete 
compensation of the cardiac lesion. The acceleration of the pulse occurs rather 
suddenly, and is usually associated with a subjective sensation of palpitation and 



328 DISEASES OE THE CIKCULATOEY OKGAHS 



distress. It may last several hours and then vanish, usually with the same sudden- 
ness. The exact cause of these attacks is unknown. They suggest a temporary 
paralysis of the inhibitory apparatus of the heart. Very often a well-marked 
acute dilatation may be demonstrated by percussion, during the attack of tachy- 
cardia. 

Arhythmia of the heart is of still greater importance than anomalies of the 
pulse-frequency. It always points to a severe disturbance of the nervous appa- 
ratus of the heart. The general circulatory disturbance which follows every valv- 
ular disease must of course make itself felt in the heart itself, and the nerves and 
ganglia of the heart can not remain undisturbed by it. Hence we generally see 
marked variations in the frequency and rhythm of the heart's action along with 
the other signs of beginning disturbance of compensation; but daily clinical 
experience teaches us that there is not a perfect parallelism between the two symp- 
toms. We find often enough in heart disease a considerable irregularity of the 
pulse without any of the other signs of marked disturbance of compensation, and, 
on the other hand, we see in many patients an almost perfect regularity of the 
pulse up to death. In mitral disease, especially in mitral stenosis, arhythmia of 
the heart is much more frequent than in aortic disease. 

We can not enter here into a complete discussion of the special varieties and 
symptoms of arhythmia. A distinction is made between the irregular pulse, in 
which the successive beats are separated by irregular intervals, and the unequal 
pulse in which the separate waves are of unequal height. In reality, both phe- 
nomena are often associated, for when the pulse is more rapid the left ventricle 

is imperfectly filled during diastole, and the pulse 
is consequently smaller. The irregularity of the 
cardiac activity may be extreme (delirium cordis) ; 
or it may be so modified as to have a certain pe- 
riodic regularity of its own (allorhythmia). One 
of the most important and frequent forms of 
allorhythmia is the pulsus bigeminus (see Fig. 
Fig. 42.— Pulsus bigeminus. 42). In this there is first a vigorous systole and 

then, before the ventricular diastole is completely 
finished, a second weaker contraction, followed by a pause. We feel alter- 
nately a strong and quite weak pulse. The latter may be imperceptible, so 
that it can be made out only by the sphygmograph. In such cases, with co-ex- 
isting tricuspid insufficiency, we sometimes find the number of the venous pul- 
sations twice as great as the number of the radial pulsations, because the sec- 
ond weaker contraction "of the heart produces a visible venous pulse, but not 
an appreciable radial pulse. It is possible that in such cases we may have 
to do with an unequal contraction of the two halves of the heart, the right 
ventricle contracting vigorously, and the left feebly. If we listen to the heart 
when there is a pulsus bigeminus we hear four sounds in quick succession, the 
first two corresponding to the distinct radial pulse, the next two to the close- 
following systole of the heart which does not give rise to a distinguishable pulse. 
Continuous and regular pulsus bigeminus, as depicted in the preceding figure, is 
an infrequent phenomenon, but we very often have a few beats of this character 
at brief irregular intervals. It is certainly the most frequent cause of the inter- 
mittent pulse. The fingers on the radial artery from time to time fail to distin- 
guish any pulse whatever, or else they perceive it merely as a short wave, closely 
following the preceding pulse ; but if we listen to the heart at the same time, we 
recognize that four audible heart sounds correspond to every intermission of the 
pulse. On the whole, the pulsus bigeminus is a bad sign, since it always points to 
a marked disturbance of the cardiac innervation ; but it may also pass away again 
and give place to a regular action of the heart. 













o - v \ 



VALVULAR DISEASE OF THE HEART 



329 



Chronic valvular disease of the heart is often combined with anatomical 
changes in the cardiac muscle, and sometimes in the pericardium. 

Among the changes in the cardiac muscle, cloudy swelling, and especially fatty 
degeneration of the muscular fibers, are the most frequent. The fatty degenera- 
tion of the muscle occurs either in a diffuse form, or in little yellowish spots, 
which are plainly visible on the papillary muscles and trabecule. The opinion 
has often been expressed that fatty degeneration of the muscles is the cause of 
the disturbance of compensation; that the cardiac muscle performs its increased 
work until fatty degeneration ensues and reduces its strength. This theory does 
not entirely correspond to the facts. We have often seen the greatest disturbance 
of compensation in valvular disease when section of the cardiac muscle showed 
no fatty degeneration ; and, on the other hand, we have seen great fatty degenera- 
tion of the heart, as in pernicious anaemia, when there were no signs of cardiac 
weakness during life. Anatomically, with our present aids to research, we can 
hardly ever decide with certainty whether the cardiac muscle is still capable of 
performing its normal functions or not. The usual state of the case is probably 
this, that fatty degeneration of the cardiac muscle is a result of the disturbance 
of compensation, and especially of the deficient supply of arterial oxygenated 
blood to the muscle (see the chapter on anaemia). 

There is as truly a passive congestion of the heart as there is a passive con- 
gestion of the liver and kidneys. The circulatory disturbance in the heart itself 
is the chief cause of cardiac insufficiency, and the phenomena of disturbed com- 
pensation. 

A frequent affection of the cardiac muscle in valvular disease is the presence 
of cicatricial changes and so-called myocarditic nodules in the substance of the 
heart. Chronic endocarditis may directly invade the subjacent parts of the car- 
diac muscles and set up a chronic inflammation there,- but the cardiac cicatrices 
usually have another origin. The connective-tissue thickening beneath the endo- 
cardium is the result of a simple atrophy of the superficial muscular fibers due to 
the increased internal pressure of the blood, as in mitral or aortic insufficiency. 
The connective-tissue nodules within the cardiac muscle, however, depend in part 
upon a deficiency in the local supply of arterial blood. Simple sclerotic thickening 
of the coronary arteries, or complete embolism or thrombosis of a small branch 
of one of them, is the evident cause of these circumscribed cicatrices. On the 
other hand, it is also probable that disease of the myocardium is associated with 
the endocarditis, and is referable to the simultaneous action of the same causes, 
such as the infection of articular rheumatism, diphtheria, and syphilis. On care- 
ful microscopic examination we find, in almost all cases of valvular disease, quite 
extensive changes in the myocardium (Krehl), and in many cases these may cer- 
tainly impair the functional powers of the Jieart. Still, we often find cicatrices 
of myocarditis without any signs of a previous disturbance in the compensation 
of the heart. A fuller discussion of this subject will be found in the next chapter. 

Pericarditis is not very rare as a result of chronic valvular disease. It is 
always a dangerous complication, and it may cause death. Regarding its origin, 
we have found that almost all the cases of heart disease complicated with peri- 
carditis show changes in the aortic valves. Hence it does not seem improbable to 
us that the secondary pericarditis in such cases is sometimes due to a direct 
invasion of the pericardium, by the excitants of inflammation passing from the 
aortic valves through the walls of the blood-vessel. 

3. Symptoms of Stasis in the Different Organs of the Body. — As has fre- 
quently been mentioned in what precedes, the results of stasis of the blood make 
themselves manifest in heart disease in various organs. We have already spoken 
of the important results of blood stasis in the heart itself and the lungs. It re- 
mains for us to discuss the symptoms of stasis in the systemic veins. 



330 



DISEASES OF THE CIRCULATORY ORGANS 



As soon as the flow of Tenons blood into the right side of the heart is hindered, 
the venous stasis is shown by the cyanotic appearance of the patient. This 
cyanosis may exhibit any degree. In heart disease which is still, on the whole, 
well compensated, it is recognized only by the practiced eye of the physician as 
a slight bluish tinge of the lips, the alse of the nose, the cheeks, or the nails. 
With the increase of the disturbance of compensation the cyanosis increases, if 
it be not modified by the co-existence of general anaemia. In mitral disease, 
especially in mitral stenosis, the cyanosis is usually more marked than in aortic 
disease. The large veins, also, become plainly visible as a result of their complete 
filling, especially the large external jugulars. 

A further important symptom which follows the venous stasis is the oedema, 
the dropsy of heart disease. As we know from general pathology, every venous 
stasis, if it reaches a certain grade, leads to a transudation of the fluid of the 
blood from the capillaries. If the lymphatics can no longer carry this transuda- 
tion away, it collects in the meshes of the tissues and leads to oedema. The 
oedema of heart disease, therefore, does not appear until the venous stasis has 
reached a certain degree, and the compensation of the heart disease has become 
impaired. It first appears in those parts where there is a particularly loose 
tissue, as in the scrotum, or where mechanical conditions favor its development. 
The legs usually swell first, especially about the ankles, because here the stasis 
of the venous blood is increased by gravity. At first, slight oedema appears only 
temporarily and by day, and disappears again while the patient is in bed at night ; 
but, as the disturbance of compensation increases, the oedema also constantly grows 
worse, especially in the dependent parts of the body, until finally it may reach the 
highest degree of dropsy. Besides the oedema of the skin, transudations into the 
internal cavities occur, especially into the abdomen and the pleural cavity. 

The relation between the degree of cutaneous oedema and the amount of drop- 
sical transudation is variable ; thus, in particular, we may have a large amount of 
ascites, with only moderate swelling of the legs. This is probably occasioned in 
most cases by special secondary changes in the liver (vide infra). 

The patient's distress is decidedly increased by marked oedema, as has already 
been said. All the motions of the swollen extremities are considerably impeded. 
Hydrothorax and ascites increase the dyspnoea, the former by compression of the 
lungs, the latter by upward pressure on the diaphragm. The passage of urine may 
be rendered very difficult by oedema of the prepuce. Besides that, we must men- 
tion that the skin, when very cedematous, is quite apt to become the seat of 
furuncular and erysipelatous inflammations. 

The results of stasis in the internal organs may be best seen in the liver, 
spleen, and kidneys. 

Passive congestion of the liver is manifested by quite a considerable increase 
in the size of the organ. The lower boundary of the liver dullness extends 
several fingers' breadth beyond the edge of the ribs, and the anterior surface and 
lower border of the liver may often be plainly felt. The liver may also be 
enlarged in cases in which there are no other marked signs of passive congestion, 
such as dropsy. Quite severe pain in the hepatic region sometimes arises from the 
tension of the capsule of the liver. In later stages the liver may grow smaller 
again through a partial atrophy of the liver cells (atrophic nutmeg-liver). In- 
deed, there may even develop, as a result of the chronic congestion, a secondary 
cirrhosis of the liver, with a distinctly granulated surface. These are the cases 
in which marked ascites is especially apt to occur (vide supra). 

Slight jaundice often develops in heart disease, as a result of passive congestion 
of the liver, or perhaps sometimes from a secondary duodenal catarrh. The 
peculiar mixture of a cyanotic and slightly jaundiced hue of the skin is very char- 
acteristic in many cases, especially in mitral disease. It should be added that 



VALVULAR DISEASE OF THE HEART 



331 



the yellowish discoloration of the skin in heart disease is probably not always 
a genuine icterus, but it may be occasioned by the deposit of other pigments in 
the skin. 

Passive congestion of the spleen arises if the stasis of the blood extends to 
the splenic vein. The spleen increases in size and becomes firm and dense. It is 
often hard to make out the congestion from the increase of the splenic dullness, 
because percussion of the spleen is uncertain if there be also ascites, hydrothorax, 
etc. We can often, however, plainly feel the enlarged spleen under the edge of 
the ribs on the left. 

In the kidneys we find passive congestion, with the final development of 
" cyanotic induration." The slowness of the circulation and the diminution of 
the arterial tension in these organs lead to marked changes in the urine. In 
particular, there is a diminution in the quantity, especially if the patient is at 
the same time dropsical. The amount of urine falls as low as 800-500 cubic centi- 
metres (27-17 ounces), or even less, in twenty-four hours. It becomes dark, con- 
centrated, of high specific gravity, and abnormally acid, and hence it usually has 
an abundant sediment of urate of sodium. In marked degrees of stasis there is 
albumen in the urine as a result of the damage done to the glomerular epithe- 
lium. The amount of albumen is usually slight, but it may equal one third or 
one fourth of the volume of urine. Under the microscope we find, in the urine 
of simple passive congestion, only an occasional hyaline cast, and a few red and 
white blood-corpuscles. 

Careful examination of the urine in cases of severe heart disease is of the 
greatest practical importance, for the character of the urine as shown by the 
color, specific gravity, and amount of albumen, is an excellent index of the vigor 
of the heart and the condition of the circulation. Any change for the worse in 
the circulation is directly shown in a diminution of the amount of urine, and an 
increase in its specific gravity, or, it may be, in the appearance of albuminuria. 
Any improvement in the circulation, whether spontaneous or due to remedies, is 
shown first and clearest by an increase in the daily excretion of urine, and a cor- 
responding diminution in its specific gravity. 

We not infrequently meet with acute and chronic nephritis, particularly 
arterio-sclerotic nephritis, complicating heart disease. It is often no easy matter 
clinically to form a correct opinion about such cases. 

We may in part refer the numerous gastric and digestive disturbances, such 
as loss of appetite, vomiting, constipation, and diarrhoea, from which such pa- 
tients often suffer, to the stasis in the blood-vessels of the stomach and intestines ; 
but of course there are not infrequently diseases such as acute and chronic catarrh 
of these organs, which are to be regarded as complications. 

4. Embolic Processes. — The slowing of the circulation, and the disturbances in 
the nutrition of the walls of the vessels, which result from it, often give rise in 
heart disease to the formation of thrombi. These are situated in the heart itself, 
on the diseased valves, in the recesses between the trabecule, in the auricles, 
etc., or else they form in the veins, especially in those of the lower extremity. 
From these thrombi fibrinous plugs may easily be set loose and enter the circu- 
lation, and thus give rise to embolic processes in distant organs. Some of the 
embolisms, whose clinical relations are especially important, have been more fully 
described elsewhere, and will be mentioned only briefly here. 

Embolism of the pulmonary arteries, proceeding from venous thrombi or from 
thrombi in the right side of the heart, gives rise to hemorrhagic infarction of the 
lungs. Its pathogenesis and symptoms have already been discussed in a pre- 
vious section (see page 273). 

Embolism of the cerebral arteries is a common cause of apoplectic attacks, 
which are not infrequent in heart disease, and usually lead to hemiplegia. The 



332 DISEASES OF THE CIKCUL AT OE Y OKGANS 



anatomical cause of the hemiplegia in these cases is the embolic softening of 
the brain which ensues. The details of this are given in the section on cerebral 
diseases (see page 1103). 

Embolism of the larger arteries of the extremities, such as the femoral and the 
brachial, is much rarer than the forms mentioned. It leads to embolic gangrene 
of the extremities, unless an adequate collateral circulation can be established. 
The skin of the peripheral parts, the fingers or toes, first becomes cool, bluish, 
and at last, if the circulation be wholly checked, almost black. The gangrene 
advances slowly, usually occupying weeks. Ulcerations develop as the necrotic 
portions are thrown off. The affection is extremely painful. The patient soon 
becomes very miserable from the pain and the septic fever that usually attend 
the ulcerations, and extensive gangrene almost always ends fatally. Sometimes 
there is embolism of the abdominal aorta. This is usually located at its bifurca- 
tion, and occasions a sudden and almost complete paraplegia, speedy disturbance 
of sensation, abolition of the reflexes, and loss of electrical excitability. No pulse 
can be felt in the peripheral arteries; the feet are pale and cold, and soon there 
are signs of gangrene in both legs. The condition is probably invariably fatal. 

Embolism of the renal arteries, with consequent anaemic or hemorrhagic in- 
farctions in the kidneys, may have no clinical symptoms at all, but it is sometimes 
indicated by sudden pains in the region of the kidneys and marked hematuria 
(see page 644). 

Embolic infarction of the spleen is often marked by swelling of the spleen 
and by severe perisplenitic pains. In other cases it is wholly without symptoms. 

Embolism of a mesenteric artery is a very rare event. Its symptoms consist of 
a sudden intestinal hemorrhage, of severe colicky pains, general collapse, and 
peritonitis. 

5. Complications on the Part of the Nervous System. — The most important 
complication on the part of the nervous system — embolic softening of the brain — 
has already been mentioned. We must also state that cerebral hemorrhage may 
occur in heart disease. It is especially frequent in aortic insufficiency, either 
as a result of co-existing atheroma of the cerebral arteries, or perhaps of the ab- 
normally high tension of the vessels during systole. 

Mental disorders have been repeatedly observed in chronic valvular disease. 
They are the result of the disturbance of the circulation, and the consequent im- 
pairment of nutrition in the brain. Hence they usually make their first appear- 
ance in the last stages of heart disease, at the same time with the other disturb- 
ances of compensation. The psychoses in heart disease most frequently have the 
character of melancholia, but conditions of confusional insanity and excitement 
also occur. 

6. Secondary Affections of the Joints are not rare in heart disease. As acute 
endocarditis develops in the course of acute articular rheumatism, so, on the other 
hand, rheumatic pains in the muscles and joints, and even acute swelling of the 
joints, associated with fever, appear in the course of chronic heart disease. Some- 
times we have the complete picture of acute articular rheumatism. Probably no 
fresh infection from without is requisite for the development of these second- 
ary lesions in the joints, but under certain circumstances there is an unusual 
development of infectious germs (staphylococci?) on the diseased valves, and 
large numbers of them passing into the circulation occasion a fresh constitutional 
infection. 

7. Constitutional Symptoms. Fever. — In congenital and early acquired val- 
vular disease, the general development of the child is ordinarily much retarded. 
In heart disease in adults, however, we by no means always see an injurious influ- 
ence on the general nutrition. In many patients we even find a remarkably good 
development of fat. A marked general disturbance of nutrition, such as great 



VALVULAR DISEASE OF THE HEART 



333 



anaemia and general emaciation, often develops in the later stages, especially in 
aortic insufficiency. The wasting is of course often hidden by the oedema. 

In general, chronic heart disease runs its course without fever, but periods 
often occur in the course of the disease when there is a moderate and usually 
irregular fever. Marked disturbances of the general condition may or may not be 
associated with it. The basis of the fever is probably an acute exacerbation of 
the endocarditis, except, of course, in accidental complications. All variations 
occur, from a mild febrile movement without further symptoms to a severe acute 
recurring endocarditis (q. v.). In other cases the fever is connected with second- 
ary swelling of the joints, or with embolic processes. 

General Course and Prognosis of Valvular Disease of the Heart 

The course of valvular disease of the heart is in most cases very chronic. It 
may last for years. So long as there is a complete compensation, the patient feels 
almost perfectly well; sometimes he even has no misgivings as to his trouble. 
The slight difficulty in respiration and the incapacity for physical exertion are 
noticed, but little attention is paid to them, because the patient is used to them. 
In other cases there is a moderate disturbance for a long time, but it may be borne 
quite easily if the patient is rational and prudent in his conduct. 

We can not make any general statement as to the length of the stage of com- 
pensation, because cases differ very greatly in this respect. It depends in part 
upon the intensity of the heart disease, in part upon the external conditions 
under which the patient lives, and in part, certainly, upon the different indi- 
vidual capacity for work and power of resistance of the heart. Thus it happens 
that many cases last for decades, while in others severe sequelae appear within a 
few months. External injurious agencies, acting on the patient, are of great 
influence on the course of heart disease. Severe physical exertion, an injudicious 
manner of living, intercurrent febrile disease, mental disturbances, care, and 
anxiety are often followed by unhappy consequences. 

If the first signs of disturbed compensation appear, if severe dyspnoea, slight 
oedema of the ankles, etc., develop for the first time, these symptoms may disap- 
pear again completely under proper treatment. Severe disturbances of compen- 
sation even, great general dropsy, associated with very weak and irregular action 
of the heart, may abate, after a few weeks' duration, and the patient may feel 
quite well again. Exacerbations of the disease may come on several times and 
as often improve. Finally, of course, the improvement is incomplete. Persistent 
oedema and the other results of venous stasis ensue, the symptoms constantly 
increase in severity, especially the dyspnoea, until the patient dies after a long 
and distressing illness. Immediately before death in heart disease, certain irregu- 
larities in the innervation of the heart and in the respiration sometimes develop. 
Among these the so-called Cheyne-Stokes phenomenon deserves especial mention. 
It consists in a peculiar periodical variation in the respiratory movements. There 
will be, first, a complete pause in the respiration (apnoea), and this will be suc- 
ceeded by feeble breathing gradually becoming stronger, then gradually abating, 
and finally ending in another complete cessation of the respiration. The patient 
usually becomes more comatose during the cessation of respiration; his pupils 
contract. During the hard breathing the patient recovers somewhat, and his 
pupils dilate again. The chief cause of this rhythmical breathing is probably to 
be sought in the decided lowering of the excitability of the respiratory center. 
During the apnoea a considerable amount of carbonic acid collects in the blood 
before the respiratory center is sufficiently stimulated to resume its activity. 

We have seen the heart behave in a precisely analogous manner, but independ- 
ently of any Cheyne-Stokes respiration. There was a series of rapid but regular 
pulsations, alternating with a series of slower contractions. 



334: DISEASES OF THE CIKCULATOKY OKGANS 



In regard to the particular forms of valvular disease, aortic insufficiency gener- 
ally gives the best prognosis, inasmuch as it may be very perfectly compensated 
for many years, but if severe disturbance of compensation once occurs in this form 
of heart disease, it gives a very unfavorable prognosis, since, as a rule, we can not 
reinvigorate the heart. Mitral insufficiency is also quite a favorable form of 
heart disease, which may be compensated for a long time. Mitral stenosis is de- 
cidedly more unfavorable in its prognosis, and is associated with more disturb- 
ance; but in all mitral diseases very severe conditions may improve once or even 
repeatedly. Aortic stenosis is also capable of quite good compensation, and in this 
respect it is even more favorable for the patient than mitral stenosis, but it often 
causes persistent cerebral symptoms, such as headache and vertigo, depending on 
anaemia of the brain, or very likely upon simultaneous changes in its blood-vessels. 

Whether established valvular disease of the heart is curable is a question which 
can not be answered unconditionally in the negative. Of course in the great 
majority of cases it is in itself incurable; only its sequelae can be prevented or 
removed to a certain degree. In children and young people, however, cases some- 
times do occur, as we ourselves have seen, in which there are all the signs of a 
pronounced heart disease, but after a long time recovery is complete. Of course 
it is very hard to decide whether we really have to do with a valvular disease that 
has been cured, because simple dilatation of the heart, relative insufficiency of 
the valves, anaemic cardiac murmurs, etc., may easily be confounded with pure 
valvular disease of the heart. 

Among the dangerous intercurrent accidents in valvular disease we must make 
especial mention of embolic processes, which may occur suddenly and without 
warning. The different forms of embolism have been mentioned above, and also 
the possibility of cerebral haemorrhage in heart disease. Intercurrent acute dis- 
eases, such as typhoid and pneumonia, often, but not invariably, take a very 
severe and dangerous course in patients with heart disease, because they make 
increased demands upon the heart. 

Treatment of Valvular Heart Disease 

1. Prophylaxis. — Our means for preventing the development of heart disease 
are very limited. To avert endocarditis in articular rheumatism by the present 
method of treating acute rheumatism with salicylic acid is impossible. The proba- 
bility of the onset of endocarditis may be lessened only so far as the whole dura- 
tion of the disease is often considerably shortened by salicylic acid. 

We can also do little in the way of prophylaxis against the development of 
heart disease that is chronic from the start, since the cause of the disease is in 
many cases wholly unknown to us. Those injurious influences deserve the most 
attention which may favor the development of arterial atheroma and its conse- 
quent chronic valvular disease. The chief factors in this connection are exces- 
sive physical exertion and high living, including the use of too much alcohol 
and tobacco; but the role which these play in the development of genuine val- 
vular disease is certainly much less important than their influence upon certain 
myopathic and nervous diseases of the heart (see the following chapter). 

[There is evidence that the alkaline treatment of acute rheumatism lessens the 
danger of cardiac complications (see page 686).] 

2. Treatment of Compensated Heart Disease. — If we have to treat a heart 
disease which already exists, but which is at the same time fully compensated, our 
treatment must be chiefly hygienic. The patient must be made aware of his heart 
disease without making him needlessly anxious. He must be told that his further 
good health depends in great part upon his own conduct, his discretion, and his 
perseverance. The patient must avoid everything which makes great demands 
upon the heart, or which may have a directly injurious influence on it. All 



VALVULAE DISEASE OF THE HEART 



335 



violent bodily exertion, too intense mental work, and also all excesses in eating, 
drinking-, smoking, etc., must be avoided. That the physician's directions will 
often collide with the demands of the patient's occupation, as well as with his 
favorite amusements and his habits, should not deter the physician from demand- 
ing the fulfillment of his prescriptions, at least so far as possible. 

Treatment by drugs is usually unnecessary in compensated heart disease. We 
do not know a remedy which has a directly favorable action on heart disease. 
The protracted use of iodide of potassium, Eowler's solution, arsenite of antimony 
("granules of antimony"), etc., has been recommended. The efficacy of these 
remedies is very questionable. We can always try them, if a mild disturbance 
makes a prescription desirable and other remedies are not especially indicated. 
Beyond this, the physician is usually contented with an endeavor to improve 
the appetite and nutrition of the patient by means of iron, quinine, and bitters. 
If there is a suspicion that the heart disease may be due to syphilis, a trial of 
iodide of potash may be made, but a brilliant result from the employment of anti- 
syphilitic measures is hardly to be expected, because the mechanical imperfections 
of the valves, leading to regurgitation and stenosis, can scarcely be remedied. 

The employment of baths in heart disease deserves special consideration. Nu- 
merous experiences go to prove that they are not only well borne by patients 
with heart disease, but that they exercise a peculiarly beneficial and invig- 
orating influence upon the action of the heart. In this regard, the greatest 
reputation is possessed by the warm mud baths, which are rich in carbonic diox- 
ide, particularly those at !Nauheim. Even where there is incipient failure of 
compensation, there will be marked improvement upon the use of these or similar 
baths (e. g., Kissingen). Patients may also employ at home either simple, or, still 
better, salt baths, at a temperature of 88°-90° (25°-26° E.). Where there is no 
marked disturbance of compensation, the methodical employment of gymnastic 
exercises, the so-called Swedish movements, has a certain value in the treatment of 
heart disease. Regular muscular movements certainly promote the circulation of 
the blood, and thus lighten the task of the heart. If they are carried out cau- 
tiously and with a proper consideration of the individual case, they are not infre- 
quently beneficial. The best measure for the amount of bodily exercise for pa- 
tients with heart disease seems, to the author, to be the subjective sensation of 
dyspnoea. Any patient who has no special signs of failing compensation may 
walk at a slow pace until he experiences distinct dyspnoea. As soon as this hap- 
pens he must stand still and rest. The author regards it as a great mistake to 
encourage patients to persist in their efforts regardless of difficulty in breathing. 
We should not forget that any disturbance of the circulation which occurs must 
involve the myocardium itself in its influence. That a change of climate may 
prove beneficial is self-evident. It is particularly appropriate that patients with 
a tendency to bronchitis or rheumatism should spend the winter South. 

3. Treatment of Ruptured Compensation. — As soon as the compensatory 
activity of the heart, in a case of valvular trouble, begins to be impaired, as soon 
as there is marked dyspnoea, diminution in the excretion of urine, and oedema, we 
must promptly lighten the burden of the heart by complete bodily rest. Many 
cases, particularly of mitral disease, are completely restored, even when there are 
marked symptoms of cardiac embarrassment, by mere rest in bed with simple diet 
and without any other therapeutic measures; but if the disturbance of com- 
pensation is more marked and persistent, the physician must have recourse to 
digitalis, a remedy which possesses undoubted value when the powers of the heart 
are impaired. Digitalis has the properties of making the separate beats more 
powerful, of lowering the pulse-rate by lengthening the diastole, and above all of 
heightening the arterial tension. Digitalis is therefore indicated in every case 
of heart disease when there is persistent disturbance of compensation, and if the 



336 DISEASES OE THE CIRCUL AT OE Y ORGANS 



pulse is small, of low tension, and, above all, frequent and irregular ; the desired 
effect of digitalis is to make the pulse slower, more regular, and especially of 
higher tension. Under the influence of the increase in tension thus produced 
and of the acceleration of the circulation, the disturbances of compensation often 
disappear in a surprising fashion; there is more abundant diuresis, the scanty, 
dark, concentrated urine of passive congestion disappears, the daily amount of 
urine increases, and the urine therefore becomes clear and of lower specific grav- 
ity. The oedema then disappears, the dyspnoea ceases, the head becomes free, the 
general condition improves, and, in brief, there may again ensue a complete com- 
pensation of the heart disease. This change is sometimes accomplished in a com- 
paratively short time, in a few days or weeks. 

It is very important to prescribe digitalis in a correct manner in order for it 
to be efficient. Much experience has shown that it is best to give it at regular 
intervals of two hours, in doses of one grain and a half (gramme 0.1) of the 
powdered leaves, either in capsules or simply in water; so that the patient receives 
in the course of a day some five or six powders — that is, eight or ten grains 
(gramme 0.5-0.6) of digitalis. If the remedy is well borne we may continue it in 
this manner, but usually it is omitted during the night, to be resumed in the same 
way on the next day. As a rule, the distinct specific influence of digitalis is 
evident after the employment of ten to fifteen powders in the course of two or 
three days. This is recognized by the marked diminution in pulse-rate, the in- 
creasing strength and regularity of the pulse, and the improvement in the general 
symptoms. Instead of the powder we may employ an infusion of the strength of 
1 or 2 parts to 150 of water. Of this a tablespoonful must be given regularly 
every one or two hours. In some cases, particularly if the patient has already 
become accustomed to the remedy, we may prescribe still larger doses, up to thirty 
or forty-five grains (grammes 2-3) and even more, daily. But in every case 
digitalis should be given in regularly repeated doses, so as to obtain by their com- 
bined action the full effect of the drug. It is entirely useless to prescribe digitalis 
in small doses at long intervals. The remedy must never be prescribed unless 
we can accurately watch the pulse and the heart's action, for only thus can we 
obtain clear indications as to the further employment or the omission of the drug. 

Often some unpleasant incidental effects appear simultaneously with the bene- 
ficial influence upon the heart's action. Among these are nausea, vomiting, and 
specks before the eyes. If the digitalis is omitted these symptoms usually cease, 
while the beneficial effect upon the heart may last for a long time. With regard 
to these incidental and disagreeable symptoms, different patients vary greatly. 
Many bear digitalis very well, others very ill. Erom a therapeutic point of view 
it is particularly embarrassing if the nausea, vomiting, and other disagreeable 
symptoms appear before the digitalis has produced an effect upon the heart; but 
in such cases we should not be too hasty in abandoning the drug, especially if 
it is urgently indicated. If the patient can not bear the infusion we should 
administer the digitalis in powders, or vice versa. If the drug absolutely can not 
be given by the mouth, it should be injected into the rectum in the form of an 
infusion of the strength of 1 or 2 parts to 100 of water. This should be warmed 
to the temperature of the body and given, after a cleansing enema has been em- 
ployed, once or twice a day. The subcutaneous employment of digitalis has also 
been recommended, in the form of an infusion of the strength of 3 parts to 100, of 
which two or three syringefuls may be injected daily (tti 25-40), but with this we 
have had no personal experience. Sometimes, especially if the patient has not 
been carefully watched, the cumulative effect of digitalis is shown in severe symp- 
toms of poisoning, such as collapse, very frequent pulse, disturbance of vision, and 
dilated pupils. Then such stimulants must be employed as camphor, ether, wine, 
and strong black coffee. How often digitalis is to be used in the case of heart 



VALVULAK DISEASE OF THE HEAET 



337 



disease can be determined by experience alone. Many patients, particularly cases 
of mitral disease, may undergo treatment with digitalis twenty to thirty times 
or more, with the best results. Every time that signs of impaired compensation 
return, we must try digitalis again. It must be confessed that it will often be 
necessary gradually to increase the dose. As is the case with so many other rem- 
edies, the patient becomes habituated to the drug. There is no maximum dose, 
and we must find out by experience in each case what the satisfactory amount may 
be. Some patients become at last genuine " digitalis eaters," and are unable to 
exist without large doses of digitalis. We have ourselves seen a patient take 
seventy-five grains (grammes 5) of the powder daily. In very many cases, how- 
ever, the beneficial effect of digitalis even in the larger doses fails at last to 
appear. The remedy is no longer borne and it must be abandoned. This usually 
marks the last stage of the disease. 

ISTot infrequently we see patients with distinct symptoms of passive conges- 
tion, in whom the character of the pulse seems at first to contraindicate the 
administration of digitalis : the pulse is perhaps frequent, but regular and strong ; 
in other cases it is not rapid at all, but yet somewhat irregular; or it may be 
even infrequent and regular. Particularly in cases of aortic insufficiency is it 
often very difficult to determine whether we should give digitalis or not. With 
all patients of this sort it is, in general, worth while to make a proper trial of 
digitalis, since it may often be beneficial, and yet we should exercise especial 
caution and vigilance with regard to its effects. 

The attempt to employ the active ingredients of digitalis in a pure form 
(viz., digitaline, digitaleine, and digitoxine) instead of the drug itself, have not 
yet proved very successful. We should admit that we ourselves, in common with 
other observers, have seen good results follow the use of digitoxine. This has been 
introduced quite recently, and is to be given in tablets containing ^-fo of & grain 
(one quarter of a milligramme) every one or two hours. It has no special advan- 
tages over digitalis, but certainly deserves to be recommended as a substitute for 
digitalis when that drug is ill borne or ineffectual. Tincture of digitalis, vinegar 
of digitalis, and other preparations are far less efficient than digitalis leaves, and, 
in our opinion, may be disregarded. The best opportunity for their employment 
is when patients with slight disturbance of compensation need to take small 
amounts of digitalis persistently. 

[Digitalis is used more commonly in this country in the form of the tincture. 
The urine affords a good guide as to the safety of the continuance of the drug ; as 
long as the renal secretion is sufficient in quantity, and increasing rather than 
diminishing, there is no danger of the toxic effects. It is, consequently, a good 
plan to follow carefully the twenty-four-hour quantity of urine when this can 
be done. 

There are cases in which digitalis must be taken for long periods, but it should 
then be given only twice a day, with twelve hours' interval between the doses, 
unless the patient has ready access to his physician; there is then less risk of 
toxic symptoms. 

In mitral cases, with or without secondary tricuspid regurgitation, where the 
cyanosis and other symptoms show that the right heart is engorged with blood 
which it can not propel onward, the relief afforded by venesection, or by a dozen 
leeches in the hepatic region, may be very great. Until the veins are relieved 
either in this way or by free purgation, digitalis and stimulants are useless, and a 
resort to them results merely in a loss of time, and perhaps in the loss of a life 
which might be saved.] 

Caffeine deserves the first mention among the substances having a similar 
action, which have of late been recommended as substitutes for digitalis by Le- 
pine, Riegel, and others. Given in repeated small doses, a total of fifteen to 
22 



338 



DISEASES OF THE CIRCULATOKY ORGANS 



twenty grains a day (gramme 1.0 to 1. 5), it often slows, regulates, and strength- 
ens the activity of the heart, and also increases the arterial pressure. The salicy- 
late of caffeine and sodium is chiefly used, three to five grains (gramme 0.2 to 0.3) 
of the powder, and also the benzocitrate of caffeine in the same or smaller doses. 
The latter is also given subcutaneously. Besides caffeine, we may also mention 
here adonis vernalis, convallaria majalis, and sulphate of sparteine; but none of 
these drugs is as reliable as digitalis. 

On the other hand, in cases of simple acute or chronic weakness of the heart, 
the tincture of strophanthus sometimes proves decidedly beneficial. It is given 
in doses of ten drops several times a day. In many cases it is an excellent way 
to combine digitalis with some of the drugs already named, or with others, par- 
ticularly diuretics. Thus, for example, we may often with advantage add one or 
two parts of the tincture of strophanthus to the infusion of digitalis, or we may 
prescribe powders containing a grain and a half (gramme 0.1) of digitalis and of 
diuretine fifteen grains (gramme 1.0) in each dose, or digitalis and calomel (vide 
infra) ; or digitalis and caffeine. A combination of this sort which is often very 
efficient is the following: Infusion of digitalis, 30 grains to 5 ounces of water 
(grammes 2 to grammes 150) ; sodio-salicylate of caffeine, 30 grains (grammes 
2) ; tincture of strophanthus, 1 drachm (grammes 4) ; liquor potassii acetatis, 2 
ounces (grammes 60); syrupi aurantii, 1 ounce (grammes 30). M. S. A table- 
spoonful every two hours. 

4. Symptomatic Treatment. — Some symptoms which often occur in heart dis- 
ease demand a special description. 

Dropsy is a symptom of venous stasis, and disappears if compensation be 
restored spontaneously or by the use of digitalis. Complete rest in bed and eleva- 
tion of the swollen parts serve as the chief aid in removing the dropsy. Dropsical 
patients ought also to change their position in bed frequently, if possible, that 
there may not be too much oedema collected in the dependent portions of the body. 
It is a good plan to wrap up the swollen arms and legs with flannel bandages under 
gentle pressure. Mild massage of the cedematous parts may sometimes be of 
advantage. The amount of liquid ingested is to be limited, if possible. Of in- 
ternal remedies, besides digitalis, which should invariably be first employed, and 
drugs of similar action, the true diuretics are to be considered, such as acetate of 
potassium, acetate of sodium, and diuretine. They are sometimes ordered in 
combination with digitalis and sometimes alone, particularly when digitalis can 
not be borne or it is not indicated. Calomel is sometimes especially efficient in 
cardiac dropsy. Its diuretic influence has lately been emphasized by Jendrassik 
and others. It is prescribed in powders of three grains (0.2 gramme) three to five 
times a day. Often a very marked diuresis will be caused after one or two days, 
with rapid abatement of the dropsy. The administration of the remedy is stopped 
as soon as the diuresis begins. It is also omitted if stomatitis develops. 

We have already mentioned the advantageous combination of calomel with 
digitalis (digitalis, one grain and a half, gramme 0.1; calomel, three grains, 
gramme 0.2), five such powders daily. 

In the last stages of heart disease the patient's condition may be particularly 
distressing from the severe general oedema. It is then justifiable to remove vthe 
ascites or hydrothorax by puncture, or to let the oedema drain out by scarifica- 
tion of the skin — long incisions into the subcutaneous cellular tissue — in order 
to procure relief for the patient. The scarification of the skin, however, is dan- 
gerous, and is not to be employed without urgent indications, because erysipel- 
atous inflammation, etc., is apt to ensue at the point of incision. We can recom- 
mend little silver capillary trocars (the so-called Southey's trocars), to which a 
thin rubber tube is attached. By the aid of these trocars we can drain off large 
amounts of serum. We must always use great cleanliness, however, and the utmost 



YALYULAK DISEASE OE THE HEAET 



339 



disinfection of the skin, wrapping the parts in sterilized gauze. In patients with 
heart disease it is not, as a rule, advisable to attack the dropsy by sweating, by hot 
packs, or pilocarpine. 

The dyspnoea of heart disease is usually the most distressing symptom of all. 
Here, too, our chief task is of course to restore the compensation ; but this failing, 
we must try to relieve the dyspnoea symptomatically. Morphine is most efficient 
in this respect. In general, morphine is, next to digitalis, the most indispensable 
remedy in the treatment of severe heart disease. It is usually well borne, and 
procures great relief, especially if given subcutaneously. If we have to do with 
the last stage of the disease, we need not spare large doses. Otherwise, of course, 
caution is necessary. 

Chloral hydrate should be cautiously employed in heart disease. It is often, 
however, well borne and gives the patient rest and comfort. We have also pre- 
scribed chloralamide in cardiac cases, with good results. 

In practice we must often prescribe external applications to the chest, mus- 
tard-plasters, hot poultices, and also hot foot-baths with mustard, ashes, etc. In 
severe cases their action is slight. Acetate of lead in large doses sometimes 
seems to have a favorable influence in severe dyspnoea, especially with threatening 
pulmonary oedema. We give the powder, up to a grain and a half (gramme 0.1), 
every two or three hours, and it is often a good plan to add half a grain or a grain 
(gramme 0.03 to 0.05) of opium. We can also frequently obtain decided relief 
for the patient, particularly if constipated, by a vigorous drastic purge, with com- 
pound infusion of senna or gamboge. Inhalations of nitrite of amyl seldom have 
a beneficial effect. 

Palpitation, constant or paroxysmal, is treated by applying ice to the cardiac 
region ; the " heart-bottles," made of tin, act very well. In patients with aortic 
insufficiency and very excited action of the heart, we may recommend the pro- 
tracted use of ice. Hot poultices also are sometimes beneficial. The narcotics are 
the most efficient internal remedies, especially morphine, which, of course, we 
should reserve for severe cases. If the palpitation is of a lesser degree, we may 
try bromide of potassium, or bitter-almond water. 

The subcutaneous use of morphine is again by far the most potent remedy in 
the anginous attacks, associated with pain and a feeling of distress. W& may 
also use cutaneous irritation, mustard-plasters, etc., hot compresses or poultices, 
and perhaps strophanthus, nitrite of amyl, or nitroglycerine. 

We may prescribe bitter remedies — tinctura amara (P. G.), or compound tinc- 
ture of cinchona — and muriatic acid for the loss of appetite, in case this is not 
improved by regulating the activity of the heart. In addition, we must always 
endeavor to get a regular evacuation of the bowels. 

Eor the attacks of faintness and vertigo, occurring especially in aortic stenosis, 
as a result of cerebral anaemia, we may prescribe a horizontal position, and stimu- 
lants — wine, ether, and Hoffmann's anodyne. If the cerebral symptoms depend 
upon venous stasis, we try to remove it by ice, mustard-plasters to the neck, and 
thorough derivation to the intestines. 

Especial accidents and complications, like pulmonary oedema, infarctions, or 
apoplexy, are to be treated according to the usual rules. 



340 DISEASES OE THE CIRCUL AT OE Y ORGANS 



CHAPTER III 

DISEASES OF THE MYOCARDIUM 

Preliminary Remarks. — In valvular disease of the heart a disturbance of the 
circulation takes place because of the functional impairment of the valves, or the 
obstruction of the orifices of the heart ; but in the diseases which we are now to 
consider we have to deal with impairment of the structure and functional activity 
of the cardiac muscle itself, while the valvular apparatus of the heart remains in- 
tact. The expression myocardial diseases of the heart, in a strict sense, is too 
narrow, inasmuch as we probably have diseases of the ganglia and nerves of the 
heart associated with the muscular diseases. Indeed these nervous lesions may 
often be the essential change, but as yet our knowledge with regard to the patho- 
logical changes in the nervous apparatus of the heart is extremely limited; and, 
on the other hand, most of the organic diseases of the cardiac nerves probably in- 
volve some secondary changes in the cardiac muscle. We may therefore, in the 
classification and consideration of these conditions of the heart, limit ourselves 
provisionally to the disturbances of the cardiac function observed during the life 
of a patient, and the anatomical changes in the muscle of the heart found after 
death. It remains to be discovered later what is the part which the degenerations 
of the nerves and ganglia of the heart have in the development of these disturb- 
ances. We must also point out that in what follows we shall consider merely the 
primary muscular diseases of the heart, in which the change in the heart is the 
cause of all the essential symptoms. We shall quickly find how difficult it is in 
these matters invariably to draw a sharp distinction between secondary and pri- 
mary disease. 

1. Interstitial Myocarditis 

{Fibrinous Degeneration of the Myocardium. Sclerosis of the Coronary Arteries) 

etiology and Pathological Anatomy. — The anatomical changes of inter- 
stitial myocarditis result in irregular-shaped spots of a whitish luster, often very 
numerous, interspersed through the cardiac muscle and corresponding to a par- 
tial or complete destruction of the muscle-fibers and the substitution for them 
of a firm, fibrinous, cicatricial connective tissue. These places, which are best 
found by making horizontal sections of the myocardium, occur particularly in 
the left ventricle, and especially at its apex and in its anterior wall; but they 
may also be found everywhere, and especially in the papillary muscles. Often 
we may observe them as somewhat glistening retracted spots on the endocardial 
or pericardial surface of the heart. The origin of this interstitial myocarditis 
was explained by the researches of Weigert, Ziegler, Huber, and others. In a 
great majority of cases, though perhaps not in all, the changes just sketched are 
directly associated with changes in the coronary arteries and their branches. In 
almost every case we find in these vessels marked changes, due to endarteritis, 
or arterio-sclerosis. In places where this change in the vessel causes "marked 
diminution of its lumen, the corresponding portion of the myocardium is imper- 
fectly supplied with arterial blood, and in consequence the muscular fibers grad- 
ually degenerate, lose their nuclei, and change into a friable, cheesy detritus. 
In place of the destroyed muscular fiber there is a new growth of connective tis- 
sue. With ordinary endarteritis these processes are slow and gradual, but under 
certain circumstances there may be a somewhat rapid occlusion of the branches 
of the coronary arteries, because of thrombosis or embolism of proximal origin. 
In such cases we have a genuine cardiac infarction, presenting a spot of anaemic 
necrosis, or sometimes a rather fresh brownish-yellow haemorrhagic infiltration. 



INTERSTITIAL MYOCARDITIS 



341 



Of course, this limited necrosis and interstitial new growth will not occur if, 
in spite of the existence of arterio-sclerosis, the direct supply of blood remains 
sufficient, or, if insufficient, is eked out by the collateral circulation. 

If the formation of connective tissue is extensive, the entire heart wall may 
become decidedly thinner, so that it yields to the internal pressure of the blood. 
This sometimes occasions in the left ventricle the bulging of a limited portion 
of the wall of the heart, so-called cardiac aneurism. A cardiac aneurism of 
this sort, and also an extensive fresh infarction, may exceptionally result in 
rupture of the heart with escape of blood into the pericardium, and sudden death. 
Of still greater importance, because far more frequent, is the formation, in 
places where the fibrinous process reaches to the endocardium, of parietal 
thrombi inside the heart. These sometimes give rise to embolism in distant 
organs. 

As to further pathologic changes in the heart we find that certain portions of 
the heart are not infrequently dilated or hypertrophied. The dilatation may, at 
least in part, be due to the diminished resistant power of the cardiac walls, but 
in case of hypertrophy we must always seek for special causes, inasmuch as sclerosis 
of the coronary arteries as such can not lead to hypertrophy of a portion of the 
heart. As a rule, the cause is easily discovered, either in an associated arterio- 
sclerosis, or in those factors, such as dissipation, which may occasion, simultane- 
ously with arterio-sclerosis, an idiopathic hypertrophy of the heart. Of course, 
we must also bear in mind the possible but exceptional presence of such compli- 
cating diseases as interstitial nephritis, or pulmonary emphysema. With regard 
to the right ventricle we know, also, that this portion of the heart must hyper- 
trophy as a result of congestion in the pulmonary circuit, when the left ventricle 
is permanently weakened. 

The causes of this most important, and by no means rare, form of myocarditis 
which we have just described, and which is due to sclerosis of the coronary 
arteries, must be the same as the causes of this latter affection. Often the sclerosis 
of the coronary arteries is merely a part of a general arterio-sclerosis, but we 
sometimes find comparatively marked changes in the coronaries, although there 
are no specially extensive atheromatous changes in the other arteries of the body, 
and again, when there is well-marked arterio-sclerosis elsewhere, the coronary ar- 
teries may show slight symptoms of disease, if any. In general, however, we have 
the same ^etiological factors to explain sclerosis of the coronary arteries as arterio- 
sclerosis in general. Often we shall find the cause in high living, and particularly 
in chronic alcoholism. In other cases, habitual muscular overstrain seems to 
favor the development of arterio-sclerosis, and clinical experience shows that an 
important cause of sclerosis of the coronary arteries, particularly, lies in great 
mental effort and excitement, which indeed are not infrequently combined with 
the above-mentioned factors — for example, in the case of extraordinarily active 
business men, speculators, high officials, and physicians. All these considera- 
tions go to explain the fact that sclerosis of the coronary arteries is seen far more 
often in the male than in the female sex. That age plays an important part is uni- 
versally acknowledged. It is true of interstitial myocarditis, as of arterio-sclero- 
sis in general, that, as a rule, persons are attacked in the second half of life, 
from forty years of age on. Finally, we must add that hereditary tendencies to 
the development of arterio-sclerosis in general, and sclerosis of the coronary 
arteries in particular, can not be denied. 

That form of disease of the coronary arteries deserves special mention which 
is of syphilitic origin, and therefore somewhat distinct from ordinary arterio- 
sclerosis, although the number of proved cases is not great. It is scarcely possible 
to doubt that there is a specific syphilitic endarteritis of the coronary arteries, 
giving rise to almost exactly the same symptoms as ordinary arterio-sclerosis. At 



342 DISEASES OF THE CIKCULATOEY ORGANS 



any rate, tliis point should in every case be considered, for therapeutic reasons 
if for none other (vide infra). 

Finally, it is to be added that there may be another form of chronic myocar- 
ditis not associated with primary chronic disease of the arteries, but with an 
antecedent acute myocarditis as a sequel of severe constitutional infectious dis- 
ease, such as typhoid, diphtheria, sepsis, or scarlet fever. The careful histological 
examination of the myocardium by Krehl, Romberg-, and others, in cases of dis- 
ease of this sort, has demonstrated acute inflammatory processes in the cardiac 
muscle. It might very well be that chronic interstitial myocarditis, with all its 
results, should gradually develop from acute processes of this sort. Still, the 
matter needs further clinical study. 

There is a secondary chronic myocarditis as a sequel of chronic endocarditis 
(valvular disease), but this is only exceptionally of any importance in itself. The 
endocarditic process may extend directly to the neighboring muscular layers of 
the heart, or there may occur, especially in association with aortic endocarditis, 
embolic infarctions, the development of which is the same as of the previously 
described thrombotic infarctions of the heart. Finally, there is the possibility 
that myocarditis and endocarditis might appear simultaneously. It has been 
maintained that myocarditis may develop as a sequel of acute articular rheuma- 
tism. The development of myocarditis in this way, if it ever occurs, is probably 
very exceptional. 

Clinical History. — We must first mention that sometimes quite extensive cica- 
tricial formation may be found in the cardiac muscle post mortem, without the 
occurrence of any manifest symptoms referable to the heart during life. We see, 
then, that the heart may, under some circumstances, undergo quite a considerable 
loss in its contractile substance without injury. 

In many other cases, however, the heart's capacity for work suffers so much 
that the same symptoms arise as in valvular disease. The course of such cases 
may be very chronic. The symptoms begin quite gradually. The patient first has 
a slight dyspnoea or palpitation, and a feeling of distress in the chest, but only 
from external causes, such as slight physical exertion. Sometimes there is marked 
general weakness and languor. The patients have an unhealthy sallow look. They 
become easily tired, feel depressed, and scarcely capable of any great bodily or 
mental exertion. The symptoms gradually increase, and just the same results of 
disturbance of the circulation appear as in all the other forms of heart disease. 
The difficulty in breathing becomes more marked, oedema occurs, signs of stasis in 
the liver, intestines, and kidneys appear — in short, the well-known type of general 
circulatory disturbance develops. 

Physical examination of the heart shows marked anomalies of the heart's 
action in all severe cases. The pulse is often irregular in regard to its rhythm 
and the intensity of its single beats, but the arhythmia may also be wholly absent 
in spite of the degeneration of the myocardium, as we have often convinced our- 
selves. The pulse is at first quite strong and full, later it becomes weaker, of 
lower tension, and at last sometimes very small and scarcely perceptible. It may 
be increased in frequency, but we quite often notice in chronic myocarditis, espe- 
cially in the early stages, a very characteristic and persistent slowing of the pulse 
to 60, 50, or even less, in a minute. With this slowness of the pulse there is also 
frequently irregularity of the heart's action, especially the appearance of occa- 
sional double beats (pulsus bigeminus). Percussion usually shows an increase 
of the heart's dullness, due to dilatation or hypertrophy of the heart, the increase 
being either general or chiefly on one side. Auscultation shows the absence of 
any murmur, and hence the absence of valvular disease. The heart-sounds are 
distinctly audible, and sometimes quite loud and valvular, but in the later stages 
often low and obscure. The pulmonic second sound is accentuated, when there 



INTERSTITIAL MYOCARDITIS 



313 



is stasis of the pulmonary circulation. In several cases we found the second sound 
for a long time very plainly divided — reduplicated. We must also mention that 
sometimes in pure myocarditis a systolic murmur is heard at the apex "which is 
due either to a relative insufficiency of the mitral valve, or to its incomplete 
closure, as a result of defective muscular action of the left ventricle. 

We must make particular mention of one symptom of sclerosis of the coronary 
arteries, which, although it is not pathognomonic, is by far most often seen in 
association with it and therefore has an important diagnostic significance. We 
refer to the attacks of so-called angina pectoris (stenocardia, heart -pang). These 
attacks of genuine angina pectoris (compare also the following chapter) consist in 
the sudden occurrence of pain in the region of the heart, extending into the 
back, the left shoulder, and the left am! even to the tips of the fingers. In severe 
cases the pain is extremely violent. It is as if the chest were squeezed in a vise. 
At the same time there is a decided feeling of anxiety and oppression, as well as 
complete loss of strength — a sense of impending death. The patient seeks some 
support, he can scarcely move, scarcely utter a few words in a whisper; the ex- 
tremities grow cool, the brow moist and cold. The attack may be directly fatal, 
but this is the exception. As a rule, the symptoms pas away in a few hours, and 
the patient gradually recovers. In many cases of sclerosis of the coronary arteries 
attacks of this sort occur very often, in varying severity. Xot infrequently an 
attack may be due to some special cause, such as the bodily exertion of a long 
walk or climb, errors in diet, or mental excitement. In such cases bad news may 
cause death. 

With regard to the true essence of angina pectoris, we are confined to hypoth- 
esis. » The ordinary supposition of a sudden paralysis of the left ventricle explains 
many symptoms, but not all. The intense pain indicates irritation of the sensory 
nerves. Sometimes during an attack the pulse grows small and irregular, but often 
also, as we have learned by experience, it may not be very greatly disturbed. There 
may or may not be, during an attack, acute dilatation of the heart. 

Eesides genuine angina pectoris, attacks of cardiac asthma are not infrequent 
in chronic myocarditis. This differs from angina pectoris in that the peculiar 
pain and constriction are not present, while the distress for breath, the parox- 
ysmal dyspnoea, is prominent. In most cases of this sort we probably have really 
to do with sudden weakness of the heart. Another symptom that has been re- 
peatedly observed in sclerosis of the coronary arteries is simple syncope, due to 
acute anaemia of the brain, and perhaps also referable to simultaneous sclerosis of 
the cerebral arteries. 

The general course of the disease varies considerably in different cases. Much 
depends upon the patient — e. g., upon his ability to take good care of himself. 
Sometimes dyspnoea, oedema, and other general symptoms of passive congestion 
are prominent, and in such cases the patient is alternately better or worse. Other 
cases are characterized by attacks of angina pectoris. The termination is in- 
variably unfavorable. It may either occur gradually with increase in the circu- 
latory disturbance, or with complete suddenness like a stroke. 

This important clinical fact of sudden apoplectiform death (" paralysis of 
the heart ") in patients with sclerosis of the coronary arteries, demands consid- 
eration. It usually happens in elderly persons in comfortable circumstances and 
good livers, who up to that time have not regarded themselves as really ill; but 
they have repeatedly had slight attacks of vertigo, of oppression, etc. Suddenly a 
sort of apoplectic attack comes on, often after some definite cause, after a ban- 
quet, or after some physical exertion or mental excitement. Death follows in 
a few moments, or after a deep coma that lasts for several hours or even days. 
The diagnosis often remains in doubt in such cases, especially if we have not 
known the patient previously. The autopsy shoAvs, as the sole pathological lesion, 



344 



DISEASES OF THE CIECULATOKY ORGANS 



a sclerosis of the coronary arteries, with a more or less extensive cicatricial forma- 
tion in the heart. Apparently in these cases the moment must suddenly arise 
when the supply of blood to the heart is insufficient, and thus death is caused. 
Experiments upon artificial closure of the coronary arteries, by Cohnheim and 
others, agree perfectly with the clinical facts above mentioned. Artificial narrow- 
ing- of the coronary arteries may also be well borne for a long time, until suddenly 
both halves of the heart stand still in a condition of diastole. In such cases, also, 
the heart seems to stop suddenly, but sometimes there are frequent anginous at- 
tacks, and death occurs in one of them. Finally, it should be mentioned that sud- 
den death in sclerosis of the coronary arteries may also be caused by embolism of 
the trunk of the coronary artery, or, as in one case seen by the author, by the 
bursting of a focus of myocarditis with haemorrhage into the pericardial cavity. 

Diagnosis. — The diagnosis of chronic myocarditis is by no means always easy 
and certain. We must first determine that there is a cardiac lesion of some kind. 
This is usually evident from the secondary symptoms of stasis, the condition of 
the pulse, the area of cardiac dullness, etc. Then the question arises whether we 
have to do with a valvular disease or with a myopathic disease of the heart. Here 
auscultation must chiefly decide. The absence of a heart murmur, in spite of 
other definite signs of heart disease, speaks against valvular disease, but not with 
complete certainty. All murmurs may be absent in the last stages, especially 
with a high degree of mitral stenosis, and hence we may easily confuse mitral 
stenosis with myocarditis, particularly when there is marked arhythmia of the 
heart. On the other hand, we have already stated that in pure myocarditis, with 
the valves intact, functional murmurs may be present, which may lead to an 
erroneous opinion as to valvular disease. If continued study of the case has en- 
abled us to exclude valvular disease, it remains to distinguish between chronic 
myocarditis or sclerosis of the coronary arteries on the one hand, and the other 
diseases of the myocardium (vide infra) on the other. We regard it as impos- 
sible to make this distinction with absolute certainty. All the diseases named 
present the same clinical picture of cardiac insufficiency, but what the anatomical 
conditions may be which occasion this cardiac insufficiency we can at present 
only conjecture with more or less probability, during life. The following symp- 
toms are most characteristic of coronary sclerosis: persistent infrequency (slow- 
ness) of the pulse, particularly if associated with arhythmia; attacks of genuine 
angina pectoris; and the evidence of arterio-sclerosis in the brachial, radial, tem- 
poral, and other peripheral arteries. Persistent rapidity and arhythmia of the 
pulse occur in interstitial myocarditis, just as in other myopathic . diseases of 
the heart; but arhythmia is, in general, far more common when there is actual 
myocarditis than when there is simple muscular weakness of the heart. There 
is self-evident difficulty in the diagnosis of cases with sudden apoplectiform 
paralysis of the heart, and in distinguishing them from apoplexy, embolism, pan- 
creatic haemorrhage, and similar causes of sudden death. 

Prognosis. — The prognosis is evident from what has been already said. Re- 
covery is impossible, but even extensive cicatricial formation in the heart may 
probably last for years without causing much disturbance. We must always be 
prepared for disturbances of compensation, and the manifold sudden accidents to 
which patients with myocarditis are exposed, but we can not foretell the time of 
their occurrence. 

Treatment. — The treatment of chronic myocarditis must be directed first to 
the dietetic and hygienic care of the patient. This is of the greatest importance. 
For obese persons accustomed to high living, a moderate, simple diet must be 
accurately prescribed. Alcoholic beverages must be greatly limited or wholly 
forbidden, and not more than two or three cigars allowed per diem. Moderate 
bodily exercise is beneficial, and indeed necessary, for the promotion of the circula- 



SO-CALLED IDIOPATHIC HYPERTROPHY OE THE HEART 345 



tion and the more rapid diminution of the obesity, but the patient must be ear- 
nestly warned against too violent exertion, nor can great mental effort be per- 
mitted. In summer, a quiet life in the country or some mountain region is to be 
advised, or, under suitable circumstances, the cautious use of the waters of Carls- 
bad, Kissingen, Marienbad, or Nauheim. Erequent tepid baths or mud baths may 
usually be employed even at home with advantage. Of internal remedies, iodide of 
potassium has been specially recommended to be used persistently, in the amount 
of eight to fifteen grains (gramme 0.5-LO) or more daily. Iodide of potassium 
enjoys a reputation for an especial specific action upon arterio-sclerosis in general, 
and ought therefore to have a beneficial effect upon arterio-sclerosis of the coro- 
nary arteries. We have ourselves seldom seen very striking results from its use. 
Probably iodide of potassium is of benefit in cases of syphilitic origin, and we 
therefore recommend it particularly when there is any suspicion of a syphilitic 
taint. With disturbance of compensation, and with abnormally frequent, weak, 
and irregular action of the heart, digitalis and similar remedies are indicated, just 
as in valvular disease. In cases with an abnormally slow pulse, we may use them, 
provided great caution is exercised, but we must also be governed by the other pre- 
vailing symptoms. In attacks of angina pectoris (see the following chapter) the 
subcutaneous injection of morphine is by far the most efficient, and often an in- 
dispensable remedy. Also, the frequently enumerated cardiac stimulants, such as 
strophanthus, camphor, ether, and wine, ought to be borne in mind, and, finally, 
one may make trial of nitro-glycerine ( ¥ V to of a grain, gramme 0.001-0.002) 
in alcoholic solution, and of nitrite of sodium (two or three teaspoonfuls daily of 
a solution containing 1 or 2 parts to 120 of water). The inhalation of a few drops 
of nitrite of amyl is also sometimes beneficial, but more often it has no effect. 
In cardiac asthma, stimulants are indicated, but often narcotics as well. Mus- 
tard-plasters, the application of cold and of heat, hot foot-baths, etc., are also 
employed. Sometimes even in the worst cases we see good results from the use of 
digitalis. 

With regard to regimen and mechanical treatment compare the following 
section on idiopathic hypertrophy of the heart. 

2. So-called Idiopathic Hypertrophy of the Heart 

{Meclianical Strain of the Heart) 

etiology and General Pathology. — ~Not infrequently cases during life pre- 
sent all the symptoms of an uncompensated cardiac lesion, and yet the autopsy 
discloses merely hypertrophy of the heart with a greater or less degree of accom- 
panying dilatation. There is no lesion of valves, coronary arteries, or myo- 
cardium. The cardiac hypertrophy, which involves the left ventricle chiefly, 
but often both ventricles, can not be regarded as secondary in the ordinary sense 
of the word, for in the heart itself and in the other organs we find nothing which 
can call forth a secondary hypertrophy of the cardiac muscle — no valvular disease, 
no chronic nephritis, no general arterio-sclerosis, and no pulmonary emphysema. 
Hence we term these cases " primary idiopathic " cardiac hypertrophy, in the 
sense that we can not discover any other primary disease. 

ISTotwithstanding, we must in these cases also seek the cause of the cardiac 
hypertrophy in some excessive demand upon the cardiac muscle, and as there are 
no macroscopic anatomical or mechanical changes involving an increase in the 
cardiac activity, we must seek other circumstances occasioning' a functional over- 
strain of the heart. Careful observation and investigation of cases of this sort 
have taught us a number of such causes. 

Among the most frequent is habitual embarrassment of the circulation by 
excess in eating and drinking. There can be no doubt that every time food is 



346 



DISEASES OF THE CIRCULATORY ORGANS 



taken in large amount there is a temporary increase in the activity of the heart, 
the frequency of the pulse, and the tension in the arteries. This is in part because 
the specific gravity of the blood is temporarily increased by the material taken into 
it, and in part because the products of metabolism in the blood have a direct 
stimulating action upon the heart or the blood-vessels, and finally, because an ex- 
cessive ingestion of liquids temporarily increases the total amount of blood. In 
brief, there are numerous persons of the more favored classes who indulge too 
freely in eating and drinking, and for years go to excess in the pleasures of the 
table; and in the case of such persons there is, during a great part of their life, 
although not all the time, that condition which the older physicians termed 
plethora. All these circumstances which we have mentioned occasion an increase 
in the demands upon the heart, especially its left ventricle. The heart performs 
this extra work laid upon it, and consequently becomes gradually hypertrophied. 
Erom what has been said, it is easy to understand why this form of cardiac 
hypertrophy is especially frequent in the obese, and particularly in men from 
forty to fifty years old, though sometimes much younger. We have seen by far 
the most frequent examples of it in great beer-drinkers, and so in persons whose 
business tempts them to excessive indulgence in beer, such as landlords, brewers, 
hop-dealers, butchers, and many others. Persons of this sort often drink for years, 
almost daily, four or five, or even eight or ten, litres (quarts) of beer. Let the 
reader consider what an amount of liquid, and at the same time of nourishment 
(for one litre of beer contains about fifty or sixty grammes [two ounces] of carbo- 
hydrates), is in this way alone introduced into the blood. This explains the 
great frequency of cardiac hypertrophy which Bollinger has shown to exist at 
Munich ; but the " Munich beer-heart " is seen with unfortunate frequency in other 
towns than Munich. The alcohol is probably not a factor in the development of 
the hypertrophy of the heart, but we may well suppose that it promotes, or at 
least hastens, the degenerative changes in the cardiac muscle, and particularly in 
the cardiac nerves, which at last render the heart's action inadequate and the 
circulation imperfect. Eor the development of cardiac hypertrophy in itself is a 
circumstance which does not impair the health, but rather preserves it ; only, ex- 
perience teaches us that no heart can uninterruptedly perform an amount of work 
which is physiologically excessive, and escape final exhaustion — the point of time 
depending upon the individual vigor and other associated factors. 

A second cause of idiopathic hypertrophy is persistent muscular strain. Every 
muscular exertion increases the demands upon the cardiac activity. There is an 
increase in the frequency of the pulse and in the amount of blood passing through 
the heart. If excessive bodily exertion is habitual for a considerable period of 
time, there finally develops hypertrophy of the heart, usually affecting both ven- 
tricles, but especially the left. Thus is explained the hypertrophy sometimes seen 
in, blacksmiths, locksmiths, baggage-carriers, laborers in vineyards ("Tubingen 
heart"), and soldiers after severe campaigns. Why this hypertrophy should 
sometimes occur and sometimes be absent, under apparently similar conditions, 
must be explained by the difference in the physiological capacity of the individ- 
ual. Here, too, the abnormality of the condition does not become evident till the 
functional ability of the heart begins to fail (" heart overstrain," " irritable 
heart "). 

In the third place, it seems that in some few cases of idiopathic hypertrophy 
of the heart, in which none of the causes yet named are operative, it is abnor- 
mal nervous irritation of the heart which increases its activity, and hence, 
finally leads to its hypertrophy. This is perhaps the explanation of many cases 
of cardiac hypertrophy in persons who have long been exposed to many sorts of 
psychical excitement. The cardiac hypertrophy of exophthalmic goitre (q. v.) 
may also be put in this category. Not infrequently we may conjecture in an 



SO-CALLED IDIOPATHIC HYPERTROPHY OF THE HEART 347 



individual case that several of the causes mentioned have been operative simul- 
taneously in the development of the hypertrophy. Thus, idiopathic hypertrophy 
of the heart is seen particularly often in individuals who have to undergo great 
mental strain and excitement, and at the same time are heavy drinkers. 

There is usually associated with the hypertrophy a dilatation, referable to the 
persistent over-distention of the ventricles during diastole. The weaker and 
more yielding the myocardium becomes with the course of time, and the more 
passive congestion affects the heart itself (particularly the auricles and right ven- 
tricle), the more the dilatation increases; and with it comes degeneration of the 
cardiac muscle, or, at any rate, functional weakness of the same, giving rise to 
symptoms of cardiac insufficiency. 

Clinical History. — Idiopathic hypertrophy of the heart may certainly exist for 
a long time without causing the patient any subjective disturbance. We have 
already emphasized the fact that it is precisely the cardiac hypertrophy which 
protects the patient for a time from the onset of marked symptoms. Prodromata 
may occur for a long time before severe disturbance sets in. Among these are 
palpitation, a certain sense of discomfort in the cardiac region, and slight 
dyspnoea. The symptoms begin when the heart can no longer respond to the de- 
mands made upon it, and when it begins to fail. Then all the symptoms of 
cardiac insufficiency arise, in just the same way as in valvular disease and in 
chronic myocarditis. Hence we need not go into the details of the disturbances 
of compensation again. The whole series of symptoms of stasis, as well as the 
attacks of angina pectoris and cardiac asthma, described in the preceding chapter, 
also occur in idiopathic hypertrophies and dilatations of the heart. 

Another subjective disturbance is the peculiar and often very annoying feel- 
ing of " fluttering " of the heart — that is, a momentary feeling of fluttering con- 
traction of the heart. This symptom indicates, probably, abnormal conditions of 
contraction, and must by no means be confounded with the numerous sensations 
which hypochondriacal and neurasthenic patients refer to the heart. If the action 
of the heart is irregular, and especially if there is a tendency to bigeminal pulsa- 
tion, many patients feel every bigeminal contraction as a jolt or stopping of the 
heart. 

The general course of the disease differs considerably in individual cases. 
Sometimes there is moderate difficulty in breathing for a long time, especially on 
any physical exertion. The patient often complains of great languor, or nervous 
irritability, and sometimes of attacks of vertigo and f aintness, and a tendency to 
perspiration. The appetite is poor, and there is very apt to be constipation. The 
condition may become quite suddenly worse after any marked injurious influence, 
especially after great physical exertion or mental excitement. Physical examina- 
tion discloses all the signs of hypertrophy of the heart. In the first place, the 
left ventricle is usually enlarged, corresponding to the direct causes of the con- 
dition. This enlargement is often better appreciated by accurate observation of 
the apex-beat than by percussion. Later the right side of the heart also becomes 
hypertrophied ; dullness on percussion then extends over the lower part of the 
sternum, with epigastric pulsation and undulatory movements in the veins of 
the neck. The heart-sounds are pure, at first valvular, later sometimes muffled 
and feeble. We lay especial value on the characteristics of the first sound of the 
heart. A dull, indistinct sound is probably a sign of considerable dilatation, while 
a normal valvular sound indicates a vigorous systole. In general, there is per- 
sistent frequency of the pulse, at least in patients who are led to seek the physician 
because of beginning symptoms. Infrequency of the pulse probably indicates, in 
most cases, co-existent sclerosis of the coronary arteries (vide supra). The fre- 
quent pulse may for a long time remain regular, but it is not always so. So long 
as the left ventricle does its work well the pulse may be tense, and the second 



34S DISEASES OF THE CIECULATOEY OKGANS 



aortic sound valvular; but if the heart becomes insufficient the pulse grows small, 
feeble, often irregular; the heart-sounds grow faint, and not infrequently that 
bad sign appears which is known as bruit de galop or gallop rhythm, and con- 
sists in a peculiar reduplication of the first sound of the heart ; * for each beat of 
the pulse we hear three sounds over the heart. At the same time the dyspnoea 
and oppression in the chest increase, the amount of urine diminishes, and oedema 
appears in the legs. We now have the complete picture of an uncompensated 
heart disease. With proper treatment the symptoms may disappear again; but, 
sooner or later, they return. Death finally ensues from general dropsy or from 
some complications or intercurrent attacks, among which we may mention em- 
bolic processes. 

Cases of sudden death (paralysis of the heart) from heart-failure occur not 
very infrequently, as we know from experience, in idiopathic hypertrophy of the 
heart independently of chronic myocarditis. 

Diagnosis. — It is by no means an easy task for the physician to make an 
absolute diagnosis of idiopathic hypertrophy of the heart. Sometimes, when the 
subjective symptoms suggest an examination of the heart, it is easy to make out 
an increase in the cardiac dullness and a displacement of the apex-beat; but in 
other cases the presence of emphysema, or obesity, or even of dropsy, makes the 
physical examination very difficult. If an enlargement of the heart has been 
demonstrated, we must then exclude valvular disease, especially mitral stenosis, 
and also secondary hypertrophy, as a result of chronic interstitial nephritis, or 
other causes. It may be difficult to rule out nephritis if the patient is suffering 
from passive congestion when he first comes under observation, for then it is often 
hard to say whether the albuminuria which may be present is to be referred 
to actual renal disease, or to passive congestion. Even if we can exclude nephritis 
we have still to determine whether there is simple hypertrophy of the heart, or 
an interstitial myocarditis. To settle this question is, as we have already said 
(page 344), very difficult. ^Etiology is always important — for example, if there 
has been an excess in beer, or in muscular exertion. Frequent attacks of angina 
pectoris, arhythmia, and a lowering in the rate of the pulse, suggest sclerosis of 
the coronary arteries. Not infrequently diseases of the myocardium are con- 
founded with chronic obliterative pericarditis. When we consider this latter con- 
dition we shall refer again to the differential diagnosis. 

Treatment. — The main points in the treatment of idiopathic hypertrophy of 
the heart are, in general, exactly the same as for valvular disease and interstitial 
myocarditis. We may, therefore, refer the reader for these to the preceding chap- 
ters. There is, however, one point which we would like to discuss in more detail 
here, because it is especially prominent in the treatment of diseases of the myo- 
cardium. We refer to the so-called dietetic and mechanical treatment of circu- 
latory disturbances. Much of what we shall say here applies also to other forms 
of chronic heart disease. 

Efforts have long been made, but with fresh zeal of late years, because of 
Oertel's recommendation, to promote and improve the circulation by mechanical 
means as well as by such internal remedies as digitalis. The following considera- 
tions lead one to regard such an influence as possible : 

1. Diminution of the Amount of Fluid in the Body, and particularly in the 
Blood ("Desiccation"). — This is the point upon which Oertel lays the greatest 



* This sign is not infrequently found in idiopathic hypertrophy of the heart, in myocarditis, and 
particularly in secondary cardiac hypertrophy following chronic nephritis. It has not yet been fully 
and definitely explained. Perhaps we have to do with an audible muscle-sound originating in the 
auricle, perhaps with peculiar irregularities in the contraction of the heart [for example, the contraction 
of the right and left ventricles not being simultaneous. — V.]. 



SO-CALLED IDIOPATHIC HYPERTROPHY OF THE HEART 349 



stress. He believes that he can diminish the amount of blood in the body by with- 
drawing liquids, and thus lighten the task of the heart and restore the normal cir- 
culation. On this view rest the proscription of excessive drinking and the limita- 
tion of liquid nourishment, such as soup. We must confess that it is difficult for 
us to decide upon this point. Numerous well-known physiological experiments 
prove that the body maintains its amount of blood with great tenacity at a cer- 
tain constant ratio. Inasmuch as the body is able by means of numerous ways 
(secretion and absorption of liquids) to make speedy compensation for variations 
arising through changes in the amount of water ingested, it is by no means proved 
that the total amount of blood in patients with circulatory derangements is in- 
creased; and if actually there is a retention of fluid in the body (as indeed is 
certainly the case where oedema has developed), yet the liquid does not collect in 
the vessels, but in the lymph-spaces of the interstitial tissue, or possibly in the 
cells of the parenchyma itself. That the total amount of water in the system may 
be subjected to great variations must certainly be admitted ; but this assumption, 
that in circulatory disturbances there is an increase in the amount of water con- 
tained in the blood, is not proved. On the other hand, there are facts which con- 
tradict it, such as the actual number of blood-corpuscles and the specific gravity 
of the blood. That there should be any increase in the labor demanded of the 
heart, requires that a large amount of fluid should be added to the blood in a 
relatively short space of time, so that an actual, although extremely temporary, 
hydrsemic plethora should exist. If this process is very frequently repeated, it 
will surely result in a permanent hindrance to the circulation. These circum- 
stances are, however, actually found only in certain patients, particularly in great 
beer-drinkers. In them, of course, to forbid the ingestion of fluid means to forbid 
the drinking of beer, and is therefore of the greatest benefit ; and we can not in- 
sist too strongly upon the necessity of this injunction in the case of corpulent 
beer-drinkers who are beginning to have some dyspnoea. It is not, however, in 
our opinion, permissible to apply this rule about liquids, as is sometimes done, to 
every patient without individualizing. For those who live temperately and are of 
spare figure, the amount of fluid ingested needs no special attention from the 
physician. 

2. Strengthening of the Cardiac Muscle and Promotion of Compensatory 
Hypertrophy hy Increased Physical Exertion. — That the fulfilling of this indica- 
tion may be of great importance is certain, and Oertel lays the greatest stress 
upon inciting the heart to more vigorous contractions by means of suitable bodily 
exertion, and especially by methodical mountain-climbing, in order by these means 
to promote as much as possible the development of cardiac hypertrophy. This 
view is probably fully justified and of obvious utility in many cases of simple 
muscular cardiac weakness. If, however, we apply it to those cases of circulatory 
disturbance in which there is valvular disease, or some other actual mechanical 
hindrance to the circulation, or in which the heart is already suffering from func- 
tional strain, the matter seems to be entirely different. For we must consider that 
we can not transfer unreservedly to the cardiac muscle our current views relating 
to the voluntary muscles of the body with regard to exercise and invigoration. 
The functional activity of the heart is minutely regulated by means of an especial 
reflex apparatus, independently of our volition. We know that every increased 
demand upon the heart's activity is in most cases directly fulfilled by an increased 
cardiac effort. Under proper conditions the most marked cardiac hypertrophy 
may develop in a completely bedridden patient. We must therefore consider 
carefully whether, in cases of this sort, the further increase of the demands upon 
the heart is judicious; whether it may not, on the contrary, contribute to a 
premature exhaustion of the myocardium. It certainly seems to us, and our 
opinion is fortified by practical experience, that the prescription of increased 



350 DISEASES OF THE CIRCULATORY ORGANS 



bodily exertion, such, as mountain-climbing, should always be given with great 
caution, and with consideration of the individual circumstances, if the physician 
desires to avoid unhappy consequences. It may indeed be claimed that a cer- 
tain measure of bodily exercise is very suitable for many patients with valvular 
and other similar cardiac lesions, but we hold that the benefit lies less in the re- 
sultant " invigoration of the cardiac muscle " than in the promotion of the 
venous circulation occasioned by the motion of the extremities and the deeper 
inspirations; or, in the obese, in the increased metabolism of fat occasioned 
by the increased muscular effort. Nevertheless, the inconsiderate prescription 
of muscular exertion has worked much harm. Long mountain trips have a great 
and unique value for those circulatory disturbances alone which are occasioned 
by obesity, or associated with simple weakness and slight dilatation of the heart. 

3. Promotion of the Circulation by Massage, Passive Movements, Gymnastics, 
and Baths. — It can not be doubted that the first three of these are suitable means 
for the promotion of the circulation, especially in the veins. We ought not to 
overestimate their value, but we are fully justified in the assertion that they may 
sometimes be employed with decided benefit in circulatory derangements. There 
are patients whom we dare not permit to take general bodily exercise, and for 
these there is sometimes great benefit in Swedish movements methodically and 
regularly pursued, especially in the form of what is called resisted movements 
with the arms and legs. The employment of massage is likewise useful in appro- 
priate cases, in which there are such symptoms as slight oedema and moderate 
dyspnoea. 

Thermic stimulation and baths are considered to have a strengthening influ- 
ence upon the heart. About this we have as yet little physiological knowledge, 
but we can not ignore the fact of the beneficial influence upon many cardiac 
patients, from the use of lukewarm, or warmer baths, and in particular the salt 
baths and natural brine baths, containing carbonic-dioxide gas, as employed at 
Nauheim and Kissingen, and other places. 

To sum up what has been said, we must, in every case of beginning impairment 
of the circulation, give full weight to the considerations just enumerated. We 
must find out the patient's mode of life, and determine and regulate his diet 
and exercise according to the individual circumstances. In this we must always 
pay great regard to the patient's constitution, whether he is obese or spare; 
whether he is full-blooded or anaemic ; whether his muscular strength is great or 
small. It scarcely seems necessary to go into every detail in this place, since all 
the points are repeatedly discussed in other portions of this book. We would 
refer particularly, however, to the chapter on obesity. 

3. Hypertrophy of the Heart, Associated with Congenital Smallness of the 

Systemic Arteries 

{Hypoplasia of the Aorta) 

For a considerable time, physicians have occasionally noticed cases, of the sort 
to be described, in which weakness of the heart and disturbance of the circulation 
appear at a comparatively early age. The patient complains of palpitation, dysp- 
noea, and slight oedema. On examination we usually observe anaemia, combined 
with more or less cyanosis. The cardiac dullness is extended toward the left, and 
the apex of the heart is displaced in the same direction. There is no marked dila- 
tation of the right ventricle till the later stages of the disease. The heart-sounds 
are perfectly clear, unless there may be a murmur due to relative insufficiency of 
the mitral valve, or due to imperfect muscular contraction. The heart's action is 
usually regular, but considerably accelerated; the pulse small and the arteries 
contracted, but often of high tension. We observe the ordinary symptoms of in- 



HYPOPLASIA OF THE AOKTA 



351 



creasing circulatory disturbance, and finally death. Upon autopsy we find the 
heart hypertrophied and usually dilated. The valves are normal, but the entire 
aorta and, in most cases, probably, the other large arteries, are hypoplastic, though 
otherwise of normal structure. Such cases are termed congenital hypoplasia of 
the systemic arteries, and it is believed that the hypertrophy of the heart is due to 
the increased effort to drive the blood through these small vessels. 

In our opinion, this condition of the blood-vessels deserves full consideration 
in forming an opinion about idiopathic hypertrophy of the heart ; but, ordinarily, 
still other factors are potent at the same time, for we sometimes find this hypo- 
plasia at the autopsy of persons who showed no material disturbance of the cir- 
culation during life, and in whom the heart is of normal or even less than normal 
size. Yirchow has called special attention to the fact that this sort of hypoplasia 
of the aorta and its branches is sometimes found in association with chlorosis, or, 
perhaps more correctly, with constitutional anaemia. In these cases the smallness 
of the reservoir diminishes the volume of blood contained in it, but it does not 
have any marked influence upon the heart, which indeed has a less than normal 
burden rather than an excessive one ; so that we believe that in those instances of 
congenital hypoplasia of the aorta in which there is severe circulatory disturbance 
there is either coincident smallness and feebleness of the heart itself (vide infra), 
or an association of the hypoplasia with other influences unfavorable to the heart. 
There have been repeatedly observed cases of cardiac hypertrophy due to muscular 
strain (for instance, in soldiers), or due to excessive drinking, in which congen- 
ital hypoplasia of the aorta and its branches has been found in association with 
the hypertrophy of the heart ; and in the cases which we have ourselves seen and 
in which the diagnosis was confirmed by autopsy, there have almost always been 
some other factors unfavorable to the heart besides this congenital abnormality 
of the blood-vessels. Indeed, one can easily understand that the same injurious 
influences which a normal circulatory apparatus might endure for a considerable 
time without much damage, would occasion premature symptoms if the vascular 
system were abnormally developed. 

The recognition of hypoplasia of the systemic arteries during life is probably 
in every case difficult, and scarcely ever absolutely certain. Important factors 
would be the existence of ansemia and a tendency to shortness of breath and palpi- 
tation from early youth; and also the discovery by palpation that the circum- 
ference of the arteries was less than normal. The condition of the heart is to be 
determined in the ordinary manner. 

Prognosis and treatment must likewise be governed by the same principles as 
in other forms of heart disease. 

4. Primary Weakness of the Myocardium 

(Congenital Weakness of the Heart; Weakened Heart; Acute Muscular Strain of the Heart; 

Toxic Weakness of the Heart) 

If there is a myopathic heart disease, and the heart is at the same time hyper- 
trophied, this indicates that for a considerable time the heart has done an un- 
usual amount of work. In such cases, therefore, it can not be that the heart 
has been feeble from the start. It must indeed have been able to do more than 
is normally demanded of it. It is not until a later period, when its power is 
impaired, that we can say that the heart is relatively or finally absolutely feeble. 
There are cases, however, in which the heart is originally feeble — that is, its 
functional powers are below normal. This weakness is certainly, in many in- 
stances, congenital. It may be expressed in the structure of the heart, the organ 
being unusually small with thin walls, or merely in physiological incapacity, the 
organ being apparently of normal structure. In either case the heart can not 



352 DISEASES OF THE CIRCULATOEY ORGANS 



satisfy even tlie ordinary demands made upon it. Patients of this sort complain, 
upon the least exertion, of palpitation, shortness of breath, and a sense of pres- 
sure over the heart. The pulse is usually frequent or, at any rate, very easily 
accelerated; a short but rapid walk, for instance, may raise, the pulse-rate to 
120 or 140 beats per minute. 

In many cases there are never any severer symptoms. The patient remains 
through life feeble, and " with a weak heart " ; but if his mode of life is favorable 
the heart manages to maintain the circulation. 'Not so, however, if unusual 
demands are made upon it — as, for example, in the course of military service, or 
in mountain climbing, or in unsuitable modes of life. Then more threatening 
symptoms of cardiac insufficiency appear, either suddenly or gradually, and ex- 
press themselves objectively in dilatation (or stretching) of the heart. In some 
cases the heart is not able permanently to satisfy even the ordinary demands made 
upon it. We observe all the symptoms of circulatory disturbance, and at last upon 
autopsy find a heart which is dilated, but not much hypertrophied. Cases of 
this sort are not very frequent, but they certainly do occur; their recognition dur- 
ing life, however, is not easy, for it is difficult to distinguish simple dilatation 
from insufficiency which is subsequent to hypertrophy. We shall probably be able 
to determine that there is some muscular heart disease because of the increase in 
cardiac dullness, the smallness and frequency of the pulse, and the ordinary 
tokens of disturbed circulation, such as dyspnoea, palpitation, oedema, and the 
urine of passive congestion. If we consider carefully the history of the case and 
the presence or absence of special serological factors, we may be able while the 
patient is still alive to make a probable diagnosis of simple dilatation of the 
heart, as a result of muscular weakness. 

Acquired muscular weakness of the heart should be distinguished from the con- 
genital variety. It is occasioned by the action upon an originally normal heart 
of influences which damage the myocardium or its nervous apparatus. We often 
see temporary conditions of muscular weakness of the heart in anaemia, or fol- 
lowing severe attacks of acute disease. Even in these cases there are such differ- 
ences as to indicate a difference in the original vigor of the heart. The same is 
true of acute muscular strain of the heart. Acute attacks of cardiac weakness 
are seen in the case of soldiers at maneuvers, or in laborious mountain climb- 
ing, such as has of late been so often undertaken in an ill-considered manner; and 
these attacks are usually associated with acute dilatation. There is a sudden and 
enormous increase in the demands made upon the heart; the amount of blood 
which, in a given period of time, must pass through the muscles is increased; 
and the heart is unequal to the task. It yields to the increased tension and dilates. 
The pulmonary circulation becomes congested, the pressure in the arteries falls, 
and we have all the clinical phenomena of cardiac insufficiency, including dyspnoea, 
cardiac asthma, and sometimes angina pectoris. If there is prompt cessation of 
the effort and medical assistance, the condition may be restored to normal and 
so remain. This, for example, we lately saw in the case of a young and healthy 
person who escaped drowning only by desperate efforts. But sometimes there re- 
mains behind a permanent weakness of the heart, whether because the single ex- 
cessive strain caused a permanent damage to the heart, or because the heart was 
already of less than normal vigor, and betrayed its weakness for the first time 
when this excessive demand was made upon it. 

Certain forms of chronic intoxication are among the causes which frequently 
lead to acquired weakness of the myocardium, or its nerves. The most important 
of these, from a clinical standpoint, is chronic alcoholism, the noxious influence 
of which upon the heart is universally recognized. Less frequent, but still of 
practical importance, is chronic nicotine poisoning, or, to speak in a more general 
and perhaps more correct manner, the influence of excessive smoking. This is 



FATTY HEAKT 



353 



especially evident in persons who have smoked many strong-flavored Havana 
cigars. The symptoms consist of an unpleasant subjective sensation in the re- 
gion of the heart (fluttering, pressure, or palpitation), of slight dyspnoea, and ob- 
jectively of a frequent, irregular, or intermittent pulse. Other objective cardiac 
signs are not present, at least at first; but there may be still other symptoms of 
chronic nicotine poisoning, such as specks before the eyes, disturbance of vision, 
and dyspepsia. If smoking is stopped in due time, the symptoms may vanish. 
Otherwise, there follow severer disturbances of the heart, although in most cases 
there are other ^etiological factors also present, such as alcoholism and mental 
strain. 

With regard to prognosis and treatment, there are few special statements to 
be made. If there are signs of congenital weakness of the heart we must 
strengthen the constitution in every way possible, and we must seek to give the 
patient, on the one hand, the proper amount of protection, and, on the other 
hand, cautious and moderate exercise of the cardiac muscle, by means of medical 
gymnastics; and in other respects regimen and hygienic precautions are of first 
importance, from a prophylactic and therapeutic point of view. The treatment 
of acute and chronic weakness of the heart by such remedies as cardiac stimulants 
and digitalis is controlled by the ordinary rules. Finally, we may mention in 
this connection that obliteration of the pericardial sac by chronic pericarditis, or 
as a sequel of antecedent acute pericarditis (vide infra), sometimes occasions 
atrophy of the myocardium, with resultant feebleness and dilatation of the heart. 
Cases of this sort may readily be confused with primary cardiac dilatation. 

5. The So-called Fatty Heart 

iEtiology and Pathological Anatomy. — By the name of " fatty heart " we 
often mean, at present, two quite distinct conditions of the heart — the one an 
abnormal deposit of fat in the heart, and the other a fatty degeneration of the 
muscular fibers of the heart. 

Fatty overgrowth and fatty infiltration of the heart are usually merely symp- 
toms of great general obesity. At the autopsy of very fat people we sometimes 
find the heart entirely inclosed in a thick capsule of fat. The fat is situated chiefly 
in the external pericardium and beneath the visceral pericardium. It is usually 
abundant along the course of the larger vessels within the grooves of the 
heart, but in marked cases the fat also involves the muscular substance, so that 
many groups of fat-cells are interspersed between the muscular fibers. The heart 
itself is otherwise quite normal or somewhat hypertrophied or dilated. There are 
in some instances also present sclerosis of the coronary arteries and indurations 
due to myocarditis. 

We have already mentioned fatty degeneration of the muscular substance of 
the heart as a frequent result of valvular disease. In myocarditis and idiopathic 
cardiac hypertrophy, and in the hypertrophy secondary to chronic nephritis 
and pulmonary emphysema, we also meet with fatty degeneration. We often find 
fatty degeneration of the heart, as well as of other organs, in severe acute infec- 
tious diseases, in phosphorus poisoning, and in all marked primary and secondary 
anaemias. Under the microscope we find the muscular fibrillse studded with little 
drops of fat, which may be so numerous that the nuclei and the transverse stria- 
tion of the fibers are quite concealed by them. We often find, besides the fatty 
granules, albuminous granules, which disappear on the addition of acetic acid 
("cloudy swelling" of the cardiac muscle). If the fatty degeneration is of high 
degree, we can easily recognize it with the naked eye. Beneath the endocardium, 
especially on the trabeculse and papillary muscles, we see very fine and delicate 
yellow points and striaB. With great fatty degeneration, as in phosphorus poison- 
23 



354 DISEASES OF THE CIECULATOKY OKGANS 



ing and pernicious anaemia, the whole cardiac muscle is manifestly yellow, and 
also soft and flabby. It is claimed that rupture of the heart may occur as a result, 
of marked fatty degeneration. 

In fatty degeneration of the heart the fat comes from the decomposition of 
albumen in the muscular cells. The occasion of it is probably a defective supply 
of oxygen, which has either a general cause, as in anaemia and phosphorus poison- 
ing, or a local cause, as disturbed circulation in the heart in heart disease. The 
details of this are given in the chapter on anaemia (page 708). 

Clinical Symptoms. — Fatty degeneration of the heart has no characteristic 
clinical symptoms. In the conditions under which we know it is apt to occur, we 
can usually suspect it during the lifetime of the patient, but we can not diagnos- 
ticate it. We must also mention that the frequently expressed opinion, that fatty 
degeneration of the heart invariably occasions general cardiac weakness, is very 
often incorrect. In pernicious anaemia there may be quite a strong and a per- 
fectly regular pulse up to death in spite of the most marked fatty degeneration, 
and many personal observations lead us earnestly to dispute the view that fatty 
degeneration of the heart is to be regarded as the regular cause of cardiac insuf- 
ficiency, and the consequent disturbances of compensation. We have made micro- 
scopic examinations in many cases, and failed to find any sign of fatty degenera- 
tion in the myocardium, although during life the signs of cardiac insufficiency 
were well developed. In general, with our present knowledge, it is impossible 
to establish definite relations between the histological condition of the muscular 
tissue of the heart and its functional activity during life. 

We can not say much that is certain in regard to the clinical symptoms of a 
deposit of fat in the heart. " Fatty degeneration of the heart " always plays a far 
larger part in popular speech than it does in reality. It is certainly a fact that 
difficulty with the heart and respiration is very often observed in fat people. Ex- 
amination of the heart, which, however, is decidedly impeded by the thick pannicu- 
lus adiposus, often shows in such cases an increase of the cardiac dullness, a small 
and sometimes irregular pulse, and faint but clear heart-sounds. The disturbance 
may be very considerable, attacks of angina pectoris and cardiac asthma may 
come on, and death may follow with increasing dyspnoea and general oedema. 

If one has opportunity to make an autopsy in such cases, there will be found 
no single, constant anatomical change as the cause of the cardiac disturbance, but 
usually idiopathic hypertrophy (vide supra), or, less often, myocarditic changes 
with sclerosis of the coronary arteries, and the like. Sometimes, but by no means 
invariably, there is, of course, a marked deposit of fat upon the heart itself, but 
the question arises whether this can directly and seriously embarrass the cardiac 
activity. The fact is that we often have seen similar well-marked cases of fatty 
heart which during life presented no special cardiac symptoms. There would be 
more reason in ascribing an unfavorable influence to the fatty infiltration of the 
cardiac muscle; but in such cases there is almost always a coincident atrophy of 
the muscular structure, so that it is questionable whether the fatty infiltration 
is to be regarded as actually the primary pathological process. We ourselves are 
far more inclined to the view that there is primary atrophy of the myocardium, 
with this fatty infiltration as a secondary phenomenon, similar to the frequent 
and well-known occurrence of secondary lipomatosis of atrophic voluntary mus- 
cles. At any rate, we are as yet entirely unable to recognize cases of this sort 
of fatty heart during life, and it is certain that they are much less frequent 
than the other myopathic diseases of the heart. 

Therefore we can not associate with the term " fatty heart " any uniform 
anatomical and clinical conception. It would be better to speak of the "heart 
of obesity " — that is, of all the manifold injuries to which the heart of obese per- 
sons is exposed. 



CAEDIAC NEUEOSES 



355 



According to our experience, simple idiopathic hypertrophy of the heart is 
certainly the most frequent of these conditions, and it would be very desirable 
if physicians would have more regard to the facts of pathology, when they are 
inclined to make an off-hand diagnosis of fatty heart. 

Treatment. — A great part of the disturbance of respiration in fat people de- 
pends not upon the cardiac weakness, but on the corpulency itself. The great 
bulk of the body, and the hindrance to the activity of the respiratory muscles, are 
very important factors. Treatment directed against the respiratory disturbance 
must hence attack the obesity chiefly, and thus in many cases we also assist the 
action of the heart. The detailed description of the hygienic methods of cure to 
be employed here is to be found in the chapter on obesity (page 784). 

In regard to the special treatment of the cardiac symptoms in the obese, this 
does not differ from the rules that obtain in other forms of heart disease. 



CHAPTEE IV 
CARDIAC NEUROSES 

1. Angina Pectoris (Stenocardia). — Angina pectoris is not an independent 
disease, but a group of symptoms, to which we have had frequent occasion to re- 
fer already; but for a considerable time this symptom-complex may be the only 
sign of disease. It is the paroxysmal occurrence of an extremely violent pain 
below the sternum and in the region of the heart, associated with a feeling of the 
greatest distress and oppression (" precordial anxiety," " sense of impending 
death"). The pain is usually described as cramp-like, boring, and constricting 
It not infrequently radiates from the heart into the shoulders and the left arm, 
sometimes as far as the tips of the fingers. The beginning of the attack is usually 
absolutely abrupt. It may last a few minutes or half an hour, or longer. The 
attacks may be infrequent with intervals of weeks or months, or they may be 
repeated several times a day. Eespiration during the attack is often unaffected, 
in which point genuine angina pectoris differs from cardiac asthma. Many 
patients indeed seek to lessen their pain by holding the breath, and sometimes 
even in angina pectoris the respiration is hurried and irregular. It must be 
pointed out that the symptoms of " pure " angina pectoris and the symptoms of 
cardiac asthma may be clinically much intermixed and confused. The pulse is 
usually rapid and small during an attack, and not infrequently irregular. Some- 
times, however, we find that, in spite of the most violent pain and distress, the 
pulse remains strong, quiet, and apparently normal. If the hand is placed upon 
the heart a peculiar wavy motion and " fluttering " is felt in a few cases, and this 
symptom the patient also perceives subjectively. The countenance is usually pale 
during an attack; the hands feel cool. Toward the end of an attack there is often 
abundant perspiration. 

We are as yet entirely ignorant as to the internal processes which are the 
foundation of angina pectoris. The condition is often compared with neuralgia, 
and spoken of as " cardiac neuralgia." Other investigators suspect that there is 
a painful contraction of the blood-vessels of the heart. It is certain that angina 
pectoris rarely occurs as an independent disease, or pure neurosis. Nothnagel 
described a vaso-motor form of angina pectoris (" angina pectoris vasomotoria "), 
in which there were at the same time distinct signs of vascular contraction in 
the extremities, as indicated by pallor, cyanosis,, and paresthesia. In the case 
of excessive smoking, also, angina pectoris sometimes appears as a result of 



356 



DISEASES OE THE CIRCULATORY ORGANS 



chronic tobacco poisoning, without any other demonstrable change in the heart. 
Similar attacks may occur after strong mental excitement, but these have more 
or less connection with certain forms of hysterical and neurasthenic attacks, 
bearing a merely superficial resemblance to angina pectoris. The true angina 
pectoris is most often seen as a symptom in association with certain diseases of 
the heart and aorta, particularly sclerosis of the coronary arteries, insufficiency of 
the valves, aneurism of the root of the aorta; less often, idiopathic hypertrophy 
of the heart, and hypertrophy secondary to interstitial nephritis. The way in 
which the other symptoms of these conditions may be conjoined with the anginous 
attacks is sufficiently clear from their presentation in a previous chapter. 

We can not speak of the prognosis of angina pectoris as a distinct entity. 
In general angina pectoris is certainly of evil omen, and occasionally death may 
occur during the attack. 

With regard to the symptomatic treatment of angina pectoris, there is no 
doubt that in severe cases the greatest relief is obtained from a subcutaneous in- 
jection of morphine. We confess that the employment of morphine in severe 
heart disease always demands the greatest caution, but yet experience shows that 
in numerous instances this remedy is excellently borne, and most beneficial. 
Among other remedies should be named chloral and chloralamide, which also are 
to be employed with caution, but which sometimes have a good effect ; nitroglyc- 
erine to the amount of A to tV of a grain (gramme 0.001-0.005), which is highly 
praised by many physicians; also nitrite of sodium, and inhalations of amyl 
nitrite, ether, or chloroform. If there are decided signs of cardiac weakness, 
camphor, strophanthus, and alcohol are to be employed as stimulants. An ice- 
bag may be placed over the heart, and sometimes, also, hot applications are of 
benefit; mustard-poultices, hot foot-baths, and the like are also frequently pre- 
scribed in practice. 

We must always bear in mind the general treatment of the underlying condi- 
tion, as well as the employment of purely symptomatic remedies. Special atten- 
tion should be directed to any serological factors, such as muscular strain, men- 
tal excitement, alcoholism, or excessive smoking. If we have to do with the 
" purely nervous " form of angina pectoris, without any physical signs of change 
in the heart, we must of course avoid the use of the stronger narcotic remedies 
so far as possible, and lay the main emphasis upon the general treatment of the 
nervous system by means of electricity, cold-water cures, and psychical influences. 

[In well-marked angina sudden death during a paroxysm is not very rare. In 
Dr. Arnold, of Rugby, the first attack proved fatal. The patient may, however, 
live for years — cases of survival for upwards of twenty, and one even of thirty, 
years being recorded. Flint has known recovery to occur. The prognosis depends 
somewhat on the condition of the cardiac valves and walls: but changes, espe- 
cially in the latter, may escape detection by any save a very skillful observer. 
Walshe states that in every one of twenty-four cases he examined during life he 
found physical signs of changes either in the heart, the aorta, or both. The 
experience of Balfour and Latham is similar.] 

2. Nervous Palpitation. — By " palpitation " we understand the subjective 
perception of the movements of the heart. It is usually excited by increased ac- 
tion of the heart, but there is no constant relation between the intensity of the 
cardiac pulsations and the subjective feeling of them. We sometimes observe 
that patients with aortic insufficiency do not perceive the very strong action of 
their hypertrophied hearts, while in other cases a patient complains of a trouble- 
some feeling of palpitation, although the action of the heart does not appear 
objectively to be especially increased. 

We term cases " nervous palpitation " if the patient complains of palpita- 
tion when a physical examination of the heart shows no anatomical change in it. 



CARDIAC LEUKOSES 



357 



As a rule, in these cases we really have to do with a heart whose action is increased 
by abnormal nervous influences. In many cases the palpitation arises from slight 
external causes, which may give rise to little or no palpitation in a healthy per- 
son, as, for example, after the slightest mental excitement, after any slight phys- 
ical exertion, after taking food, after indulging in certain drinks, such as tea, 
coffee, wine, or beer, or after assuming certain positions, as in lying on the left 
side. Here, then, we have to do with an abnormal sensitiveness of the heart to 
external irritation. Usually the increase in vigor of the heart's action is associ- 
ated with a decided increase in its frequency. We have often seen patients with 
nervous palpitation who had a pulse-rate of 140 to 160 beats a minute after com- 
paratively slight exertion; but in other cases there is apparently a sort of hyper- 
esthesia of the patient with regard to the motions of the heart, so that contrac- 
tions of normal strength and rapidity give rise to disagreeable sensations. 

The patient rarely complains of continuous palpitation; it usually occurs in 
more or less sharply defined paroxysms. Very commonly in pure nervous palpi- 
tation we have to do with persons who, in general, suffer from nervous, hysterical, 
and neurasthenic symptoms, or they are anaemic persons, chlorotic girls, etc. ; but, 
on the other hand, nervous palpitation may occur in very full-blooded, " plethoric " 
subjects. 

Often hypochondriasis plays an important part, and dread of heart disease 
and the thought of its possible consequences excite a palpitation which confirms 
the patient in his delusion. 

The diagnosis of nervous palpitation can be made only when repeated careful 
examination shows no objective abnormality in the heart. In many cases, as 
when there are anaemic murmurs, the decision may be quite difficult. We must 
always pay particular attention to the whole constitution and the general impres- 
sion which the patient makes. 

It is often especially difficult to distinguish between purely nervous palpita- 
tion in a heart otherwise functionally normal, and conditions of congenital or 
acquired weakness of the heart (vide supra). 

The prognosis is so far favorable in that the disease is not dangerous. In 
many cases improvement and final recovery may be effected, but other cases, of 
course, resist all therapeutic efforts very obstinately. 

The treatment must first be directed to improving the patient's general con- 
stitution. The anaemic are to be given iron, quinine, and strengthening diet. 
We put full-blooded persons, however, on scanty fare, and prescribe for them 
bitter waters, or a bath cure at Marienbad or Kissingen. When there is 
hysteria or neurasthenia, it requires special treatment. If the patient is hypo- 
chondriacal, of course the main thing is for the physician to reassure him. We 
should avoid all the influences which seem to excite palpitation. As a symptom- 
atic indication during an attack we should recommend the patient especially to 
keep quiet. The use of cold to the cardiac region — cold compresses and ice-bags 
— often acts beneficially. On the other hand, however, it is to be noted that a 
tendency to palpitation associated with cardiac weakness may often be allayed 
by methodical exercise and the invigoration of the cardiac muscle consequent 
thereupon (see the preceding chapter). Among internal remedies we must employ 
nervines, and in severer cases even narcotics. Among the former we would men- 
tion especially ethereal tincture of valerian and bromide of potassium, which have 
repeatedly done us good service. Digitalis is usually of little value in pure neu- 
roses of the heart, but we may give it as an experiment, say fifteen to twenty drops 
of the tincture with the same amount of cherry-laurel water. 

3. Tachycardia (Paroxysmal Tachycardia). — A peculiar and quite rare neu- 
rosis of the heart, tachycardia, consists of an enormous frequency of the pulse, 
coming on in paroxysms, up to 160-200 beats and more a minute. 



358 DISEASES OF THE CIRCULATORY ORGANS 



We have already mentioned these attacks as a rare symptom in mitral and 
aortic valvular disease and in diseases of the myocardium, but precisely similar 
attacks occur as a pure neurosis without demonstrable lesion of the heart, particu- 
larly in anaemic, nervous, or obese individuals. We saw one very well-marked case 
in a lady with extreme neurasthenic melancholia. The attacks occurred many 
times a day, each lasting only a few minutes. We were often able while feeling 
the pulse to notice that it suddenly became extremely rapid, and then in a brief 
time almost with equal suddenness resumed its approximately normal rate. We 
have seen many similar attacks of genuine tachycardia, although not so extreme, 
in young and neurasthenic individuals, following muscular exertion — for example, 
in soldiers. Similar states develop sometimes after diphtheria (q. v.), and after 
other acute infectious diseases ; but in such instances the tachycardia is usually 
more continuous and not so distinctly paroxysmal. 

In men we must consider the possibility of the action of injurious habits, such 
as drinking and smoking. The individual attack usually begins quite suddenly, 
by day or by night, sometimes without any cause, but often it is apparently pro- 
duced by certain exciting causes, especially at times by overdistention of the 
stomach. The patient feels that the attack is coming, he becomes anxious and 
restless, and looks pale; but there are not, as a rule, at least according to our 
experience, any symptoms like precordial anxiety, dyspnoea, or attacks of faint- 
ness. We notice in the heart itself, during the attack, chiefly a great acceleration 
of the heart-sounds. We sometimes hear indefinite, functional murmurs. The 
action of the heart is often quite regular, but there is not infrequently manifest 
arhythmia during the attack. Acute increase of the heart's dullness has been 
observed during the attack. We have repeatedly been able to verify a marked 
temporary dilatation of this sort, particularly in patients with heart disease, and 
also in one case of paroxysmal tachycardia affecting a sufferer from cirrhosis of 
the liver. In other instances and especially when the tachycardia is a mere neu- 
rosis, no such dilatation of the heart can be made out. 

We know little that is definite as to the nature of the attacks. The affection 
is usually regarded as a temporary paralysis of the vagus. 

We may also state here that paroxysmal and constant tachycardia have also 
been repeatedly observed in anatomical lesions of the cardiac nerves and their 
centers, in tumors and other affections in the vicinity of the medulla oblongata, 
and in compression of the vagus in the neck from new growths, and aneurisms. 

The prognosis of tachycardia depends first upon the nature of the underlying 
disease. We do not know whether a permanent recovery is possible in idiopathic 
cases, but we can always succeed in improving the condition. The treatment dur- 
ing the attack consists in enjoining complete bodily rest, and in applying ice to 
the heart. Such sedatives as bromide of potassium, water of bitter almonds, and 
tincture of valerian are particularly beneficial in the " purely nervous " cases. 
Sometimes the physician may even be constrained to the cautious injection of 
small amounts of morphine. In other respects our treatment is determined mainly 
by the underlying condition, if known. [If there is reason to think that the 
stomach is overloaded, gentle measures should be taken to empty it. — V.] The 
best way to guard against the return of the attacks is to give precise hygienic 
directions, suited to the patient's constitution and manner of life. The contin- 
ued use of iodide of potassium has sometimes seemed to us to be of service. 



PERICARDITIS 



359 



SECTION II 

Diseases of the Pericardium 

CHAPTER I 

PERICARDITIS 

(Inflammation of the Pericardium) 

iEtiology. — Pericarditis seldom appears as a primary idiopathic disease. It is 
usually merely a sequel or a complication of other diseases. Thus, it is observed 
with particular frequency in the course of acute articular rheumatism, where it 
appears sometimes alone, sometimes in combination with acute endocarditis. It 
is not impossible that some few cases of apparently primary acute pericarditis 
belong, from an aetiological standpoint, to acute articular rheumatism — that is, 
they are excited by the same pathogenic factors which exceptionally attack the 
pericardium alone, without simultaneous participation of the joints in the disease. 
This supposition is rendered probable from the later course of many such cases. 
For instance, arthritis may ensue. Cases of secondary pericarditis, unassociated 
with articular rheumatism, occur, although much less often, in other acute infec- 
tious diseases, among which scarlet fever, measles, and septico-pyaemic processes, 
as well as scurvy and purpura haemorrhagica, deserve especial mention. In sepsis 
and pyaemia the pericarditis is purulent, and in purpura, haemorrhagic. Among 
the chronic diseases in the course of which pericarditis sometimes appears we 
must mention especially chronic nephritis. We have seen hsemorrhagic peri- 
carditis in association with leukaemia. Pericarditis sometimes occurs also in the 
victims of carcinoma, but here it is probably dependent upon a secondary septic 
infection. Finally, it should be mentioned that severe haemorrhagic pericarditis 
is seen comparatively often in alcoholic subjects, and apparently as a primary 
disease. Often it is really tubercular, but by no means always; and if not, the 
author is inclined to regard it as a primary haemorrhagic inflammation, analogous 
to haemorrhagic pachymeningitis or haematoma of the dura mater. 

A large number of cases arise from an extension of the inflammation from the 
vicinity. Thus we not infrequently see pericarditis as a result of pleurisy, espe- 
cially on the left side, and in pneumonia complicated with pleurisy. New growths 
and ulcerative processes in the oesophagus, in the vertebrae, in the bronchial glands, 
or in the lungs, also lead at times to perforation into the pericardium and a con- 
sequent inflammation. It is not settled whether the pericarditis, which appears in 
the course of chronic valvular disease, is also to be regarded as arising from ex- 
tension by contiguity. We have thought of this possibility, because we have been 
struck with the fact that secondary pericarditis is especially frequent in valvular 
disease of the aorta, suggesting a direct propagation of the inflammatory germs 
through the aortic wall to the pericardium. Still, it must of course be allowed 
that this form of pericarditis may have an independent origin, particularly in 
cases of mitral disease. Pericarditis may also develop as a result of myocarditis, 
abscess of the heart, etc. 

Tuberculosis plays a very important part in the aetiology of pericarditis. ~No 
small number of apparently primary cases of pericarditis turn out at the autopsy 
to be tubercular. This seems to come on in quite an isolated way, or as one 
symptom of a special localized form of tuberculosis, which we term tuberculosis 
of the serous membranes. In many cases we can discover the origin of a tuber- 
cular pericarditis in the direct extension of a tubercular pleurisy. In apparently 
primary cases the occurrence of the infection may sometimes be explained by the 



360 



DISEASES OF THE CIECULATOKY OKGANS 



discovery of a tubercular lymph-gland, which has broken through into the peri- 
cardium. 

Pericarditis is usually a disease of youth and middle life, but it may also occur 
in advanced age. 

Pathological Anatomy. — Ordinary pericarditis involves the internal surface 
of the pericardium in either a circumscribed or diffuse manner. Inflamma- 
tion of the outer surface of the pericardial sac is distinguished as external 
pericarditis (vide infra). The anatomical processes in pericarditis are precisely 
analogous to those in inflammations of the serous membranes in general, especially 
of the pleura. 

We usually divide pericarditis into fibrinous, sero-flbrinous, hemorrhagic, and 
purulent (or ichorous) forms, according to the character of the exudation. The 
fibrinous and sero-flbrinous forms, with an abundant fluid effusion into the peri- 
cardial cavity, are the most frequent, occurring in articular rheumatism, in valvu- 
lar disease of the heart, etc. Both layers of the pericardium are covered with 
masses of fibrine, which often show a reticular or villous arrangement (cor 
villosum) . Besides this, we find more or less of a fluid effusion which distends 
the pericardium. The fluid is of a serous nature, contains more or less numer- 
ous flakes of fibrine, and is turbid from the admixture of cells — pus-corpuscles,, 
and, in part, desquamated endothelium. A purulent pericarditis is always the 
expression of a specific infection of the pericardium. It is seen in pyemic dis- 
eases, as a result of empyema, and in perforation of abscesses, cancers of the oesoph- 
agus, etc., into the pericardium. A hemorrhagic effusion is seen chiefly in tuber- 
cular pericarditis. In this we find miliary tubercles, and little cheesy nodules in 
the inflammatory new growths, besides all the signs of inflammation. The specific 
tubercular changes are sometimes recognizable with the naked eye, but at other 
times we have to use the microscope to find them. Hemorrhagic pericarditis also 
occurs in general hemorrhagic diseases, such as scurvy, and in weak and debili- 
tated persons, especially drunkards (vide supra). 

In long-continued pericarditis the cardiac muscle almost invariably undergoes, 
changes. The heart is usually flabby and dilated, and the muscle often shows 
fatty degeneration. After the pericarditis has lasted a long time there is often 
considerable atrophy of the cardiac muscle, which is partly replaced by fat tissue. 
We have already mentioned the occurrence of pericarditis in connection with 
valvular disease and degenerations of the myocardium. 

In favorable cases of pericarditis we may have a perfect recovery. The so- 
called macules tendinece sometimes remain in the pericardium as residua of a 
past circumscribed pericarditis. In some cases the pericarditis leads to an adhe- 
sion of the two layers of the pericardium to each other, and obliteration of the 
pericardial cavity (vide infra). In many cases a chronic pericarditis finally de- 
velops from the acute form, or the whole affection takes a more chronic course 
from the outset. In this way chronic adhesions of connective tissue arise, and 
great thickening of the pericardium, but the amount of fluid is usually small. 
Sometimes the chronic pericarditis is interrupted by an acute exacerbation of the 
disease. 

Clinical Symptoms. — 1. Suhjective Symptoms, General Symptoms, and Fever. 
— Mild forms of pericarditis may develop, as in the course of an acute articular 
rheumatism, without causing any subjective symptoms. They are discovered only 
by a careful physical examination of the heart. In severe cases, however, the peri- 
carditis causes violent subjective symptoms, which of course have in themselves 
little that is characteristic. 

On careful questioning we often find that there is pain in the cardiac region, 
or not infrequently in the epigastrium. This pain is of decided diagnostic impor- 
tance, but it does not always exist. 



PEEICAEDITIS 



361 



A general feeling- of constraint and distress is almost constant in all acute cases 
of any severity, and so is a feeling of dyspnoea, which may increase to the highest 
degree of orthopncea. The patients often complain of headache. In severe cases 
they become stupid and comatose. 

It is easy to understand that extensive pericarditis must impede the motions 
of the heart. Probably the most important way in which it does this is by in- 
creasing the tension in the pericardium, and thus embarrassing the diastole of the 
ventricles, so that the cavities of the heart are not normally filled and general dis- 
turbance of the circulation ensues. Furthermore, the pericarditic deposits and 
adhesions, and such changes in the myocardium as may occur, interfere with the 
cardiac systole. Thus are explained the early signs of diminution in the amount 
of blood received by the arteries, as shown by pallor and cerebral ansemia; the 
distention of the systemic veins, as shown by cyanosis ; and the disturbance of the 
pulmonary circulation, causing dyspnoea. 

The dyspnoea is also increased in large pericardial effusions by the mechanical 
pressure of the distended pericardium on the left lung. 

Acute pericarditis is usually associated with fever. This has no special type, 
and usually keeps at a moderate height— 102° to 103.5° (39°-39.8°C.)— but it 
often exhibits considerable variations. In cases of recovery the fever declines by 
lysis. Chronic pericarditis may run its whole course without fever. 

2. Physical Signs — Inspection. — The general hue of a patient with severe 
pericarditis is pale, but also more or less cyanotic. He has an anxious expression. 
He lies with the upper part of the body raised, or he sits up in bed. The breath- 
ing is usually rapid, labored, and somewhat irregular. The veins in the neck are 
swollen and prominent. We very often see marked undulating or pulsating 
movements in the jugular veins, as a result of stasis. The cardiac region seems 
unusually prominent in all cases with much effusion, and the intercostal spaces 
there are flattened out. We sometimes detect a slight oedematous swelling of the 
chest-wall itself. 

If the action of the heart is powerful and the exudation small, the heart's 
movements may be distinctly visible. In other cases they are seen only faintly, 
and they may be noticeably diffuse. If the exudation is abundant, or if adhesions 
occur (vide infra), they may disappear altogether. 

Palpation in the milder cases shows the apex-beat in its normal position and 
of about normal strength ; but if the amount of the pericardial effusion increases, 
the heart is pushed away from the chest-wall by it, and hence the heart-beat 
grows weaker until it disappears entirely. In such cases it is sometimes to be felt 
again if the patient bends forward or lies on his left side. In the rest of the car- 
diac region we sometimes feel the movements feebly, but they entirely disappear 
as the effusion increases. There is diagnostic importance in the contrast between 
the great extent of cardiac dullness (vide infra) and the faintly distinguishable 
motions of the heart, with absence of a distinct apex-beat and any marked epi- 
gastric pulsation. In some cases, by laying the hand flat on the chest, we can 
feel the rub of the rough pericardial surfaces against each other. 

The pulse is usually accelerated, and in severe cases it becomes irregular. In 
every large effusion, as we have already said, the tension and height of the pulse 
are diminished. In severe cases the pulse sometimes becomes very small and weak, 
but, when the heart is otherwise normal and strong, it may also remain quite 
strong — and indeed this condition of the pulse, in contrast to the great weaken- 
ing of the heart -beat, is sometimes of diagnostic significance. In some cases with 
a large pericardial effusion we have seen a manifest pulsus paradoxus — that is, a 
diminution or a complete disappearance of the radial pulse on every inspiration. 

Cha nges in percussion-resonance are evident as soon as the pericardial sac is 
distended with exudation. The so-called triangular shape of cardiac dullness is 



362 



DISEASES OF THE CIRCULATORY ORGANS 



regarded as especially characteristic of large pericardial exudations. The blunt 
apex of the triangle is found above in the second or third left intercostal space, 
near the edge of the sternum. The lateral boundaries run obliquely to the right 
and downward to about the right parasternal line, and to the left and downward 
to the left mammillary line, or beyond. The broad base of the triangle which lies 
below is usually not to be defined by percussion, on account of the adjacent left 
lobe of the liver. On the border of the dullness we often find a tympanitic reso- 
nance due to the retraction of the adjacent lung. 

In general, the author's personal experience forces him to say that we must 
not be too dogmatic in the establishment of special shapes of cardiac dullness, 
as peculiar to pericarditis. The fact of enlargement of the area of cardiac dull- 
ness, and the marked sense of resistance upon percussion, are important signs, but 
there is a considerable variety in the shapes of the dull area, although extension 
of the dullness upward and to the right may be regarded as particularly frequent. 
According to Ebstein's observations, the first change in percussion in incipient 
exudation is usually an extension to the right of the heart's apex, in a triangle 
between the heart and the liver. 

The area of the dullness depends, of course, in the first place, upon the amount 
of the effusion, but we must take special notice that in regard to this the relation 
is not constant. In old cases of pericarditis especially we sometimes find the 
cardiac dullness very extensive, while the autopsy detects only a little fluid in the 
pericardium. This is explained partly by a secondary dilatation of the heart, and 
partly by a persistent retraction of the lung. 

It is an often-mentioned but seldom available diagnostic sign of pericarditis 
that in many cases the still perceptible apex-beat lies within the cardiac dullness, 
since the pericardial effusion extends farther to the left than the heart itself. It 
is also worthy of note that the dullness in pericarditis often shows very great 
changes when the patient changes his position. The dullness is more extensive 
when the body is erect than when lying down, and when the patient lies on his 
side it sometimes shows a lateral displacement of several centimetres. The same 
changes, however, though rarely so marked, also occur in a hypertrophied heart. 

The characteristic pathognomonic auscultatory sign of pericarditis is the peri- 
cardial friction-rub. This arises during the movements of the heart from the 
rubbing of the rough and inflamed pericardial surfaces against each other. The 
friction-rub is absent in pericarditis if the rough surfaces of the two layers of the 
pericardium are separated from each other by a considerable fluid effusion, or if 
they can no longer rub against each other from an adhesion of the layers of the 
pericardium. We usually hear the friction-rub loudest in the neighborhood of 
the base of the heart, but it may also be heard at other parts of the heart. In 
general the adventitious sounds of pericarditis are not transmitted to any great 
distance. The quality of the sound is described as rubbing, grating, or scratching. 
The friction-rub may be heard chiefly either during the systole or during the 
diastole of the heart, but it is in general not often closely associated with the 
phases of the heart's action. We sometimes find it intermitting frequently, and 
jerky. The intensity of the friction-rub sometimes varies with the phases of the 
respiration. It is usually louder on inspiration, but sometimes on expiration. If 
the patient changes his position, the intensity of the sound is sometimes altered. 
It is louder when sitting up than lying down, etc. The friction-rub often sounds 
louder if the stethoscope is pressed firmly against the chest, since in this way the 
layers of the pericardium are approximated to each other. 

The heart-sounds, when the valves are intact, may sometimes be heard as well 
as the friction-rub, or they may be completely drowned by the loud rub, at least 
in some parts of the heart. In general, they are faint in every case of pericardial 
effusion, since their conduction to the ear is impaired. In large effusions where 



PERIGAEDITIS 



363 



no friction-rub is to be heard, we hear the heart-sounds, especially the first, but 
only very faintly and obscurely. This condition, in connection with the increase 
of the cardiac dullness, is of diagnostic importance. If there is also valvular dis- 
ease with the pericarditis, the pericardial and endocardial murmurs are some- 
times hard to distinguish from each other, but usually the former greatly pre- 
ponderate. 

3. Sequelae of Pericarditis. — A large pericardial effusion may excite special 
symptoms from pressure on the neighboring organs. Thus we have already said 
that compression of the left lung must increase the dyspnoea. In many cases we 
also notice a moderate dullness over the left lower back, from compression of the 
left lower lobe. Not infrequently there is a combination of pericarditis and left- 
sided pleurisy with effusion. In rare cases difficulty in deglutition has been ob- 
served as a result of pressure on the oesophagus, and paralysis of one vocal cord 
from pressure on the recurrent nerve. 

In cases of long-continued pericarditis the same sequelae may develop as in any 
chronic disease of the heart. The amount of urine diminishes as a result of the 
low arterial pressure. The venous stasis finally leads to general dropsy and to 
symptoms of passive congestion in the liver, spleen, and kidneys. We would also 
state that we have repeatedly met with large effusions in the cavities of the body, 
especially hydrothorax, without any cedema of the skin. All the symptoms of 
stasis mentioned, however, are often due much less to the pericarditis itself than 
to the atrophy and dilatation of the heart which frequently follow it {vide 
supra). 

Special Forms of Pericarditis 

1. Pericarditis externa and Mediastino-pericarditis (Pleura-pericarditis).— 
Py pericarditis externa we mean an inflammation of the external surface of the 
pericardial sac, which is usually combined with an inflammation of the mediastinal 
connective tissue and the neighboring- pleura, especially over the lingula of the left 
lung. This form of pericarditis may exist by itself, or it may be combined with 
internal pericarditis. It is a rare disease, and is most frequently seen as a result 
of tubercular pleurisy. 

The physical signs must differ so much, according to the localization and extent 
of the process, that we can give few general data in regard to them. There are 
only a few peculiar signs, which must be noted as characteristic of many cases. In 
the vicinity of the apex-beat, or at the left border of the cardiac dullness, we some- 
times hear a so-called extra-pericardial (pleuro-pericardial) friction-rub. This 
depends both upon the cardiac movements and upon the respiratory movements. 
The friction sound often becomes louder during- inspiration, or, again, it may be 
audible only when the lungs are fully inflated. On holding- the breath we hear 
merely the sound due to the pulsations of the heart, while on deep breathing' the 
pleuritic friction-sound is also to be heard. In individual cases there are many 
modifications, which can not all be mentioned. Another interesting- sign, first 
found by Griesinger and Kussmaul in a cicatricial mediastino-pericarditis, is the 
so-called pulsus paradoxus. This consists of a diminution of the pulse at each 
inspiration. This condition arises, in part of the cases at least, from the fact that 
the bands and adhesions of connective tissue at the origin of the aorta mechan- 
ically nick into and contract its lumen at every inspiratory movement of the 
thorax. This explanation, of course, does not suffice for all cases, since the pulsus 
paradoxus also occurs under other conditions, as with large pericardial effusions. 
In some cases there may be seen a marked swelling of the jugular veins in the 
neck at each inspiration, at the same time with the pulsus paradoxus, since 
the large venous trunks also undergo a mechanical nicking and constriction at 
each inspiration. We have ourselves seen a very pronounced slowing of the pulse 



364 



DISEASES OF THE CIRCULATORY ORGANS 



at every inspiration, in a complicated case of extra-pericardial adhesions (vagus 
irritation?). We must also mention that Riegel observed a disappearance of the 
apex-beat on expiration in some cases where there were bands of connective tissue 
between the lungs and the outer surface of the heart. At every expiration the 
bands were stretched more tightly, and hence checked the movements of the heart. 

2. Obliteration of the Pericardial Cavity (Adhesive Pericarditis; Adhesions 
of the Layers of the Pericardium; Concretio seu Synechia pericardii) . — We may 
have a more or less complete adhesion of the two layers of the pericardium with 
each other as a result of pericarditis. We can sometimes observe the occurrence 
of this condition during the course of a pericarditis. Quite frequently, however, 
we meet with extensive adhesions of the two layers of the pericardium at autopsies, 
without being able to gather any history of a previous acute pericarditis. The 
pericarditis must have occurred here in a chronic way, and without symptoms from 
the outset. 

Even extensive adhesions of the pericardial surfaces may develop and remain 
entirely without symptoms, and be met with accidentally at the autopsy. In 
other cases, however, the obliteration of the pericardial sac causes special physical 
signs and severe clinical sequela?. Of the physical signs, one of the best-known and 
most discussed is the systolic retraction of the chest, either limited to the apex or 
involving a larger area. This is most comprehensible if there is an adhesion of 
the pericardium with the heart, and also with the chest-wall (Skoda) ; but we cer- 
tainly find this retraction at the systole without co-existing extra-pericardial adhe- 
sions. It is not, however, an absolutely certain sign of an intra-pericardial adhe- 
sion, especially if we have to do with a systolic retraction at the apex alone, or 
limited to the third or fourth intercostal space, since systolic retractions may some- 
times occur in other disturbances of the heart's motions, or even under normal 
conditions ; but systolic retractions of the whole cardiac region are, in the major- 
ity of cases, a certain sign of pericardial adhesion. The amount of this retraction 
is often dependent upon the respiration, it being usually more marked on inspira- 
tion. 

On the other hand, it must be noted that very often there is no retraction of 
the prsecordia during systole, in many cases of undoubted obliterative pericar- 
ditis. In brief, the symptom under consideration is extremely ambiguous, and it 
must always be viewed with considerable reserve in forming a diagnosis. Of at 
least equal importance, in our opinion, is the obscurity or absence of any cardiac 
motion either to sight or touch. We can lay great diagnostic value upon the 
absence of a normal cardiac impulse, when the cardiac dullness is increased, al- 
though the heart-sounds are normal; and when the adjacent borders of the lung 
do not move with respiration, because of the adhesions due to the associated 
pleurisy (vide infra) ; and finally, when the history of the case and the general 
course of the illness are confirmatory, for instance, if there are indications of a 
previous acute pericarditis. % 

The other symptoms of obliteration of the pericardial cavity are more rare and 
in their diagnostic significance still more uncertain. Friedreich observed a sudden 
collapse of the jugular veins at each diastole — the " diastolic collapse " — while 
they became well filled again at the next- systole. He explained this phenomenon 
by supposing that the conditions for emptying the veins, at the moment of the 
diastole of the ventricle, were especially favorable, since the chest-wall, which had 
previously been drawn in by the systole, went back again quickly. But we have 
ourselves seen distinct diastolic collapse of the veins in a case of adhesive peri- 
carditis, the diagnosis of which was confirmed by autopsy, in which there was 
no systolic retraction of the prsecordia. Riess described some cases of pericardial 
adhesions in which the heart-sounds had a metallic character from the resonance 
of the stomach, which had been drawn up. All things considered, we must say 



PEEICAKDITIS 



365 



that although the diagnosis of pericardial adhesions can be correctly made in 
many cases, yet the signs given for it are more or less uncertain, since they may 
be absent in obliteration of the pericardial sac, and they may also be caused by 
other conditions without such an obliteration. In a word, it is no easy matter to 
establish the diagnosis of obliterative pericarditis, and in cases of this sort the 
autopsy not infrequently brings surprises, as our own experience has shown. 

The general constitutional symptoms of obliterative pericarditis are also sub- 
ject to great variations. In many cases the affection, as we have said, has no 
symptoms at all or at least no grave results. In other cases, however, there is 
distinct evidence of circulatory disturbance. This disturbance is sometimes due 
directly to the mechanical embarrassment of the heart, but more often to sec- 
ondary changes in the myocardium. We find atrophy, fatty infiltration, and 
fatty degeneration, with consequent dilatation. In such cases the pulse becomes 
small and frequent, and the ordinary picture of ruptured compensation is dis- 
played, characterized by oedema, dyspnoea, and congestion of the liver and kidneys. 
In these cases the diagnosis is often very difficult. It is scarcely possible to dis- 
tinguish between this form of pericarditis and chronic myocarditis, or the " idio- 
pathic " enlargement of the heart. 

There is another symptom-complex, somewhat different from the above, which 
deserves special mention. We have been acquainted with it for years, but it 
has only lately received general attention. Sometimes, when there is obliteration 
of the pericardial sac, there is developed a condition so like that of hepatic cir- 
rhosis (q.v.), that the name of " pericarditic pseudo-cirrhosis of the liver" has 
been applied to it. There are increasing dyspnoea and great ascites, with subse- 
quent oedema of the lower extremities, so that we have dropsy of the lower half 
of the body, while the upper half remains free from oedema (see Fig. 43). There 
may be, however, a serous effusion demonstrable in one or both pleural cavities. 
At the autopsy we do not find the hepatic cirrhosis which has in many cases been 
supposed to exist, but instead, a total obliteration of the pericardial sac, with 
which is often associated a nutmeg liver (sometimes atrophic, vide supra, page 
330), and often, also, chronic peritonitis and chronic pleurisy. The peritonitis 
causes a marked fibrous thickening of the peritoneum, apt to be especially marked 
on the surface of the liver, in the form of what is called " frosted liver." This 
condition, therefore, in many cases, should be classed as one of " chronic inflam- 
mation of the serous membranes" (vide supra, page 289). We may have a 
similar group of symptoms not associated with inflammation of the peritoneum, 
if the circulatory disturbance resulting from the obliteration of the pericardium 
affects chiefly the portal circulation. We have also observed a combination of 
obliterative pericarditis with genuine hepatic cirrhosis. In a word, the cases are 
not all after one pattern. The diagnosis can not be correctly made unless one 
is acquainted with the symptom-complex, and pays special attention not only 
to the history of the case but to the cardiac signs, such as increase in the area of 
•dullness, absence of apex-beat, or presence of systolic retraction. 

3. Tubercular Pericarditis. — Tubercular pericarditis is an important disease 
clinically, since in many cases it is apparently primary. It may be either quite 
acute or chronic. The patient falls ill suddenly, or more gradually, with indefi- 
nite thoracic symptoms, dyspnoea, general weakness, moderate fever, etc. If the 
disease is of long duration, there is more or less oedema. When we find on phys- 
ical examination, in such cases, the signs of pericarditis, the diagnosis of tubercu- 
lar pericarditis is probable, if we discover a general " phthisical habit," hereditary 
predisposition, and also co-existing disease of other serous membranes, especially 
pleurisy, or more rarely chronic peritonitis. In the latter case the tubercular 
pericarditis forms one symptom of the so-called tuberculosis of the serous mem- 
branes, but, as has been said before, apparently isolated primary tubercular peri- 



366 



DISEASES OE THE CIRCULATORY ORGAXS 



carditis does occur (vide supra). We have seen such cases repeatedly, especially 
in old people. In these cases the disease is not easy to diagnosticate. The patient 
gives one the impression of having heart disease, but the physical signs in the 
heart are sometimes of a very indefinite nature. Eriction-rubs may be entirely 




Fig. 43.— Pseudo-hepatic cirrhosis due to pericarditis. (Personal observation.) 



absent, on account of adhesions or of large effusions. This leads to confusion 
with myocarditis or mitral stenosis. In other cases, of course, all the physical 
signs of pericarditis mentioned above may be manifest, and a correct diagnosis 
can be made. 

Diagnosis. — From what precedes, it follows that the diagnosis of pericarditis is 
very easy in many cases, but is very difficult or impossible in others. The most 
unequivocal sign is the characteristic friction-rub. The practiced ear can often 
distinguish it from an endocardial sound by its quality. The pericardial sound 
is a rubbing, grating noise, near the ear; the endocardial is blowing, distant from 
the ear. The following features may serve as marks of distinction in doubtful 
cases : 1. "We hear the pericardial sounds at first, and also later, over the base of 
the heart in the vicinity of the pulmonary valve : the endocardial are often loudest 



PERICAKDITIS 



36T 



at the apex. 2. The pericardial murmurs are not so closely associated with the 
phases of the heart's action, with systole and diastole, as the endocardial. 3. 
We find that the pericardial sounds are not transmitted far. A loud rub may be 
audible at one spot which can not be heard a few centimetres away. Loud endo- 
cardial murmurs, however, are audible over almost the whole heart. 4. Some- 
times the peculiarity of the pericardial murmur — -that it becomes louder when 
the patient sits up, on pressure with the stethoscope, etc. — may be of diagnostic 
value. In many cases the loud, functional, so-called anaemic murmurs over the 
base of the heart may give rise to confusion with pericarditis. 

If no pericarditic friction has been heard during any part of the illness, it is 
seldom possible to make an absolute diagnosis of pericarditis. At least, we must 
confess that we have made many errors in the diagnosis of such cases. Important 
factors to be considered are the general course of the disease, including the acute 
onset and precordial pain, and also the shape of the cardiac dullness (triangular), 
and the signs furnished by the apex-beat, the pulse, and the heart-sounds. We 
have already pointed out the possibility of confusion between pericarditis and 
myopathic disease of the heart, and mitral stenosis if unattended by murmur. E"o 
rules of universal application in these cases can be laid down. It is very often 
advisable, and absolutely devoid of danger, to make an exploratory puncture in 
doubtful cases with a hypodermic syringe. This is done at the left edge of the 
sternum, or a little way in from the left limit of cardiac dullness. 

Course and Prognosis. — Many cases of pericarditis in articular rheumatism,, 
pneumonia, or heart disease, and also many of the rare and apparently primary 
forms, may recover completely. The disease lasts, in the mild cases, only about 
a week, in severe cases much longer. 

Many cases of pericarditis, however, terminate fatally. The unfavorable issue 
depends either upon the severity of the primary disease, or upon the intensity 
of the pericarditis itself. In extensive croupous pneumonia, in valvular disease 
of the heart, or in severe chronic nephritis, an attack of pericarditis is often the 
terminal affection — the immediate cause of death. In otherwise healthy persons, 
however, a severe pericarditis with a large effusion may be the direct cause of 
death, as a result of the impairment of the movements of the heart. Yet one need 
not wholly despair, particularly in rheumatic pericarditis, even in cases which 
seem very bad. The prognosis of tubercular pericarditis is always very unfa- 
vorable. This form may, indeed, run quite a chronic course, but it is hardly 
ever capable of definite recovery. The prognosis of pysemic pericarditis is also- 
unfavorable. 

In one class of cases pericarditis takes a chronic course from the start, or 
chronic pericarditis develops from an acute attack. The ultimate prognosis of 
these cases is usually unfavorable, since the secondary atrophy and dilatation of 
the heart gradually lead to severe disturbances of the circulation. We have 
spoken above of the termination of pericarditis in obliteration of the pericar- 
dial sac. 

Treatment. — Since pericarditis is a severe affection under all circumstances, we 
must see especially that the patient has perfect rest and care. Extreme caution 
must be enjoined upon him, especially in the cases in which at first the subjective 
symptoms are slight. We must keep the patient strictly confined to the bed, and 
not let him leave it even temporarily. 

The remedies which are used against pericarditis aim partly at keeping the- 
inflammation in check, and partly at aiding the action of the heart. For the first, 
the continued application of ice to the cardiac region deserves especially to be 
recommended. Local blood-letting, ten or twelve leeches to the cardiac region 
■ — formerly very often but now more rarely used — may, in otherwise strong and. 
healthy persons, afford great relief in cases with marked subjective symptoms. 



368 



DISEASES OE THE CIRCULATORY ORGANS 



Painting with tincture of iodine and blistering, however, deserve little confi- 
dence. Digitalis is our chief means to bring down an accelerated pulse, and to 
strengthen the heart's action. It is a drug which is most active and most fre- 
quently used in pericarditis, and is always indicated when the pulse is rapid and 
of diminished tension. Of course, the action of the remedy must be carefully 
watched, as in all cases where digitalis is prescribed. Tincture of strophanthus is 
also useful. As a palliative, morphine often does indispensable service when the 
subjective symptoms are marked and the patient is very restless. Diuretics are 
also employed, as in pleurisy with effusion (q. v.). 

If the symptoms are threatening, the question arises whether a large fluid peri- 
cardial effusion is the cause of the severe symptoms. In this case the evacuation 
of the exudation is of course imperatively indicated. The difficulty of forming 
a correct opinion, however, is very great, because in any individual case it is rarely 
possible to determine the amount of fluid that may be present. In the first place, 
we must consider the size of the cardiac dullness and the weakening of the move- 
ments of the heart, but both factors may give rise to deception. Hence we always 
first make an exploratory puncture with a Pravaz's hypodermic syringe. The best 
point for insertion is, in general, the sternal end of the fourth or fifth [left] inter- 
costal space with the patient on his back, partially raised in bed. If the explora- 
tory puncture gives a positive result, we make a puncture with Billroth's, Fraent- 
zel's, or some similar trocar. With regard to the details, we will refer to the 
description of puncture of the pleura. Puncture of the pericardium is always 
performed by the aid of aspiration. It is less dangerous than might be feared. 
Even injuries to the heart during the operation have scarcely ever had grave re- 
sults. The temporary relief to the patient, in cases of successful puncture, is 
usually very striking, but the permanent results of pericardial puncture are, of 
course, much less favorable than those of puncture of the pleura, which is chiefly 
due to the character of the underlying disease. In some cases of purulent peri- 
carditis, incision of the pericardium has also been practiced after the analogy of 
the treatment of empyema. In other forms of pericarditis with an abundant 
fibrino-serous exudation, it might often be preferable to make an incision rather 
than to aspirate, but there has not yet been much experience with the former 
method. 

[The experiments of Rotch show that pericardial effusion causes dullness in the 
fifth right interspace, a sign which he thinks is not produced in cardiac enlarge- 
ment. So far as is known to the editor, he is the only person who has acted on 
this observation, and punctured on the right of the sternum for pericardial effu- 
sion. In the case referred to, the signs pointed to a very large acute effusion of 
rheumatic origin. The first puncture was made in the fifth left interspace, but 
only about an ounce and a half of bloody serum was obtained. The needle was 
then withdrawn and immediately inserted in the fourth right space near the sternal 
border with absolutely negative result. The gravity of the symptoms led to two 
more punctures on the left some days later, one with small though positive result, 
the other with negative. Absorption and recovery ultimately took place. 

The recommendation of the author to make a preliminary puncture with a 
hypodermic syringe for diagnostic purposes seems unnecessary, just as with pleural 
effusions.] 

If there is a condition of cardiac weakness, stimulants are indicated — strong 
wine, subcutaneous injections of ether or camphor, or wine of musk. We try to 
keep up the patient's strength by the best of nourishment. 

The resulting conditions of disturbance of the circulation, such as oedema, in 
chronic pericarditis, are treated in the same way as in valvular disease (vide 
supra). Digitalis and diuretics are the chief remedies. 



HYDRO-PERICARDIUM 



369 



CHAPTER II 

HYDRO-PERICARDIUM, HiEMO-PERICARDIUM, AND PNEUMO- 
PERICARDIUM 

1. Hydro-Pericardium 

{Dropsy of the Pericardium) 

The collection of a serous transudation in the pericardial sac, without any in- 
flammatory symptoms in the serous membrane itself, we term hydro-pericardium, 
or dropsy of the pericardium. Dropsy of the pericardium, which formerly played 
quite a great role in pathology, is never a disease of itself, but is always a sec- 
ondary condition. It may occur in anaemic and cachectic persons as a result of 
hydrsemia, but it usually depends upon a local or general venous stasis in the 
pericardium. In the latter case the hydro-pericardium is one symptom of general 
dropsy, and hence is found chiefly in heart disease, renal disease, or pulmonary 
emphysema. 

The clinical symptoms of hydro-pericardium are only exceptionally distinct, 
being obscured by the underlying affection. Large amounts of fluid in the peri- 
cardial sac, which may amount to a quart (a litre) or more, must of course impair 
the action of the heart, weaken the heart-beat objectively, and cause an increase in 
the cardiac dullness. The distinction from pericarditis is rendered possible by 
the absence of a friction-rub, but especially by attention to the existence of an 
underlying disease. In other respects the distinction between a pericardial tran- 
sudation and an effusion during life is not always easy. 

The prognosis and treatment depend wholly upon the nature of the underlying 
disease. Only exceptionally do we need to puncture, when the exudation is very 
large. 

2. Hsemo-Pericardium 

{Blood in the Pericardial Sac) 

In rare cases haemorrhages occur into the pericardial sac. The source of the 
haemorrhage is most frequently an aneurism of the aorta, which perforates into 
the pericardium. Other causes of haemorrhage are the bursting of aneurisms of 
the coronary arteries and rupture of the heart. The latter has been seen after 
injuries, and also as a result of cardiac aneurism and the cicatricial formations 
in myocarditis (see myocarditis). Finally, direct injuries to the heart, especially 
bullet-wounds, may also cause haemorrhages into the pericardial sac. 

In most cases death occurs in a few moments from compression of the heart, 
when a haemo-pericardium comes on. Hence the amount of blood poured out into 
the pericardial sac is usually not very considerable. Only in the cases in which 
the blood oozes out more slowly can a great distention of the pericardial sac be 
reached. The diagnosis is rarely possible. With regard to treatment we can 
merely note that, in some traumatic cases, the aspiration of the blood has been 
performed with success. 

3. Pneumo-Pericardium 

{Air in the Pericardial Sac) 

The entrance of air or gas into the pericardial sac has been observed in rare 
cases, apart from external wounds, as a result of the perforation of a pyopneumo- 
thorax, or of some other suppurating process in organs that contain air. Thus 
cases are known in which the rupture into the pericardial sac comes from the 
oesophagus, as in cancer; from the stomach, in cancer or ulcer; or from the lungs, 
24 

! 



370 DISEASES OF THE CIRCULATORY ORGANS 



in tubercular or gangrenous cavities. Since the agents of inflammation enter the 
pericardium along with the air, a purulent pericarditis almost always develops, 
besides the pneumo-pericardium, or it may rarely be simply a sero-fibrinous peri- 
carditis. 

The most characteristic and striking sign of pneumo-pericardium is the pres- 
ence of a metallic sound, due to the movements of the heart. Either the heart- 
sounds themselves, or some existing friction-rub, may acquire a metallic timbre 
from the increased resonance, or splashing metallic sounds may be produced in 
the pericardial sac from the movements of the air and the fluid, which may often 
be heard at a distance from the patient. In regard to diagnosis, however, it is 
important to know that signs similar to those of metallic resonance in the heart 
may arise from the stomach, when it is drawn or pushed upward. 

In true pneumo-pericardium percussion gives a more or less complete absence 
of the cardiac dullness. On rod-percussion (see page 297) a metallic sound is some- 
times heard, whose pitch may vary somewhat with the phase of the heart's action. 
If fluid is also present in the pericardial sac besides the air, the dullness caused 
by this will rise on raising up the patient. 

The other symptoms of the disease and the treatment are the same as in a 
severe pericarditis. The prognosis, however, corresponding to the primary dis- 
ease, is wholly unfavorable. 



SECTION III 
Diseases of the Vessels 

CHAPTER I 

ARTERIO-SCLEROSIS 

{Endarteritis chronica deformans. Atheroma of the Vessels) 

-ZEtiology. — Atheromatous degeneration is probably in most cases an expres- 
sion of the wearing out of the arteries, because of the many ways in which the 
intima of the arteries is damaged during life, both chemically and mechanically. 
Atheroma of the arteries is then mainly a change incident to age, and as such 
is often regarded as not a true disease. 

On the other hand, if arterio-sclerosis appear in earlier life, say before the 
fortieth year, we must look for such circumstances as would tend to make the 
ordinarily efficient causes unusually active. We must not forget that there is 
an apparent predisposition to the condition, which often seems to be hereditary; 
but without doubt there are more appreciable causes. The reason that arterio- 
sclerosis is so common and occurs comparatively so early in hard laborers, is the 
great mechanical strain which the arteries undergo during persistent, severe, bodily 
exertion. Again, in diseases which are associated with a persistent elevation of 
arterial tension, such as hypertrophy of the left ventricle in interstitial nephritis, 
arterio-sclerosis develops probably as a result of the constant high tension. It 
must be confessed that here a decision is often very difficult, inasmuch as the ar- 
terial disease may be simultaneous with the nephritis, or even the actual cause of 
it. Again, excessive chemical irritation must be considered, as experience shows 
that a continued excess in eating and drinking, particularly in the use of alcohol, 
is apt to occasion arterio-sclerosis ; and in the same connection are to be named 
such constitutional diseases as syphilis, gout, and chronic nephritis, and perhaps 
also definite poisons such as lead. INTor can we disregard the possibility that the 



AKTEKIO-SCLEKOSIS 



371 



disease may follow persistent mental strain and excitement. All these circum- 
stances explain why well-marked atheroma is far more frequent in men than in 
women. 

Pathological Anatomy. — Atheroma is almost exclusively confined to the arte- 
ries; only exceptionally do like processes occur in the veins. Among the arteries 
the aorta is almost always the most intensely and extensively diseased; we also 
find disease in the iliac and femoral arteries, the brachial, radial, and ulnar, the 
coronary arteries of the heart, and the arteries of the brain. In some of the other 
arteries, however, like the gastric artery, the hepatic, and the mesenteric, we very 
rarely find atheromatous changes. 

The atheromatous process is easy to recognize macroscopically. Instead of the 
normal smooth internal surface, we find more or less numerous irregularities and 
thickenings on the intima, which appear either more or less gelatinous and trans- 
lucent, or dense and fibrous, or ossified as a result of calcification, in which case 
they also feel perfectly hard. In many cases we find the surface of the thicken- 
ings destroyed — atheromatous ulcers — and covered with masses of fibrine. 

The wall of the arteries is usually increased in thickness, making the vessel 
feel stiff and hard. Very frequently the calcareous plates may be felt by the 
finger. The frequently associated increase in arterial tension gradually stretches 
the walls of the arteries, rendering them tortuous. This is best seen in those 
of medium size, such as the brachial and radial. 

Microscopic examination shows that the chief changes are situated in the 
intima of the arteries. This appears three or four times as thick as normal, 
partly from the swelling of its elements and partly from the new growth of con- 
nective tissue and the deposit of round cells. In the connective-tissue cells of the 
intima, and in the endothelial cells of its surface, we usually find a marked fatty 
and hyaline degeneration, to which the yellowish, translucent appearance of the 
surface is due. Finally, in the deeper layers there is a complete breaking down of 
the tissue into a mixture of fat, detritus, and cholesterine crystals, which has 
given the whole process the name of atheroma [ = pulp] . If this destruction ex- 
tends to the surface, an atheromatous ulcer is formed. In other places, however, 
it does not reach ulceration, but the superficial layers of the intima become scle- 
rosed, and are finally changed to lamellae of bony hardness from the deposition of 
lime-salts. The atheromatous spots on the -intima of the vessels often give rise 
to the formation of parietal thrombi. 

The media and adventitia of the arteries also show changes, in the later stages 
of the process. Here, too, we may finally get fatty degeneration and calcification. 
In other cases, however, there is a marked atrophy of the media. 

The immediate result of the atheromatous changes is a loss of elasticity in the 
walls of the vessels. The ability to resist the blood-pressure is reduced, and this 
is why diffuse or circumscribed aneurismal dilatations of the vessels so often arise 
as a result of arterio-sclerosis (see the following chapters). 

Another result of extensive atheromatous degeneration of the vessels is an 
increase of the resistance to the blood-current, and a consequent elevation of the 
arterial pressure. Furthermore, the loss of elasticity in the coats of the medium- 
sized and smaller arteries removes an important factor for the propulsion of the 
blood. The left ventricle, in consequence of these additions to its task, becomes 
almost invariably hypertrophied in cases of extensive arterio-sclerosis, provided 
the general nutrition of the patient is still well maintained. 

We see, therefore, how close the mutual relations are between increased 
arterial tension, hypertrophy of the left side of the heart, and arterio-sclerosis. 

The thickening of the intima in the smaller vessels often causes so marked a 
diminution of the blood-supply that secondary disturbances of nutrition are not 
wanting in the various organs. The lumina of the vessels may be still further 



372 



DISEASES OF THE CIRCULATORY ORGANS 



narrowed, or even completely closed, by the formation of thrombi on such por- 
tions of the wall of the vessels as have undergone atheromatous changes. We 
have already in part learned to recognize the sequelae which necessarily arise in 
the various organs, such as indurations in the heart as a result of atheroma of 
the coronary arteries, and we will return later on to the analogous changes in 
some other organs, such as cerebral softening and certain forms of contracted 
kidney. 

Clinical Symptoms. — In order to decide whether an arterio-sclerosis is present 
in the living subject, we are of course restricted exclusively to the examination of 
those peripheral arteries that are accessible to palpation. We must examine, first 
of all, the radial, brachial, femoral, and temporal arteries. If there is atheroma, 
we feel the hard and partly calcified vascular tube. In marked cases we have a 
feeling, especially in the radial, as if we had hold of a goose's neck. We some- 
times notice a diffuse dilatation of the femoral arteries. In many cases the 
marked spiral form of the vessels is very striking, and it is, as we have said, a 
direct result of the loss of elasticity of their walls and of the increased blood- 
pressure. The spiral form is most frequently observed in the temporal, brachial, 
and radial arteries. 

Although we can often directly demonstrate atheroma in the vessels men- 
tioned, we must always be cautious in deciding from this that there is also an 
atheroma of the internal arteries, for the radial arteries often feel very rigid, 
while the autopsy later on shows little or absolutely no atheroma of the internal 
arteries. In other cases, however, we find at the autopsy marked atheromatous 
changes in the arteries of the brain, the kidneys, the heart, etc., although the 
external arteries during life felt perfectly normal. We see from this how hard it 
is to make an absolute diagnosis of general arterio-sclerosis. 

It is impossible to give a uniform picture of arterio-sclerosis, since its results 
appear now chiefly in this organ and now chiefly in that, whereby entirely dis- 
tinct types of disease arise. Hence we must confine ourselves here only to men- 
tioning briefly the most important sequelae. Eor the most part, they are described 
separately in other portions of this work. 

In the heart we find a hypertrophy of the left ventricle as a result of the in- 
creased resistance to the arterial circulation. This is often apparent during life 
from the strength of the apex-beat and its displacement to the left, and also from 
the extension of the area of cardiac dullness to the left. On auscultation, the 
increased tension in the aortic system is made manifest by the strength of the 
aortic second sound. The examination of the heart, however, is often rendered 
difficult by the presence of pulmonary emphysema. On the other hand, we some- 
times can not decide how far a manifest hypertrophy of the left ventricle is due 
to an arterio-sclerosis, and not to other co-existing processes, such as contracted 
kidney. We often find other anatomical changes in the heart besides hypertrophy 
of the left ventricle. We have already spoken of the important and interesting 
results of atheroma of the coronary arteries, the formation of the so-called indura- 
tions of myocarditis in the heart (see page 340 et seq.). Sometimes, from an 
invasion of the aortic valves by the atheromatous process, we get an insufficiency, 
or much more rarely a stenosis of the aortic orifice. Finally, we may also mention 
here that atheroma, especially of the ascending aorta or the arch, is the common- 
est cause of the formation of aneurism of the aorta. 

We have already described the character of the peripheral arteries. The radial 
pulse is hard and tense, and the wave is either quite large, or, when the tube is 
very narrow, small. Since the wall of the vessel contracts only slowly, in conse- 
quence of its loss of elasticity, the radial pulse is usually sluggish — pulsus tardus. 
This condition is also pronounced in the sphygmographic tracing, which shows 
a slow ascent, and a still slower descent, of the pulse-curve, and an absence of the 



AETEEIO-SCLEKOSIS 



elevation in the descending limb of the curve, due to the normal elasticity. The 
frequency of the pulse is quite different in different cases ; it is often rather slow 
as a result of sclerosis of the coronary arteries. The pulse is very often irregular 
as a consequence of changes in the heart. We sometimes find an abnormal delay 
in the radial pulse, or in the pulse in other arteries, in comparison with the heart- 
beat, from the lessened rapidity of transmission of the pulse-wave. 

Besides the heart, the brain is the chief place in which we observe definite 
results of arterial sclerosis. The increased tendency to rupture which the athe- 
romatous vessel-walls show, and the co-existing heightened blood-pressure, explain 
the comparatively frequent occurrence of cerebral haemorrhages. Cerebral haemor- 
rhages often result from little miliary aneurisms, which have formed in the athe- 
romatous cerebral arteries. Atheroma is also the most frequent cause for the 
formation of foci of softening in the brain, since the arterial changes may give 
rise to a closure of the cerebral arteries from thrombosis or embolism. Finally, 
so-called senile dementia, or, at any rate, many cases of that condition, are ref- 
erable to cerebral atrophy, resulting from the faulty nutrition of the brain 
through the sclerosed arteries. 

In the kidneys, too, atrophic processes often develop from the diminution of 
the blood-supply owing to the narrowed lumina of the vessels, and they lead to 
a special form of contracted kidney. The origin of the granulated " senile kidney " 
is in large part atheroma of the renal arteries. 

The lower extremities display symptoms of arterio-sclerosis less often than 
the parts already mentioned, but if present the symptoms may be very striking. 
Here belongs a peculiar group of symptoms, which has been specially studied by 
Charcot, Erb, and others. It is termed intermittent claudication or lameness, or 
dysbasia intermittens angio sclerotica (Erb). It is sometimes associated with 
lesions of one or both femoral or iliac arteries, more often with obliterative arter- 
itis of the distal arteries of the lower leg and foot. It usually begins with dis- 
agreeable paraesthesise of crawling, tickling, or coldness in the feet and calves. If 
the patient walks even for a short time the symptoms increase, the feet grow cold ; 
and blue, there is actual pain, and the patient becomes completely incapable of 
walking farther. After a short pause he can resume his walk, but soon he has to 
stop again. Upon examination we find the feet and legs cold and bluish-red. If 
we palpate the arteria dorsalis pedis, or the tibialis postica, we can detect no pul- 
sation whatever. This is the diagnostic sign. The course of the trouble is chronic, 
but decided improvement may ensue under correct treatment (vide infra). Erom 
a prognostic point of view there is an unfavorable tendency to the development of 
gangrene of the toes, as the arteritis increases. With regard to causation, an im- 
portant part in the development of intermittent lameness is played by syphilis, 
excess in tobacco, glycosuria, damage from thermic influences, and other causes. 

Sometimes gangrene of the lower extremities occurs as a result of marked 
atheroma without any previous appearance of intermittent lameness. So-called 
" spontaneous gangrene," senile gangrene, and diabetic gangrene are probably, 
without exception, due to primary lesions from arteritis and consequent impair- 
ment in the arterial blood-supply. 

All this shows how different the symptoms of arterio-sclerosis may be in differ- 
ent cases. The symptoms in the vascular apparatus often predominate over all 
others. The heart, which is simply hypertrophied, or which has undergone in part 
cicatricial degeneration, is finally paralyzed, and then all the symptoms of a 
chronic heart disease develop — dyspnoea, oedema, etc. If there is also albumi- 
nuria, a type of disease is produced which resembles that of contracted kidney. 
In other cases, however, the symptoms in the brain are especially manifest, either 
alone or in combination with the other symptoms mentioned, and, finally, in rare 
cases we have the above-described symptoms relating to the lower extremities. 



374 



DISEASES OF THE CIKCUL AT OEY OEGAXS 



"We must remark, however, in conclusion, that all the results of arterio- 
sclerosis mentioned may be absent for a long time or altogether. Many persons 
have practically no symptoms at all from their arterio-sclerosis, and reach an 
advanced age, but we must always consider the possibility of the sudden occur- 
rence of severe symptoms, and make our prognosis accordingly. 

Treatment. — If we recall the above-mentioned causes of arterial sclerosis, we 
see at once the possibility and importance of prophylaxis, and of course if the 
disease already exists we must endeavor to avert these injurious influences, so as 
to limit the progress of the disease as far as possible. There is little direct influ- 
ence upon the arterio-sclerotic process to be expected from drugs. Iodide of 
potassium has won the highest reputation in this regard, and it is employed 
extensively in all cases of arterio-sclerosis. Probably it is most efficient in those 
cases which are associated with a syphilitic taint. In general, treatment must be 
symptomatic, according to the indications in each instance. In the symptom- 
complex known as intermittent lameness, Erb recommends iodide of potassium, or 
iodide of sodium; local applications of warmth (for instance, by means of the 
warm pack) ; galvanic foot-baths ; such cardiac tonics as strophanthus ; and 
careful regulation of bodily exercise. If gangrene has set in, prompt amputa- 
tion of the necrotic part is necessary, for we have no means of influencing the 
process itself. In each case treatment must be adapted to the sequelae which 
ensue. Prophylaxis is important. It may hinder, or at least delay, the develop- 
ment of the process if the patient avoids the causes already enumerated. 



CHAPTEK II 

ANEURISM OF THE THORACIC AORTA 

etiology and Pathological Anatomy. — The circumscribed dilatation of an 
artery is termed an aneurism. The cause of its formation is almost always to 
be sought in a primary disease of the vessel-wall, which weakens its resistance to 
the blood-pressure. As we have already said in the previous chapter, it is chiefly 
arterio-sclerosis which lies at the foundation of aneurisms in many cases. The 
same factors, therefore, which favor the origin of arterio-sclerosis belong to the 
aetiology of aneurism. This explains why the root of the aorta, where arterio- 
sclerosis is most marked, is also the most common seat of aneurism, and further, 
why aneurisms are especially seen in advanced life and in men. Still, the develop- 
ment of aneurism is a rare occurrence in comparison with the great frequency 
of arterio-sclerosis ; so that there are probably other circumstances of importance 
which we shall some day know more about. Possibly there is a congenital weak- 
ness of certain portions of the arterial wall. Traumatic influences, also, are not 
wholly out of the question. Lately many authors have laid special weight 
on syphilis affecting the intima of the aorta. Indeed, syphilis is said by some 
to be by far the most frequent factor in the aetiology of aneurism of the aorta. 
This seems to us an exaggerated view, but certainly the point deserves consid- 
eration. 

[The occurrence of aneurism in early middle rather than in advanced life shows 
that too much stress can be laid on atheroma as a cause. That sudden strain often 
plays an important part in the aetiology can scarcely be doubted, though the cases 
in which a perfectly healthy aorta yields locally to internal pressure must be very 
rare. It is highly probable that violent exertion tends to produce changes in the 
walls of the aorta. The far greater frequency of aneurism in the male sex is 



ANEURISM OF THE THORACIC AORTA 



375 



notable. Syphilis, gout, alcoholic excess, and lead-poisoning appear to be factors 
in some cases.] 

The size of aneurisms of the aorta varies jrery much, of course, in different 
cases. They most frequently are about the size of an apple or the fist ; but in rare 
cases much larger aneurisms are observed. According to their shape we distin- 
guish the more diffuse or spindle-shaped dilatations from the saccular aneurisms 
(aneurisma diffusum sen cylindricum, aneurisma fusiforme, et aneurisma sac- 
ciforme). Intermediate forms and combinations of the different forms occur in 
manifold ways. 

As we should expect from its origin, we never find the Trail of the aneurism 
formed of a normal vessel wall. The intima almost always shows the same 
changes that are characteristic of arterio-sclerosis, only in a much higher degree. 
The media, too, is usually changed, and its muscular structure often shows fatty 
degeneration. The adventitia is usually thickened by chronic inflammatory pro- 
cesses. The media, and sometimes the intima, are in many cases so much atro- 
phied that the wall of the aneurism, at least in part, is formed only of the adven- 
titia. 

In the cavity of the aneurism the blood is only partly fluid. We usually find 
it more or less full of new and old masses of thrombi. The oldest thrombi, which 
lie upon the wall of the aneurism, are firm, yellowish, adherent to the wall, and 
sometimes calcified. At other points the thrombi are softened and broken down. 
The most marked coagulation is usually found in the saccular aneurisms with a 
narrow entrance, because in this form of aneurism the blood is almost completely 
stagnant in the aneurismal sac. 

Aneurisms of the aorta usually have their seat in the ascending aorta, or in 
the arch. Aneurisms of the descending thoracic and of the abdominal aorta are far 
more rare. The following description refers principally to aneurisms at the be- 
ginning of the aorta. 

"We do not give separate consideration to aneurism of the ascending aorta and 
of the arch of the aorta, respectively, for it is impossible clinically to draw a sharp 
distinction between them. Other aneurisms will be considered further on. 

Clinical Symptoms. — The subjective sensations of the patient, relating directly 
to the aneurism, are of a very uncertain nature, and are often entirely absent. In 
other cases there is pain in the region of the aneurism, either only a slight sense 
of pressure, or very severe and subject to paroxysmal increase, sometimes rather 
localized, sometimes radiating into the back, the shoulders, and the extremities. 
Sometimes, too, the patient feels the beating and pulsation of the aneurism. 
The remaining symptoms of aneurism may be divided into two groups. The first 
group embraces those symptoms which are directly related to the aneurism itself, 
and most prominent in this group are the physical signs. The second group of 
symptoms includes the resultant phenomena which the aneurism occasions in the 
circulatory apparatus and by pressure upon the neighboring parts. 

1. Physical Signs. — It depends entirely upon the position of an aneurism of 
the aorta whether it causes physical signs or not. Deep aneurisms, which no- 
where approach the chest-wall, may, of course, be quite inaccessible to direct ex- 
amination. 

Aneurisms of the ascending aorta, however, and of the arch, often extend so. 
near to the anterior wall of the chest that they cause an abnormal pulsation. "We 
feel this most frequently at the sternal end of the second right intercostal space, 
or over the upper part of the sternum. The pulsation of an aneurism of the arch 
of the aorta may sometimes be felt in the root of the neck. It often occurs a 
moment later than the systole of the heart. In many cases the pulsation is clearly 
double, analogous to the normal dicrotism of the pulse. We sometimes feel a 
slight systolic thrill with the flat of the hand. In the rare aneurism of the de- 



376 



DISEASES OF THE CIRCULATORY ORGANS 



scending thoracic aorta the pulsating swelling may make its appearance in the 
back, between the vertebral column and the left scapula. If the aneurism has 
reached a certain size, the pulsating part protrudes as a tumor. The protrusion is 
either merely slight, or in many cases it forms a large prominent swelling. It 
then shows usually a marked pulsation, not only from below upward, but also in a 
lateral direction, which is of diagnostic significance. In large aneurisms, how- 
ever, the pulsation sometimes is only very weak, and scarcely perceptible, from 
the formation of many coagula. 

[The Roentgen ray furnishes a most valuable means of searching for thoracic, 
aneurism, as the latter casts a shadow which dilates with each cardiac sys- 
tole— V.J 

The marked prominence of large aneurisms is possible only because the cover- 
ing parts, not only the muscles and skin, but also the cartilages and bones, the 
ribs and sternum, are brought to a gradual atrophy and wasting by the persistent 
pressure. The skin over large aneurisms gradually becomes thinner and thinner, 
until finally it may even become necrotic. 

There is of necessity more or less dullness on percussion over every aneurism 
of any size. The dullness is usually evident in the upper right intercostal spaces, 
or the adjacent parts of the sternum. Sometimes it even precedes the palpable 
pulsation, although then its significance is usually still very uncertain. In rare 
cases of aneurisms of the ascending aorta and of the arch, dullness and abnormal 
pulsation have been observed to the left of the sternum. 

Auscultation gives varying results. In some cases (probably chiefly when 
many coagula form) we hear nothing at all over the aneurism. In other cases we 
hear one or two sounds, which are usually the audible heart-sounds transmitted. 
Perhaps a systolic sound may also arise from vibration of the wall of the aneu- 
rism. In other cases, we hear a murmur over the aneurism. A dull and usually 
not very loud systolic murmur often arises from the formation of eddies in the 
aneurismal sac. If we also hear a diastolic murmur, it is almost always due to a 
co-existing insufficiency of the semi-lunar valves of the aorta (vide supra). 

2. Sequelce. — An aneurism of the aorta by itself probably never causes such an 
increased resistance to the blood-current as to give rise to the development of 
a hypertrophy of the left ventricle. In the quite frequent cases in which hyper- 
trophy of the left side of the heart exists, it may almost always be referred to a 
co-existing insufficiency of the aortic valves, and sometimes to very extensive 
atheroma of the arteries. During life a hypertrophy of the heart may be simu- 
lated, because the heart is pushed to the left by the aneurism. 

In many cases the signs in the peripheral arteries are important. Marked 
inequality of the pulse in symmetrical arteries is often an especially valuable 
diagnostic sign. Either the trunk of an efferent vessel is compressed by the 
aneurism, or the lumen of the exit of the vessel is itself involved in the aneurism, 
and hence the opening of the vessel is distorted or contracted, or partly stopped 
by a coagulum. This readily explains why, in aneurism of the ascending aorta, 
the radial, and sometimes the carotid pulse, are plainly weaker on the right than 
on the left, as a result of implication of the trunk of the innominate, while in 
aneurism of the arch or of the beginning of the descending aorta the opposite 
condition may obtain. Abnormal differences, too, in the intensity of the pulse in 
the upper and lower halves of the body may arise under some circumstances. 

[W. S. Oliver has described a valuable sign to which he gives the name of 
" tracheal tugging." In aneurism of the transverse arch with pressure on the 
left primary bronchus, a distinct downward pull, synchronous with the heart- 
beat, can be felt by the thumb and forefinger on either side of the inferior bor- 
der of the cricoid cartilage, when the patient, in the erect or sitting posture and 
with the mouth shut, raises the chin as far as. he can. The late R. L. IfacDon- 



ANEURISM OF THE THORACIC AORTA 



377 



nell, of Montreal, has shown that non-aneurismal tumors in this region are not 
accompanied by this sign, and that pressure on the trachea, from whatever cause, 
does not produce it. It may be the sole sign of aneurism present, and may then 
possess the double diagnostic value of indicating both the nature and exact seat of 
the disease. — Editor. Very exceptionally, tracheal tugging is caused by other 
conditions than thoracic aneurism. — V.] 

A marked delay of the pulse in the arteries arising below the aneurism is a 
symptom that is occasionally seen. Thus, we see in aneurism of the arch of the 
aorta that the left radial pulse is later than the right, and that in aneurism of the 
descending aorta the pulse in the lower extremities is later than the radial pulse. 

We see very striking signs in the veins if the large venous trunks in the 
thorax, the superior vena cava, or an innominate vein, are compressed by the 
aneurism. The veins swell in the neck, in the upper extremities, or upon the sur- 
face of the thorax, according to the seat of the compression. Local oedema may 
also be produced in this way. 

The respiratory organs are exposed to the pressure of aortic aneurisms in many 
ways. Compression of the lungs by large aneurisms actually contributes toward 
increasing the dyspnoea in many cases. This may be still more distressing if the 
trachea be compressed. Of the two main bronchi, the left bronchus, which lies 
beneath the arch of the aorta, is more apt to be compressed. This produces the 
symptoms of a unilateral bronchial stenosis (vide supra). The comparatively fre- 
quent compression of one recurrent nerve, especially the left, is also of diagnostic 
importance, as it results in paralysis of one vocal cord. 

Pressure on the vagus may occasion changes in the rate of the pulse, and per- 
haps sometimes attacks of dyspnoea. The dyspnoea in most cases, however, takes 
the form either of angina pectoris or of cardiac asthma, and is referable to the 
other coincident lesions of the heart and the coronary arteries. 

Very prominent symptoms sometimes arise from compression of the intercostal 
nerves or branches of the brachial plexus by the aneurism. As a result of this 
pressure, extremely severe and distressing neuralgias are felt in the nerve terri- 
tories affected, and sometimes we see motor paresis in the arm. 

Finally, disturbances of deglutition arise in many cases from compression of 
the oesophagus. If this be falsely interpreted, it may lead to a mischievous use of 
the oesophageal sound. Cases have repeatedly occurred in which perforation of 
the aneurism has been caused by passing a sound into the oesophagus. Hence we 
must always remember this possibility in practice. 

Course and Termination of the Disease. — Aneurisms may remain latent for a 
long time without causing any symptoms. In such cases a sudden perforation may 
lead to a speedy and unexpected death. 

In the cases which have shown the above symptoms to a greater or less extent 
for a long time, and often for years, sudden death quite frequently results from 
rupture of the aneurismal sac and perforation into a neighboring organ. In per- 
foration into the pericardium death follows almost instantly from cessation of the 
heart's action. In perforation into the oesophagus a fatal haemorrhage occurs. 
In perforation of the aneurism into the air-passages (the trachea or bronchi) or 
into one pleural cavity, two factors, haemorrhage and suffocation, unite in causing 
death. In aneurisms which gradually erode the anterior wall of the chest, the per- 
foration is in rare cases external; but here a sudden, immediately fatal haemor- 
rhage seldom ensues ; much more commonly a slowly increasing anaemia develops 
as a result of repeated slight haemorrhages which may sometimes go on for weeks. 
Death then is due to the gradually increasing weakness, or to a final severe haemor- 
rhage. Perforation of an aneurism into the right side of the heart, into the 
pulmonary arteries, or the vena cava, is a rare termination. Here death does 
not follow at once, but severe general disturbances of the circulation, such as 



378 



DISEASES OE THE CIRCULATORY ORGAXS 



dropsy, soon arise. In many of these rare cases peculiar physical signs also appear 
— a venous pulse, a loud systolic murmur over the point of perforation, etc. 

If, in patients with aneurism of the aorta, death does not ensue from a sudden 
perforation, the general type of the disease takes a form similar to chronic heart 
disease. The aneurism, as we have said, is often also combined with aortic insuffi- 
ciency. The left ventricle gradually becomes paralyzed, and the well-known dis- 
turbances of compensation set in — increasing dyspnoea, oedema, etc. In other 
cases the patient gradually becomes duller and weaker from the distressing pain, 
the sleeplessness, and the other symptoms, and dies with the signs of increasing 
general weakness. 

Recovery from aneurism of the aorta scarcely ever occurs. 

Diagnosis. — The diagnosis of aneurism of the aorta can in many cases be made 
with great ease and certainty, but in other cases it is very difficult and even 
impossible. If the direct physical signs are plain, especially if we feel an abnor- 
mal pulsation, we shall not be apt to commit an error; but the diagnosis presents 
great difficulties in those cases in which the aneurism is not accessible at all, or 
accessible only with great difficulty, where it merely causes indefinite symptoms, 
pain in the chest, occasional oppression, symptoms of pressure on neighboring or- 
gans, etc. A very stubborn intercostal neuralgia, which no remedy can relieve, 
may be for a long time the only symptom, often misinterpreted, of a latent aneu- 
rism. The disease is often not recognized, however, because in such cases we do 
not generally think of the possibility of an aneurism, and hence we neglect a care- 
ful examination of the heart and the arteries, and also the search for other symp- 
toms of compression, such as paralysis of the vocal cords; but sometimes, even 
with the most careful examination, the diagnosis can not amount to more than 
a suspicion. 

If there is a loud systolic murmur in the second intercostal space on the right 
without other decisive signs, it may be difficult to make a differential diagnosis be- 
tween aneurism and aortic stenosis. 

The distinction between aneurism and other tumors in and about the thorax 
sometimes presents difficulties in diagnosis. Mediastinal sarcomata and abscesses, 
circumscribed empyemas, tumors arising from the sternum, or new growths in 
the lungs and bronchial glands, may all give rise to confusion. We can scarcely 
lay down any general rules for diagnosis, since the conditions differ in almost 
every case. If we feel a swelling, its pulsation is the symptom which points most 
to an aneurism, but we must be certain that the pulsation is not merely trans- 
mitted, but that it really takes place in all directions within the swelling itself. 
We must also consider the auscultatory symptoms, the condition of the heart and 
the arteries, and any symptoms of compression; yet in such cases we can not 
always make a definite diagnosis. 

Treatment. — Many attempts have been made to bring about an obliteration of 
the aneurism, and thus a recovery. Although the methods of treatment aiming 
at this have obtained decisive results in the aneurisms of peripheral arteries, their 
results in aneurism of the aorta are still of a very doubtful character ; yet we are 
always justified in any given case in trying one of the methods recommended. 

Persistent compression by a pad can of course be employed only in those cases 
where the aneurism projects at one part of the chest-wall. The pressure, how- 
ever, usually causes great pain, and hence is ill borne. 

Tying the carotid, the subclavian, or both vessels, has also been repeatedly 
performed in aneurism of the arch of the aorta, sometimes with apparent success, 
but oftener without any benefit. 

" Acupuncture " of the aneurism (Yelpeau) consists in inserting a needle or an 
iron wire into the aneurismal sac in order to excite coagulation in it. The 
results obtained by it in aneurism of the aorta are not very encouraging. 



ANEURISMS OF THE OTHER VESSELS 



379 



Better results are reported from galvano-puncture. Two needles inserted into 
the aneurism are connected with the poles of a galvanic battery, by which a weak 
current is passed through the aneurism. Here we must regard the chemical and 
electrolytic action of the current as well as the mechanical action of the needles. 

Injections of chemical substances into the aneurismal sac, in order to produce 
coagulation, are dangerous, since the coagula caused by them may give rise to 
emboli. Hence we have abandoned making trial of liquor ferri sesquichloridi and 
similar substances. We can better recommend injections of ergotine into the 
vicinity of the sac, two to five grains (gramme 0.1-0.3) of the aqueous extract of 
ergot dissolved in water or glycerine, injected every day or two. This method 
was first employed with success by Langenbeck in peripheral aneurisms. Its ac- 
tion depends upon a contraction of the smooth muscles in the wall of the aneu- 
rism, caused by the ergotine. 

We can expect little action on an aneurism from the use of internal remedies, 
although favorable results have been reported. Especially recommended is the 
long-continued use of iodide of potassium or iodide of sodium, drugs which have 
obtained a great reputation in all arterio-sclerotic lesions and, in particular, in 
syphilitic disease of the arteries (vide supra, aetiology of aneurism). Yet it is 
easy to see why one should not expect too much from the iodides. Acetate of lead, 
5 to 10 grains (gramme 0.3-0.6) daily has also been employed. Its value, however, 
is questionable. 

The symptomatic treatment of aneurism, which tries to relieve the patient's 
sufferings, and the dietetic measures prescribed, follow the generally customary 
principles. In a rupture of the aneurism externally we try to avert the fatal 
catastrophe by absolute rest, ice-bags, styptic cotton, etc. Treatment is powerless 
against internal perforations. 

[Tufnell's method, so-called, which has given good results in abdominal and 
peripheral aneurisms, proves sometimes useful in palliating the symptoms and 
lengthening the course of aortic aneurism. The aim of this method is to diminish 
the force and rapidity of the circulation, and, if possible, to increase the fibrinous 
deposit. It is carried out by enforcing absolute rest in the recumbent position, 
and by limiting the amount of food, especially of liquids. About ten ounces of 
solid food and eight of liquid are allowed daily, divided into three meals.] 



CHAPTER III 
ANEURISMS OF THE OTHER VESSELS 

Aneurism of the Abdominal Aorta.— Its favorite seat is the vicinity of the 
cceliac axis. In many cases it may be felt through the abdominal wall as a pul- 
sating tumor, over which a systolic sound or a whirring murmur can be heard. 
The possible symptoms of compression are very numerous. The stomach, intestine, 
and liver (jaundice) may be implicated. Pressure of the aneurism upon the nerve 
trunks, or even pressure on the spinal cord after gradual erosion of the vertebra?, 
with consequent severe neuralgia, paralysis, etc., has been repeatedly observed. 
Death usually ensues from rupture of the aneurismal sac and internal hemor- 
rhage. 

Aneurism of the trunk of the innominate is rare. Its symptoms are very 
much like those of an aneurism of the arch of the aorta. If we feel a pulsating 
tumor, it is usually situated somewhat higher up than the aneurism of the aorta, 
in the first right intercostal space, or the tumor even extends into the supra- 



380 DISEASES OF THE CIKCULATOKY ORGANS 



clavicular fossa. In rare cases aneurisms of the subclavian and of the carotid 
have been observed. We have ourselves seen an aneurism of the internal carotid 
the size of a cherry pressing on the Gasserian ganglion, which caused an extremely 
severe trigeminal neuralgia lasting for years. 

Aneurism of the pulmonary artery may appear as a pulsating tumor in the 
second left intercostal space. It is usually impossible to distinguish it with cer- 
tainty from an aneurism of the aorta. 

We have already mentioned, in the description of pulmonary tuberculosis, the 
great importance of small aneurisms of the branches of the pulmonary artery in 
pulmonary cavities, as a frequent cause of haemorrhage. 

Aneurisms of the arteries of the brain, which are relatively most frequent in 
the basilar artery and the artery of -the fissure of Sylvius (the middle cerebral 
artery), may cause severe cerebral and bulbar symptoms (see page 1052). As has 
already been mentioned, miliary aneurisms of the cerebral arteries play an impor- 
tant part in the aetiology of cerebral haemorrhage (q. v.). 

The symptomatology and treatment of aneurisms of the peripheral arteries 
belong to the domain of surgery. 



CHAPTEK IV 
RUPTURE OF THE AORTA 

A rupture of a previously healthy aorta, with fatal haemorrhage, after violent 
traumatic influences, has been seen only in a very few cases. In the majority of 
the very rare cases of rupture of the aorta we have to do with a vessel that is 
already atheromatous. In some cases a special exciting cause is present, and in 
others it is absent. We once saw sudden death caused by rupture of the ascend- 
ing aorta in a young man about twenty-five, who before that seemed perfectly 
healthy. 'No trace of atheroma was found ; but at the point of rupture there was 
a slight protrusion and a decided thinning of the wall, which was probably con- 
genital. The formation of a so-called dissecting aneurism, which has often been 
seen in the aorta, is of anatomical interest. Here only the intima and media are 
torn. The blood burrows between them and the adventitia or between the layers 
of the media. Most of the cases of dissecting aneurism of the aorta also result, 
like rupture of the aorta, in sudden death. In many cases death results from the 
secondary perforation of the aneurism into the pericardium. On the other hand, a 
sort of recovery from dissecting aneurism may occur. A secondary perforation 
takes place into another part of the aorta itself (Bostrom). Cases of this sort were 
formerly more than once mistaken for double aorta. If the capsule containing the 
blood is preserved for a considerable length of time, the symptoms may assume the 
character presented in ordinary aortic aneurism. 



CHAPTER V 
NARROWING OF THE AORTA 

Congenital narrowness of the aorta and its branches is a condition to which 
Rokitansky first, and later Virchow, have directed attention. We find this anom- 
aly especially in those, mostly women, who during life have shown the signs of 



ZSTABROWHSTG OF THE AORTA 



381 



persistent chlorosis. Sometimes such persons are backward in their whole devel- 
opment; they retain a puerile habit, and show a defective development of the 
genitals. They often suffer from palpitation, f aintness, and a tendency to haem- 
orrhages. In many cases the heart is also small, but in others it is dilated and 
hypertrophied. We have already pointed out (page 350) that congenital hypo- 
plasia of the aorta may be regarded as the cause of certain cases of " idiopathic 
hypertrophy of the heart." Valvular disease of the heart has been repeatedly 
found combined with general narrowness of the arterial system. During life this 
anomaly of the vascular system may sometimes be suspected, but it can never 
be recognized with certainty. 

Narrowing of the aorta at the point of insertion of the ductus arteriosus is a 
lesion observed in rare cases, whose origin probably always falls in the period 
directly after birth, and is associated with obliteration of the foetal ductus arteri- 
osus. Other congenital anomalies of the heart are usually present at the same time. 
If the narrowing of the aorta is not very marked, it may be properly equalized by 
a secondary hypertrophy of the left ventricle and the development of a collateral 
circulation. The latter is brought about by dilatation of the anastomoses between 
the first intercostal artery, the dorsalis scapulas, the subscapularis, and the trans- 
versalis colli on one side, and the lower intercostal arteries, which come off from 
the descending aorta below the narrowing, on the other. Anastomoses are also 
formed between the mammary and the superior epigastric on one side and the 
lumbar and femoral arteries on the other. During life the dilated arteries are 
prominent, in part abnormally tortuous, and perceptibly pulsating, especially the 
dorsales scapulas, the subscapulars, the mammaries, and the epigastrics. In some 
cases a systolic murmur has been heard over some of these vessels. The pulse 
in the arteries of the lower extremities, the femoral and popliteal, is very weak 
and scarcely perceptible. 

In many cases the collateral circulation is so complete that the person affected 
may feel no subjective disturbance at all, and may attain an advanced age, but in 
other cases disturbances of the circulation appear sooner or later, and the patient 
finally succumbs to dropsy. Sudden death from rupture of the heart or of the 
aorta has also been observed. 



DISEASES OF THE DIGESTIVE ORGANS 



SECTION I 

Diseases of the Mouth, Tongue, and Salivary Glands 

CHAPTER I 

CATARRHAL STOMATITIS 

{Catarrhal Inflammation of the Mouth) 

.ZEtiology. — Inflammation of the buccal mucous membrane is not infrequently 
the direct result of mechanical or chemical causes. As mechanical causes we may 
mention particularly the sharp edges of broken or carious teeth. It should be 
said that often infectious organisms (vide infra) are active at the same time, 
because they gain a much easier foothold on account of the presence of bad teeth. 
Chemical irritation may come from highly spiced food, or from tobacco-chewing 
or excessive smoking. Chemical and mechanical irritation provokes stomatitis 
in many trades which expose the artisan to lime, copper, coal, or other varieties 
of dust. In drunkards we find not infrequently a chronic stomatitis, which is 
characterized by a thickly coated, moist, and shiny tongue, which is somewhat 
swollen and exhibits indentations on its side due to its pressure against the 
teeth. Inflammation of the mucous membrane of the mouth from poisoning 
with corrosive acids or alkalies is also the result of direct chemical irritation. 
It may take the form of severe ulcerative stomatitis (see the following chapter). 
The mercurial stomatitis, which results from acute or chronic poisoning with 
mercury, is caused indirectly by the particles of mercury deposited from the 
blood in the mucous membrane. This mercurial stomatitis when severe always 
takes the form of ulceration or necrosis. The stomatitis attendant upon the 
cutting of teeth in children will be discussed below. 

In many instances stomatitis comes from a direct propagation of inflammation 
from neighboring parts. It thus forms a frequent complication of pharyngeal 
catarrh, and less often of rhinitis. 

Infection plays an important part in the setiology of stomatitis. The local in- 
flammation may be merely part of a constitutional infectious disease, as in mea- 
sles, variola, and syphilis. Stomatitis is still more frequently a complication of 
some severe and protracted illness, when the mouth is not properly attended to 
and cleansed. The bits of food and the mucus quickly begin to decay. Great 
numbers of fungi and bacteria invade the buccal cavity, and excite inflammation 
in its mucous membrane. Even the cases of primary stomatitis which sometimes 
occur are probably all of an infectious character. They usually soon assume 
the ulcerative form. Scorbutic stomatitis will be considered under scurvy. 

Clinical History. — The usual symptoms of an inflammation of mucous mem- 
brane — namely, redness, swelling, and increased secretion — are exhibited in 
stomatitis. The redness is usually most intense on the inside of the cheeks and 
on the gums. Indeed, we have the special name — gingivitis — for inflammation 
382 



ULCEEATIVE STOMATITIS 



383 



of the latter. The swelling is best shown by the indentations made by the teeth 
in the cheeks and the edges of the tongue. The tongue and gums are smeared 
with mucus. There is often considerable salivation. If the inflammation is 
more active, we find a muco-purulent coating on a greater or less portion of the 
membrane. The tongue is almost always thickly coated. If we scrape off a little 
of the coating and put it under the microscope, we find a great abundance of 
pavement epithelium, in part fatty-degenerated, pus, micrococci, and remains of 
food. White spots made up of epithelium may also be seen on various parts of the 
oral mucous membrane. Here and there little vesicles appear which burst and 
leave superficial ulcers. 

The local discomfort of severe stomatitis is by no means trifling. There is 
burning pain, which interferes with taking food, and usually the processes of 
decomposition occasion a constant bitter or disgusting taste in the mouth, as well 
as a foul and offensive breath. 

The duration of the disease depends on the nature of the immediate cause or 
the character of the primary disorder. Usually a stomatitis which gets well in 
one or two weeks is called acute, and a more tedious attack, chronic. The chronic 
form is seen in topers, inveterate smokers, and persons with bad teeth. It may 
last for years, with the symptoms described above, only milder. (For lingual 
psoriasis, vide infra.) 

Treatment. — If the inflammation is considerable, the diet must be liquid. 
Sometimes cold drinks are most agreeable, but usually lukewarm are pre- 
ferred. Often the pain is relieved by taking from time to time a sip of iced 
water or a bit of ice ; but in most cases the patient will prefer to rinse the mouth 
with lukewarm water. The important indication, to keep the mouth as clean and 
pure as possible, is best met by having the mouth frequently rinsed out with a 
one- or two-per-cent. solution of carbolic acid, a two-per-cent. solution of chlorate 
of potash, or one or two teaspoonfuls of a one-per-cent. solution of perman- 
ganate of potash in a glass of water. It is also advisable to rinse the mouth 
with a two-per-cent. solution of peroxide of hydrogen, and with thymol, which lat- 
ter is the chief constituent of Miller's mouth wash, the ingredients of which are : 
Thymol, \ part ; benzoic acid, 30 parts ; tincture of eucalyptus, 4 parts ; distilled 
water, 750 parts. In children who can not do this, the mouth is to be carefully 
washed or sprayed. If the gums are spongy, they should be painted with a mix- 
ture containing equal parts of tincture of myrrh and tincture of rhatany. If 
there are superficial ulcers scattered about, it is sometimes an excellent plan to 
touch them lightly with lunar caustic, to hasten their healing. 

Chronic stomatitis is often very obstinate, resisting all sorts of treatment for a 
long time. The first thing is to remove any such injurious agencies as tobacco 
or bad teeth. It is recommended, besides the above-mentioned remedies, to swab 
out the mouth with a solution of corrosive sublimate (1 to 5,000) or of lunar 
caustic (1 to 30-50). 



CHAPTER II 

ULCERATIVE STOMATITIS 

(Stomacace) 

Etiology. — By ulcerative stomatitis is meant a severe disease of the buccal 
mucous membrane, with superficial necrosis and the consequent formation of 
ulcers. The abnormal processes are not in all cases identical, and their cause 
may vary. Still it is probable that infection is the important factor, at least in 



384 



DISEASES OF THE DIGESTIVE OKGANS 



the primary cases. The disease has repeatedly been epidemic, chiefly among sol- 
diers in barracks or on a campaign, and among* the inmates of jails. We have 
repeatedly seen sporadic cases of primary ulcerative stomatitis with fever. In 
children the disease is especially common at the time of the second dentition. 
Here, too, endemic and contagious influences are frequently in evidence. 

Mercurial stomatitis is, from a practical point of view, the most important 
of those forms of ulcerative stomatitis which are referable to definite chemical 
action. It is due to the inhalation of the fumes of mercury in those whose 
trade or scientific occupation exposes them to this danger, and very frequently 
also to the therapeutic employment of mercury in the form of calomel or mer- 
curial ointments, and the like. (For the scorbutic form, see page 741.) 

Symptoms. — The disease usually attacks the gums of the lower jaw first, grad- 
ually spreading thence to neighboring portions of the lips and cheeks. The 
tongue end palate are generally not very much affected, though often the seat of 
a simple catarrhal inflammation. In severe mercurial stomatitis the gums are 
especially apt to be affected. The ulcers also show a preference for the angles 
of the lower jaw, and those portions of the mucous membrane of the cheeks 
which rest upon the teeth. 

Inspection shows that the mucous membrane in the places mentioned has a 
pasty, purulent coating. The gums are swollen, spongy, and red, and bleed 
easily. The mucous membrane on the edges of the gums becomes necrotic, giving 
rise to ulcers. The incisor teeth are so loosened by gingivitis that they may even 
fall out. There is usually profuse salivation. The lymph-glands at the angle 
of the lower jaw and on the chin are generally swollen. The breath is very 
offensive, poisoning the air of the whole room. 

The local discomfort of the patient is the same as in simple stomatitis, only 
much worse. It is very difficult to take nourishment. In many cases there are 
marked constitutional symptoms. The patient feels very weak and languid. 
The primary, and sometimes also the toxic, cases of ulcerative stomatitis are 
associated with moderately high fever— 100.5 °-102° (38°-39° C). Now and 
then severe symptoms of constitutional sepsis have followed the disease. 

The course of ulcerative stomatitis is favorable in the great majority of cases. 
With good treatment and nursing, the ulcers gradually clean up, and at the end 
of one or two weeks recovery is complete. Exceptionally, the disease may be 
more chronic. The most frequent way in which recovery is delayed is that the 
disease extends to the periosteum of the lower jaw, causing necrosis of small 
portions of the bone, which must be expelled before the patient gets well. 

The treatment does not differ essentially from that of the milder forms of 
stomatitis. The mouth must be still more carefully and more frequently cleansed 
and disinfected. A solution of potassic chlorate (1 to 30) is the favorite mouth- 
wash. Good results are also obtained from permanganate of potash, boric acid, 
peroxide of hydrogen, and similar remedies. Some authors strongly recommend 
the simultaneous internal administration of potassic chlorate; but we must 
employ it cautiously in children, as it has repeatedly caused poisoning. For 
children two or three years old we ought not to give over fifteen to thirty grains 
(grammes 1-2) in a day. 

As to prophylaxis, we should mention that all patients who are using mercury 
should employ a gargle of potassic chlorate faithfully from the beginning of 
treatment, in order to prevent the occurrence of mercurial stomatitis. If saliva- 
tion occurs, the mercury must be stopped. 



APHTHOUS STOMATITIS 



385 



CHAPTER III 

APHTHOUS STOMATITIS 

(Aphthae,. Disseminated Fibrinous Stomatitis) 

Aphtha is a name given by physicians to several entirely distinct diseases. 
Many doctors call every disease aphthae in which there are white spots upon the 
buccal mucous membrane. It is thus frequently confounded with thrush. The 
same name (Schwdmmclien, or fungus) is often applied indifferently to thrush 
and to aphthae. 

There is a special form, known as Bednar's aphthae. In new-born children 
white patches are not infrequently found lying symmetrically on both halves of 
the hard palate near the alveolar processes, and persisting till about the third 
month. These plaques are not syphilitic, although often thought to be. They 
are probably due merely to the tongue pressing upon the thin mucous membrane 
during nursing. Generally they do no harm; but in marantic, neglected chil- 
dren, they may develop into quite deep ulcers. In that case, repeated cauteriza- 
tion with a five-per-cent. solution of argentic nitrate is required. 

The genuine aphthae are roundish spots upon the mucous membrane, grayish 
white, and of small size, unless made larger by the confluence of several into one 
another. They usually have a narrow, red areola. They are most numerous on 
the edges and dorsum of the tongue and on the fraenum, but they also occur 
on the lips and cheeks. The attempt to remove the white spot with forceps 
never succeeds, but it causes bleeding. In addition to the genuine aphthae there 
are almost always the signs of a common stomatitis, which may be mild or severe. 
The white spots are due in part to a thickening and opacity of the epithelium, and 
in part are said to be caused by the formation of a fibrinous exudation, which 
penetrates the most superficial layers of the mucous membrane. If the necrotic 
epithelium is cast off, the aphthous spot develops into a little ulcer, which often 
heals promptly, but which may be very obstinate. 

The disease occurs chiefly in children, and at the time of the first dentition. 
The child is usually restless, often somewhat feverish, and evidently suffers pain 
when nursing. Generally there is considerable salivation. The lymph-glands 
may be a little enlarged. On the outer skin in the neighborhood of the mouth 
there may also appear a few blisters and pustules. These, as a rule, have no con- 
nection with herpes, although now and then genuine herpes may appear in asso- 
ciation with aphthous stomatitis. The disease is not rare in adults. Many indi- 
viduals seem especially liable to it, and very frequently have little, white, and 
often very painful spots here and there on the tongue or elsewhere in the mouth. 
These have a tendency to develop into ulcers which are usually superficial, but 
sometimes deep. They may prove very troublesome, from their frequent recur- 
rence and the hindrance they cause to speaking and mastication. If there are 
fairly deep ulcerations on the tongue and mucous membrane, the patient's condi- 
tion for a time is very painful and distressing. 

With the exception of the form just described, which is constantly relaps- 
ing, aphthae almost always run a favorable course. There is usually complete 
recovery in a week or two. The treatment of children consists in carefully wash- 
ing out the mouth with cold water, and in administering potassic chlorate. Of 
a mixture consisting of three parts of potassic chlorate, twenty of syrup, and a 
hundred of water, we may give a dessertspoonful every two hours. If the spots 
do not disappear, we can paint them with a solution of permanganate of potash 
(1 to 150), a five-per-cent. solution of sulphate of zinc, or a solution of borax 
(1 to 30). If some of the places are especially painful, particularly in adults, 
25 



386 



DISEASES OE THE DIGESTIVE ORGANS 



we may touch them with lunar caustic, when they usually are soon cured. In the 
constantly recurring form, treatment sometimes proves almost unavailing 1 . Local 
cauterization, which unfortunately in such cases is often of no benefit whatever, 
and the use of a mouth-wash containing chlorate of potash or carbolic acid in 
weak solution, may be employed, and, furthermore, some physicians strongly rec- 
ommend the internal administration of iodide of potassium. Calomel also 
appears sometimes to have a beneficial influence. 

It is often a very difficult matter to treat chronic, recurrent, aphthous stoma- 
titis, and the ulcerations which are occasioned by it in adults. Cauterization 
with lunar caustic, chromic acid, and similar agents usually does more harm 
than good. None of the ordinary mouth-washes has any great effect. A much 
praised remedy is the chewing of bilberries, either fresh or boiled, for several 
minutes several times a day, and we have ourselves employed it in some cases 
with good results. Some physicians also recommend the internal use of iodide 
of potassium, or small doses of calomel. It is remarkable that habitual aphthous 
stomatitis sometimes ceases completely for months — for example, upon change of 
residence or during a visit to the country — but then appears afresh without 
special cause. 

In conclusion, as to aetiology, infection is a not unlikely cause, if we consider 
that small epidemics or endemics have repeatedly occurred. Lately attention has 
been called to the possibility that the milk of cows suffering from hoof-and- 
mouth disease may be a source of infection. That infection of this sort may 
occur seems to us indubitable, from the experience of others, as well as our own. 
In such cases there is not only a severe aphthous stomatitis, but a development 
of vesicles, pustules, or even extensive purulent inflammation affecting the 
fingers and nails, and occasionally other parts of the body. Most cases of this 
kind also pursue a favorable course, but a few epidemics have been described in 
which the disease became dangerous to life because of constitutional sepsis. 
Probably the various forms of stomatitis aphthosa are connected with various 
infectious germs. 



CHAPTER IV 

THRUSH 

(Soor. Muguet) 

^Etiology. — Weak and artificially nourished children are particularly liable to 

this disease; but it also attacks adults who are suffering from phthisis, carcinoma, 
and severe typhoid or typhus fever. In it, grayish-white deposits are developed 
upon the buccal and pharyngeal mucous membrane. The microscope shows these 
collections to be fungi; there are a multitude of oval spores, or conidia, and a 
tangled mass of long mycelium threads. Until lately the fungus of thrush was 
called o'idium albicans, and was held to be identical with the o'idium lactis found 
in sour milk. This view is now abandoned, although no other has as yet been 
established with regard to the botanical position of the thrush fungus. Grawitz 
maintained that the thrush fungus is a sprouting fungus, and nearly related to 
the mould fungi (mycoderma vini,* or saccharomyces albicans — Rees). It seems 
to be a sort of transitional form between the sprouting fungi and the thread 
fungi, inasmuch as it appears both in the yeast form and also in the form of 



* Mycoderma villi is that fungus which is found in the development of vinegar from alcohol, when 
alcoholic beverages sour. 



THKUSH 



387 



threadlike rrrycelia. Plant, according" to his investigations, makes the thrush 
fungus identical with the monilia Candida, -which belong to the Torulacese. At 
any rate, the thrush fungus is widely distributed, for the development of thrush 
upon the mucous membrane of the mouth and throat is a frequent phenomenon, 
especially in ill-nourished children. JSTursing-bottles and the nipples used upon 
them are probably not infrequently the agents by which the disease is conveyed. 

Symptoms, — The mucous membrane of the tongue, cheeks, and soft palate is 
usually somewhat red and swollen. Upon it we see at first small white spots, 
which may gradually spread. Microscopic investigations have shown that the 
fungus develops first in the middle layers of the epithelium. From this starting- 
point it grows not only upward, but also downward into the mucous membrane. 
If the growth is abundant, it is easy to scrape off the upper layers, and make a 
diagnosis by aid of the microscope. In exaggerated cases the growth may even 
extend from the pharynx into the upper part of the oesophagus and the entrance 
of the larynx; but we never find thrush in the larynx itself, or the nostrils, or 
the stomach — briefly, in no place where there is cylindrical epithelium. Yet in 
exceptional cases the thrush fungus may extend its growth through the wall of a 
blood-vessel, and so reach the circulation. Usually thrombosis of the affected 
vessel takes place, but the metastasis of thrush to the brain and the kidneys has 
been observed. If abscesses are associated with these processes they depend upon 
the simultaneous intrusion of pyogenic cocci. 

As a rule, thrush is accompanied by a more or less severe stomatitis. The 
fluids of the mouth have an acid reaction. jSTursing, or chewing, and swallowing', 
are painful. Still, it is a question whether the stomatitis is due to the fungus, or 
whether it prepares the territory for the fungus to settle in. Xursing* infants, 
who suffer from thrush, often have diarrhoea or marasmus at the same time, which 
latter affections are more probably the cause than the result of the thrush. If 
vigorous and healthy sucklings are attacked by thrush, the disease is usually 
quite harmless, quickly vanishing if proper cleanliness is maintained. In sickly 
children, particularly if bottle-fed, the appearance of the disease is very ominous. 
If there is a large amount of thrush in the oesophagus, the ingestion of food 
may be seriously interfered with. In adults, as we have said, thrush is with few- 
exceptions confined to persons greatly prostrated by such diseases as severe 
typhoid fever or tuberculosis, and from this point of view it is an unfavorable 
symptom. 

Treatment. — To prevent the development of thrush in children, the mouth 
must, if possible, be wiped out, each time they drink, with a cloth wet in cold 
water; and if adults are very ill, they require equal attention in this regard. As 
soon as we see the first traces of the disease, we should touch the parts attacked 
with a brush wet in an aqueous solution of borax (1 to 20). Honey should not 
be added to the borax solution, as is often unwisely done. Another good solution 
is permanganate of potash (1 to 150) . If the thrush extends into the cesophagus 
the most efficient remedy (Baginsky) is said to be the internal administration of 
resorcin, in a one-half- to one-per-cent. solution, the dose being a teaspoonful 
every two hours. The food should contain as little sugar as possible, as this fur- 
nishes a favorable culture medium for the thrush fungus. Mild cases can usually 
be cured by the remedies named. If the thrush has once got a vigorous start in 
the mouth of marantic children, or of adults suffering from an incurable disease, 
it must be confessed that we often fail to check its growth. 



388 



DISEASES OF THE DIGESTIVE OKGAXS 



CHAPTER V 

GLOSSITIS 

(ParencJtymatous Inflammation of the Tongue) 

Inflammation of the true lingual parenchyma is rare, although, the tongue's 
mucous surface is frequently involved in the various diseases of the mouth. 

1. Acute parenchymatous glossitis is the name given to an inflammatory in- 
filtration of the whole or a part of the tongue, usually ending in abscess. The 
most frequent cause is the sting of a bee or wasp, or it may follow burns or severe 
cauterization. In the rare instances when it is apparently spontaneous, it is 
probable that some little wound has afforded ingress to the inflammatory poison. 

The symptoms of acute glossitis are very violent in the severer cases. The 
tongue is enormously swollen, so / as sometimes to protrude from the mouth. It 
has a thick, soft, purulent coating, and often presents excoriations and ulcera- 
tions. The subjective symptoms are very disagreeable. The patient has violent 
pain. Talking and eating are almost impossible. There is usually catarrhal 
inflammation of the rest of the mouth. The cervical lymphatic glands are 
swollen. The salivation is profuse and very annoying. In many cases the 
tongue swells so much as to cause dyspnoea and more or less suffocation. There 
is usually fever. 

Treatment consists in the employment of ice, which the patient should keep 
constantly in his mouth, if possible. Very great relief follows deep scarification 
done in a few places where the swelling is greatest. As soon as fluctuation is 
obtained, we must give exit to the pus. This is usually followed by a rapid 
abatement of the discomfort, and complete recovery. It is the exception that the 
increasing dyspnoea necessitates tracheotomy. 

2. Glossitis Dissecans. — This is a chronic disease, of comparatively rare occur- 
rence and unknown aetiology. It causes the gradual development upon the sur- 
face of the tongue of a number of deep fissures and indentations, giving the organ 
an uneven and ragged look. The pain is due to the frequent presence of excoria- 
tions and ulcers in these fissures. 

The trouble is not intrinsically dangerous, nor does it need special treatment. 
We must try the same remedies which have been mentioned above in connection 
with the various forms of stomatitis, such as antiseptic mouth-washes, the chew- 
ing of bilberries, etc. If ulcers are present they sometimes require cauterization 
with lunar caustic. 

3. Lingual Psoriasis. Leucoplacia. (Tylosis; Ichthyosis lingua? et oris.) — 
This, again, is a superficial disease, the aetiology of which is unknown. It consists 
in localized circular hyperplasias of the epithelium of the tongue, rarely conjoined 
with similar spots upon the cheeks and lips. The central portion of mucous mem- 
brane which is surrounded by this whitish, slightly raised, and more or less 
circular, wall of epithelium, is abnormally smooth and of a, reddish color. Usu- 
ally the tongue takes on a resemblance to a map (lingua geographica). The dis- 
ease generally persists for years, and without symptoms except in severe cases. 
Often it is found by chance in individuals who have known nothing about the 
unusual appearance of their tongues. Still, it may cause a hypochondriac endless 
anxiety, especially if he takes it to be syphilitic. 

This last statement applies still better to a peculiar disease allied to psoriasis. 
It is called leucoplacia, and affects the mucous membrane of the tongue and 
mouth. Usually it causes the appearance, on the lateral borders of the tongue, of 
dull-whitish spots, which have the look of scars, and are generally somewhat 
notched. As a rule, the lower surface of the tongue and the cheeks display at the 



NOMA 



389 



same time similar white spots, which are evidently due merely to thickening of 
the epithelium. Certain spots may disappear, out they are sure to be replaced by 
others, so that, so far as has yet been observed, the disease must be regarded as 
incurable. Still, it is not of great importance, as a rule, for in many cases the 
local discomfort is very slight. If the indentations along the sides of the tongue 
become cracked or ulcerated, then there may be great pain. Leucoplacia is very 
often associated with bodily states of neurasthenia, or hypochondriasis, particu- 
larly if the leucoplacia appears in a person with a syphilitic taint, which happens 
with remarkable frequency. But it is certainly not to be regarded as a tertiary 
symptom, rather perhaps as a sort of sequel to syphilis, although many cases have 
no connection whatever with the latter disease. Anti-syphilitic treatment is 
invariably useless. It is for this very reason important that the physician should 
be well acquainted with leucoplacia, that he may spare his patient needless anx- 
iety and ineffectual, or perhaps actually harmful, treatment with mercury. The 
disease has no relation to excessive smoking, one proof of which is that we have 
seen the condition in women. The only danger of leucoplacia is that sometimes 
lingual carcinoma may eventually develop on the spot affected with it. We have 
in this case to deal with a process which is analogous to the development of ven- 
tricular carcinoma in the scars of old ulcers, or of cancer of the gall-bladder sub- 
sequently to gall-stones. Treatment is, as we have said, usually unsuccessful. 
Still, thorough cleanliness and good care of the mouth may avert any great dis- 
comfort. We may try the effect of painting the spots with a four-per-cent. solu- 
tion of borax, or a five-per-cent. solution of chromic acid. Lately the frequent 
chewing of boiled bilberries has been recommended for leucoplacia, and we have 
had good results from this procedure. 



CHAPTEE VI 
NOMA 

( Water-cancer. Cancrum oris) 

Noma is a gangrene of the cheek, apparently of spontaneous origin, and attack- 
ing chiefly feeble and sickly children. The disease is rare. It may be primary, 
but it is usually a sequel of severe diseases, such as measles, scarlet fever, typhus 
and typhoid fevers, and pneumonia. Now and then it has been observed in adults. 
A priori, it is extremely probable that noma is due to some parasitic micro-organ- 
ism ; but the matter has not yet been minutely investigated. It deserves mention 
that noma is said to occur with much greater relative frequency in moist regions 
along the coast — for example, in Holland — than in Germany. 

The disease begins, without any evident occasion, in an insignificant spot of 
gangrene on the inner surface of the cheek — that is, in the mucous membrane. It 
is usually situated near the corner of the mouth. Externally, the parts are soon 
swollen by collateral oedema, and the whole cheek gradually becomes hard and 
infiltrated. At first, all we see upon the mucous membrane is a dirty-greenish 
spot not much larger than a silver dime, but soon the whole cheek and the neigh- 
boring parts are one mass of gangrene. Bits of dead tissue come away, and foul- 
smelling ichor flows continuously into the mouth. The collateral oedema may 
finally pervade that entire half of the face. The neighboring lymph-glands are 
always greatly swollen. 

This condition is as a rule accompanied by fever, often reaching or ex- 
ceeding 104° (40° C). The general health may indeed for a time be astonish- 



390 



DISEASES OF THE DIGESTIVE ORGANS 



ingly little affected; but gradually prostration comes on, or even general sepsis 
develops, with, fever, stupor, and delirium. Erequently lobular pneumonia, which 
may have a gangrenous character, is produced by the inhalation of sloughing bits 
of tissue ; and often the ichor, being swallowed, excites violent and offensive diar- 
rhoea. The local discomfort is not really very considerable in most cases, com- 
pared to the severity of the disease. There may even be no pain felt whatever. 

The prognosis is almost always fatal. Death sometimes occurs suddenly from 
collapse. Sometimes it comes at the end of three or four weeks, from a gradual 
sinking of the bodily powers. Recovery has been seen in only a few cases : there 
is a line of demarkation formed, the sloughs come away, and a slow convalescence 
follows, leaving extensive and usually very disfiguring scars behind. 

Treatment must have for its chief object to check further extension of the 
gangrene, by removing all parts that are already destroyed. Local cauterization 
with concentrated hydrochloric acid, or fuming nitric acid, or lunar caustic, or 
chloride of iron, is usually futile. It is probably the best way to remove all the 
gangrenous portion by means of Paquelin's thermo-cautery. At least in the early 
stages of noma we may hope something from this method of treatment ; but if the 
case is far advanced, we can hardly expect to accomplish much. 

We should also disinfect the mouth as thoroughly as possible. The most 
efficient means is to syringe it out with solutions of salicylic or carbolic acids, or 
permanganate of potash. We should do our best to maintain the patient's 
strength. 



CHAPTER VII 

PAROTITIS 

(Mumps) 

Parotitis, or inflammation of the parotid gland, appears not only as a pecul- 
iar, primary, infectious disease, usually epidemic, but also as a secondary compli- 
cation of numerous other severe diseases. These two forms should be considered 
separately. 

1. Idiopathic, Primary Parotitis (Epidemic Mumps). — etiology. — The dis- 
ease occurs in epidemics that, although not very frequent, may be quite extensive. 
Endemics also occur, in barracks and schools ; and here and there a sporadic case 
is seen. Children and young adults are most liable to it. Nursing infants enjoy 
a marked immunity, as well as elderly persons. Males are much oftener attacked 
than females. 

There can be no doubt that mumps is a specific infectious disease, and claims 
have already been made of the discovery of its specific bacillus, but these lack 
confirmation. Still, it is natural to suppose that the infectious matter reaches 
the gland by way of Steno's duct. Numerous observations support the view that 
the disease is directly contagious; but the degree of contagiousness is not great. 
Perhaps the saliva of patients has something to do with the extension of epidemic 
mumps. The period of incubation seems to vary. On the average, it is about 
fourteen days. 

Clinical History. — There may be a prodromal stage of one or two days, with 
mild feverish symptoms. The disease itself begins with swelling of one parotid 
gland. The swelling is directly below and in front of the lobe of the ear, which 
is gradually pushed upward. In the next few days the swelling rapidly increases, 
and it and the collateral oedema of the cheek and floor of the mouth may become 
very considerable. The face is much distorted, but often makes a very comical 



PAEOTITIS 



391 



impression, especially as everybody knows how harmless the disease is. In most 
cases the other gland also swells a few days later. 

Suppuration scarcely ever occurs in genuine mumps. If it is seen as a rare 
exception, it is probably due to secondary infection. The swelling often becomes 
very hard. Generally it has a somewhat doughy consistency. The corresponding 
portion of skin is usually pale and shiny. The submaxillary gland not infre- 
quently swells also in addition to the parotid, and this may occur upon one or 
both sides of the neck. Penzoldt has observed cases in which the submaxillary 
and sublingual were swollen, but not the parotid. We ourselves have seen a 
swelling of the submaxillary precede the parotitis. The sublingual gland also 
seems sometimes to be involved with the parotid. 

The local discomfort is moderate in most cases. There are local pain and 
difficulty in chewing, but less in swallowing and talking. Often quite a severe 
stomatitis develops, with foul breath. 

There sometimes seems to be no fever whatever. Usually there is a moderate 
elevation of temperature. Often, however, it reaches 102.5°-104° (39°-40° C). 
Only occasionally has there been a case with grave typhoidal symptoms, 

Complications. — It is not rare for men to have a swollen testicle with inflam- 
matory serous exudation into the tunica vaginalis, which may be quite painful, 
but which usually subsides in a few days. The orchitis is usually ushered in with 
a fresh rise of fever. Resultant suppuration is a rare occurrence. Once we saw 
the orchitis appear several days before the swelling of the parotid gland. Double 
orchitis is rare. In boys this complication is much more exceptional than in 
adults. Some observers have mentioned analogous swellings of the female geni- 
tals (oophoritis) and mammae, but this is very rare. Sometimes mumps is asso- 
ciated with herpes labialis. 

The prognosis of epidemic parotitis is, as we have said, almost always favor- 
able. The trouble seldom lasts more than a week or ten days, when the swelling 
goes down, and the patient completely recovers. Possible but exceptional sequelae 
are: ptyalism; cessation of the salivary secretion; chronic swelling of the paro- 
tid; deafness; and atrophy of the testicle. 

The diagnosis is easy. The only thing to exclude is swelling of the lymph- 
glands, and they never have exactly the same location as the parotid. 

Special treatment is hardly necessary. Children should be kept in bed. Usu- 
ally some salve, or vaseline, is applied to lessen the feeling of tension. If reso- 
lution is tedious, we may paint the swelling with iodoform collodion (1-15) or 
with tincture of iodine; or we may prescribe iodoform ointment (1-15). If there 
is orchitis, the testicle must be elevated, as by a suspensory bandage. If the 
pain and swelling are marked, an ice-bag should be applied. 

2. Secondary Suppurative Parotitis. — This secondary form may be a compli- 
cation of any grave disease. In most cases it is due to inflammatory agents, 
probably staphylococci in most cases, generated by decomposition of the contents 
of the mouth, which agents reach the gland through Steno's duct. It was formerly 
the universal belief that the infection was metastatic, being conveyed through 
the blood-vessels; but it is not certain whether this occurs. It is probable that 
the pysemic form is in many instances thus produced. Secondary parotitis is 
most frequently observed in typhus and typhoid fevers. It is also seen occasion- 
ally in all other severe acute diseases, and in phthisis and carcinoma. 

The parotid gland swells, just as in the primary disease. It is, however, much 
oftener of excessive size, and in the majority of cases suppurates. If one has an 
opportunity to make an autopsy on such a case of secondary parotitis in its early 
stages, the cross-section of the swollen gland presents a large number of rather 
small discrete abscesses. These finally unite to form one larger abscess, which 
usually discharges outward through the skin or into the external auditory meatus. 



392 



DISEASES OE THE DIGESTIVE ORGANS 



Sometimes the parotid suffers from gangrenous inflammation, and there is ex- 
tensive sloughing. If such a case finally gets well, still, as a rule, some permanent 
injuries have been inflicted: there is facial paralysis, due to destruction of the 
facial nerve, or deafness, caused by an extension of the inflammation to the 
middle ear. 

The treatment of secondary parotitis is that of any suppurative inflammation. 
We may at first try to scatter the swelling by ice or iodoform ointment, but this 
usually fails. As soon as fluctuation is detected, the spot must be incised, and a 
drainage-tube inserted. The prognosis depends chiefly on the nature and course 
of the original disease. 



CHAPTER VIII 
ANGINA LUDOVICI 

The name angina Ludovici is applied to a rather rare phlegmonous inflam- 
mation of the floor of the mouth. Probably this is not occasioned by a specific 
cause, but is only a special localization of the ordinary germs which occasion 
suppuration. Its starting place seems to be the submaxillary gland, at least in 
most cases. It may be primary, or a complication of other severe acute diseases. 

Angina Ludovici usually begins with swelling in the neighborhood of the sub- 
maxillary gland. The swelling rapidly increases, and comes to involve the whole 
floor of the mouth and the anterior surface of the throat. It causes great discom- 
fort. Talking, chewing, and swallowing are almost impossible. There is usually 
fever, and in many cases we even find the symptoms of general sepsis. There 
may be great dyspnoea, due either to compression of the larynx or to oedema of 
the glottis. The final result in some cases is an extensive sloughing of the soft 
parts. This has the special name of cynanche gangrenosa. In other cases an 
abscess forms, and points outward or into the oral cavity. The swelling is some- 
times, though seldom, reabsorbed. 

The prognosis should always be guarded, for severe constitutional symptoms 
and a fatal ending are not infrequently seen, particularly if the patient has a 
weakly constitution. There may also be repeated exacerbations and relapses. 

Treatment. — At the commencement of the disease we may make the attempt, 
in suitable cases, to check the process by local depletion and by ice; but, as soon 
as suppuration or gangrene begins, the case becomes a surgical one. ISTow and 
then the threatening asphyxia demands tracheotomy. 



CHAPTER IX 

ANOMALIES OF DENTITION* 

(Difficult Dentition) 

The processes of dentition play so important a role in the disorders of child- 
hood that we feel obliged to discuss the subject, at least briefly. 

The first appearance of any of the milk-teeth usually takes place when the 
child is seven to nine months old ; it may,- however, occur either earlier or later 
than this period. As a rule, the two lower central incisors are cut first ; then the 
upper central incisors appear, a few weeks later, and next the lateral incisors of 



ANOMALIES OF DENTITION 



393 



the upper jaw. In the beginning of the second year come the lower lateral inci- 
sors, and almost simultaneously the four anterior molars. The four canine, or 
" eye " and " stomach " teeth, are cut in the second half of the second year ; and 
last of all comes the eruption of the four posterior molars. The first dentition is 
therefore completed by the end of the second or in the beginning of the third year, 
with the development of all the twenty milk-teeth. The accompanying diagram 
(Eig. 44), after Vogel, represents the order in which the separate teeth appear. 
In the fifth or sixth year the milk-teeth 
begin to be replaced by the permanent teeth 
of the second dentition. " Trouble with 
teething," however, almost invariably refers 
to anomalies of the first dentition. 

Noticeable delay in teething is frequent 
in weakly, and particularly in rachitic chil- 
dren, in whom the teeth may develop not in 
pairs and in symmetrical groups, as in Fig. 44, 

healthy children, but in irregular succes- 
sion. In such cases, sometimes 5 all the teeth are not cut till the end of the third 
year. 

On the other hand, it sometimes happens that certain teeth appear very early, 
or even are present at birth. If an abnormally early tooth is only loosely in- 
serted in the gums, it should be removed with the forceps ; for it interferes with 
nursing, and injures the opposing surface of the mouth; but if the tooth is firm 
in its place, we let it be. 

During the eruption of the teeth there is in every child considerable redness of 
the mucous membrane and an increased flow of saliva. The child evidently feels 
an itching in the mouth, and therefore a constant desire to bite something. This 
simple catarrh is sometimes accompanied by a slight rise in temperature. Occa- 
sionally there is a severe stomatitis, with which fever and thrush may be asso- 
ciated. These troubles should be treated as already described. 

In consequence of the salivation, and the large amount of saliva which is swal- 
lowed, in which the various processes of decomposition are apt to develop, we 
often see gastro-intestinal diseases in teething children. In most children a tem- 
porary and mild diarrhoea occurs. We should be particularly careful at this 
period about the child's nourishment, and in treating any marked gastro-intes- 
tinal symptoms. Experience shows also that teething children are unusually 
liable to simple or even capillary bronchitis, and catarrhal pneumonia. 

Nervous disturbances are often referred to dentition. The most important 
symptom of this kind is eclampsia. The attacks are sometimes called " teething- 
convulsions." Although the laity go too far in ascribing all sorts of nervous dis- 
orders to teething, still experienced specialists do recognize the possibility of such 
an origin for many cases. Some of the convulsions may in fact be regarded as 
reflex (vide infra the chapter on the convulsions of children, page 1151). 

When the upper canines, or " eye-teeth," are being cut, there is sometimes a 
unilateral purulent conjunctivitis, which is perhaps to be explained as an exten- 
sion of the inflammation by way of the antrum of Highmore and the nostrils. 
Eczema and other cutaneous eruptions have been often ascribed to dentition, 
whether justly or not is doubtful. Yet it is remarkable that little children 
sometimes have an eruption of facial eczema with the appearance of every tooth. 

There is, of course, no special treatment for difficult dentition; and the vari- 
ous disturbances which it may indirectly produce are to be treated on general 
principles. 




394 



DISEASES OE THE DIGESTIVE ORGANS 



SECTION II 

Diseases of the Soft Palate, Tonsils, Pharynx, and Naso- 
pharynx 

CHAPTER I 

SORE THROAT 

{Inflammation of the Soft Palate and of the Tonsils) 

iEtiology. — Acute inflammation of the soft palate and tonsils, in its various 
forms, is one of the commonest of diseases. Almost everybody has had personal 
experience with it. It is chiefly a disease of early life, being infrequent after the 
thirty-fifth year. Individual predisposition to it varies greatly. There are per- 
sons who have one or more attacks almost every year, while with others attacks 
are rare and insignificant. In many instances exciting causes have evidently 
been potent. Chief among these is catching cold; the sufferer has had wet feet, 
or has been talking in a damp, cold atmosphere. Most cases, therefore, occur in 
cool weather, although now and then attacks may occur in the hottest days of 
summer. Again, direct injuries of the pharynx may produce the disease, e. g., 
the smoky atmosphere of inns, combined with loud talking or shouting; the 
inspiration of poisonous vapors; cauterization of the mucous membrane with 
concentrated acids, alkalies, and other chemical agents; and burns. 

Apart, however, from these last-named external irritants we have many 
cases of primary angina, for which we must assume an infectious origin. This 
supposition is suggested by the severity of the constitutional disturbance, with 
fever, the nature of the local process (giving rise to suppuration), and the occa- 
sional appearance of the disease in an epidemic or endemic form. At the same 
time, exposure to cold and the other exciting causes above mentioned, may often 
favor its development. [Especially when tonsillitis recurs in an individual, or 
attacks several members of the same household about the same time, it is well to 
have the drainage carefully examined. The precise connection between bad 
drainage and sore throats we do not know, but that they are often connected there 
seems to be no doubt.] With regard to the nature of the infectious organism, 
there is as yet great uncertainty. When the tonsillitis is of the suppurative par- 
enchymatous variety, it is almost certain that we have to deal not with specific 
germs, but with staphylococci and other ordinary pus-organisms. The same is 
probably true of follicular tonsillitis also, although several different kinds of 
pathogenic organisms may be concerned; thus we may find not only staphylo- 
cocci, streptococci, and particularly diplococci, but probably, in many cases, even 
the genuine diphtheria bacillus. 

Erequently the inflammation is due to extension from neighboring parts, as 
in coryza, laryngitis, and stomatitis. In many cases both affections are simulta- 
neous results of one common cause. Finally, sore throat may be a symptom of 
many acute infectious diseases, such as scarlet fever, measles, small-pox, and ery- 
sipelas. 

To distinguish between an inflammation of the soft palate by itself and an 
affection of the tonsils is not practicable. In most cases the tonsils are the 
stronghold of the disease ; less often we find the inflammation limited to the soft 
palate. 

Clinical History. — The most important subjective symptom of sore throat, 
and that by which it is usually first recognized, is the difficult and painful deglu- 
tition. The pain is sometimes manifest before any objective changes are to be 



SOEE THEOAT 



395 



seen. It may in a severe case be very violent and distressing. The pain has a 
" darting " character, or sometimes is " burning " ; and it is most acute whenever 
the patient swallows, although in well-marked cases it seldom entirely intermits. 
Swallowing is not only painful, but it is laborious; it requires more than usual 
effort and time. The patient feels constantly as if he had to swallow a big lump. 
This sensation is worse if the tonsils are swollen. It is a matter of experience 
that not infrequently an " empty " swallowing hurts more than swallowing a 
liquid or some half -solid substance. 

Talking is also difficult. Every word may be painful, so that the patient 
expresses his wishes as briefly as possible. Even in a mild case, speaking for any 
length of time will produce a burning pain in the throat. The impaired mobility 
of the soft palate often prevents the complete cutting off of the nasal passages in 
talking, so that the voice has a nasal twang ; and often it sounds as if the patient 
were talking with his mouth full : he has the " voice of sore throat." 

Further local discomfort results from the mucus and saliva collecting in the 
mouth. Salivation is not infrequent, probably as a result of the stomatitis usu- 
ally present. In other cases the patient complains that his mouth feels dry and 
sticky. Frequently there is a persistent bad taste in the mouth, and the breath 
is disagreeable. 

With these local disturbances, more or less severe constitutional symptoms are 
almost always conjoined. Indeed, these latter may begin a day or two earlier 
than the local symptoms. The patient is indisposed, languid, has anorexia and 
headache. The general disturbance may be surprisingly great in comparison 
with the slight objective changes in the tonsils. 

There is fever in most of the well-marked cases; it may even be quite high. 
Temperatures of 103° or 104° (39.5°-40° C), or even higher, are not rare. Sore 
throat can not be said to have one particular type of fever. Usually the fever 
appears rather abruptly, remains high for several days, with an occasional slight 
interruption, and then falls with equal abruptness to normal again. 

The entire attack usually lasts only a few days, seldom more than a week. 
Even when a person is quite ill for several days, convalescence is almost always 
rapid and complete — that is, if the patient has a good constitution. 

Special complications are very infrequent, except that the neighboring parts — 
the larynx, mouth, and throat — are not seldom involved. Herpes labialis is quite 
frequent. Beyond this there is nothing to mention. 

Various Forms of Sore Throat 

The symptoms thus far mentioned are much the same in all cases of sore 
throat, varying only in intensity and duration. But the objective changes to be 
observed in the soft palate and tonsils are noticeably different in different cases. 
Whether the setiology differs also we have no certain information. In some 
instances it seems probable that it does. 

We shall distinguish five chief varieties of acute sore throat. Transitional 
forms are, however, by no means rare. Genuine diphtheria, which is a specific, 
acute, infectious disease, and which has already been discussed, does not need to 
be brought up again here. 

1. Catarrhal Sore Throat (Simple Catarrhal Inflammation of the Mucous 
Membrane of the Soft Palate). — There is a more or less vivid reddening of the 
mucous membrane, either uniform or in patches. The swelling is most marked 
in the pillars of the fauces and the uvula. The surface of the tonsils is likewise 
reddened; their size may be somewhat increased, or remain unchanged. The 
mucous membrane of the palate and uvula may be covered here and there with a 
thin layer of muco-pus, which can easily be wiped off. The tonsils may present 
small, superficial erosions, scattered about. These little ulcers are apt to lie at 



396 



DISEASES OE THE DIGESTIVE OKGAtfS 



the openings of the follicles. The small " blisters " which are often seen on the 
mucous membrane of the soft palate may be caused in various ways. Either they 
are mucous glands or solitary follicles, swollen; or, rarely, they are real vesicles 
rilled with a clear fluid and produced by a raising up of the epithelium. The cer- 
vical lymph-glands are usually but slightly swollen, if at all. 

This is the common and mildest form of sore throat ; and it may be over in a 
day or two. In some instances, however, it causes considerable local and gen- 
eral discomfort ; but the disease seldom lasts longer than five to eight days. 

2. Follicular Tonsillitis. — In this form there is not only more or less catarrhal 
inflammation of the soft palate, but a decided swelling of one or both tonsils. 
On the reddened surface of these swollen bodies are whitish-yellow spots, varying 
in number from two or three to ten or more, and corresponding to the follicles. 
These spots are often seen to be plugs projecting from the openings of the folli- 
cles. It is usually easy to press out the pasty contents of the follicle, represented 
by the white speck, with a spatula. The microscope shows it to consist of numer- 
ous epithelial cells and pus-corpuscles, bacteria, and detritus, and sometimes there 
are also crystals of the fat acids and cholesterine. The pus-corpuscles may so 
predominate that we may have small follicular abscesses, which, on being opened, 
leave superficial ulcers behind. The parenchyma of the tonsil is swollen with a 
serous and cellular infiltration, increasing the bulk of the part. The trouble is 
usually bilateral, though often more marked and extensive on one side than on 
the other. In the severer cases the cervical lymph-glands are swollen. The 
local symptoms and still more the constitutional disturbance in follicular ton- 
sillitis may be decided. The fever not infrequently reaches 104° (40° C.) or 
even higher. The patient feels very languid, has no appetite, and complains of 
headache; but there are mild as well as severe cases. The disease never lasts 
longer than a few days, even when the fever is high at first. The yellow spots 
vanish from the tonsils, and there is rapid recovery; severe complications are 
hardly ever seen. Often there is a herpes labialis and there may be slight albu- 
minuria, but this very rarely amounts to a genuine acute nephritis. It should 
be mentioned that sometimes the contents of a few of the follicles remain in 
them for a considerable length of time, and become inspissated and calcified. It 
is not a rare thing to find such plugs in the tonsils of those who are subject to 
sore throat. Timid and hypochondriacal individuals are sometimes badly fright- 
ened by expectorating these old chalky plugs, which they believe to be " tuber- 
cles " ! 

From an serological standpoint, follicular tonsillitis is in most cases entirely 
distinct from genuine diphtheria, and so far the search for the Klebs-Lofner 
bacillus in the plugs contained in the follicles has almost invariably proved 
negative. Still it is noteworthy that precisely at the time of diphtheria epidem- 
ics follicular tonsillitis is remarkably frequent. It might, after all, be pos- 
sible that the mildest degrees of diphtheria present themselves in the garb of an 
apparently simple follicular tonsillitis. The latter is very probably an infec- 
tious disease; but this matter has not yet been settled by pathological investi- 
gations. 

3. Tonsillar and Peritonsillar Abscess {Parenchymatous Sore Throat; 
Quinsy). — In this form the swelling of the tonsils is the most striking symptom. 
They may be more than twice their natural size. The anterior pillars of the 
fauces are pushed forward and become convex. The swelling extends so far 
toward the median line that the tonsil touches the uvula; or, if the affection is 
bilateral, the two tonsils press against each other, grasping the uvula between 
them, or pushing it forward. The soft palate is very much reddened, particularly 
at first. Its surface is usually thickly covered with mucus. If this be wiped off, 
the mucous membrane is seen to have a moist, oedematous luster. The mucous 



SOEE THROAT 



397 



membrane of the tonsils not infrequently suffers a superficial necrosis. Follicular 
and parenchymatous tonsillitis are often combined. 

In well-marked cases of abscess the local discomfort is usually great. With 
every attempt to swallow there is pain which shoots into the ear. The patient 
is in a pitiable condition ; he can neither talk, nor swallow, nor gargle. The few 
words which he painfully utters have in an extreme degree the nasal quality of 
the " voice of sore throat." 

In the milder cases the trouble seldom lasts but a few days before the swell- 
ing goes down, and the discomfort and usually rather moderate fever gradually 
abate. In other cases an abscess of the tonsil develops, usually on one side only, 
but it would be more correct to say a peritonsillar abscess, for the pus usually 
collects mainly in the connective tissue between the tonsil and the arch of the 
palate. In such cases the mucous membrane bulges out, usually at a point in 
the velum of the palate, and on palpation there is a sense of fluctuation, and 
finally the abscess ruptures. In other cases, however, a tonsillar abscess forms, 
as a rule, on only one side. The mucous membrane bulges out more in one spot ; 
fluctuation is detected; and, finally, the abscess breaks. With the discharge of 
the pus the pain is relieved very rapidly, or it may vanish at once. The rest of 
the tonsil soon regains its former size, and in a few days the patient is well. Re- 
lapses are possible, but rare. 

Phlegmonous sore throat, in which the soft palate and not the tonsil is chiefly 
affected, is infrequent. Its usual cause is some severe external injury, such as 
burns, and cauterization with concentrated acids or alkalies. The swelling ex- 
tends deep down into the submucous tissue. The uvula may have the diameter of 
one's finger. There is intense hyperemia. Sometimes there are haemorrhages 
into the mucous membrane : this is called hemorrhagic sore throat.* 

4. Necrotic Tonsillitis, or Necrotic Sore Throat. — This name is applied to a 
disease which is very frequent in Leipsic, but seems to be rather rare in Erlangen, 
and in which the tonsils are the main seat of the pathological processes. The 
pillars of the fauces and the uvula are but slightly affected with a simple ca- 
tarrhal inflammation. The tonsils are, as a rule, moderately swollen, seldom at- 
taining great size. The mucous membrane covering them presents a whitish or 
grayish-white discoloration, often quite extensive, and most marked on the side 
toward the uvula. These spots are often erroneously said to be a white " coat- 
ing " ; but a more careful investigation shows that there is in reality a necrosis. 
The process may be superficial ; sometimes it reaches quite deeply into the struc- 
ture of the mucous membrane. It is not possible to pull off this white matter, 
as one can loosen croupous membranes, although little bits may perhaps be 
scratched off with a spatula or a pair of forceps. These particles are found, on 
microscopic examination, to be made up merely of detritus, bacteria, epithelium, 
and pus-corpuscles. The necrosis is almost invariably confined to the tonsils, 
and a sharp boundary-line separates it from the reddened and inflamed pillars 
of the fauces. After a few days the slough may come away, leaving behind an 
ulcer, which, though usually shallow, has sometimes a considerable depth. This 
generally cleans up rapidly. In severe cases, however, the floor of the ulcer 
consists for a number of days of a dirty necrotic material, which comes 
away only gradually. The worst cases may be properly called " gangrenous ton- 
sillitis." 

^Necrotic tonsillitis is almost always attended by considerable fever and 
marked constitutional disturbance, Children particularly seem very ill in the 



* Another form with the same name occurs where there is violent tonsillitis with necrosis or gan- 
grene. There is also a necrotic, hemorrhagic sore throat accompanying scurvy, leukaemia, and analo- 
gous diseases. 



398 



DISEASES OE THE DIGESTIVE OEGAIs T S 



first days of the attack. The cervical glands are usually swollen, but seldom as 
much so as in genuine diphtheria. 

Despite the rather ominous commencement, the disease does not last a great 
deal longer than the other forms of sore throat. It seldom continues more than 
five to eight days before a speedy convalescence begins. 

The necrotic tonsillitis is distinguished from the follicular form by the greater 
area of the white or grayish-white spots. Still it should be particularly noted 
that sometimes combinations of these two varieties, or transitional forms, occur. 

^Etiology. — In our opinion, necrotic tonsillitis is in many instances an en- 
tirely different disease from genuine diphtheria. Perhaps it is often a very 
intense form of follicular tonsillitis, not limited, as it usually is, to the follicles. 
On the other hand, our experience in several epidemics of diphtheria in Leipsic 
and Erlangen has taught us that in all probability mild cases of genuine diph- 
theria of the tonsils do occur, and that these objectively resemble necrotic ton- 
sillitis. This is the only way to explain what other physicians as well as our- 
selves have often observed — namely, that necrotic tonsillitis appears not infre- 
quently in families at the same time with severe cases of genuine diphtheria. 
Besides, these cases of necrotic tonsillitis are sometimes followed by the char- 
acteristic " diphtheritic " paralysis. Still, more extensive pathological investiga- 
tion is needed to settle the question of the aetiology of necrotic tonsillitis. 

Diagnosis and Prognosis. — It is never very difficult to recognize a sore throat, 
and a little practice makes it easy in most cases to decide what particular vari- 
ety is present, if we examine the objective changes carefully. It is very important 
in practice to distinguish diphtheria from the benign forms of inflammation. 
Follicular and necrotic tonsillitis are very frequently mistaken for diphtheria — 
an error which explains the success of a large number of remedies said to cure 
diphtheria. Many physicians call every case of sore throat, where there is any- 
thing white to be seen, " diphtheria." Certainty in diagnosis of genuine diphthe- 
ria can be gained only by practice ; no description, however complete, can take the 
place of personal observation. It may be a help to remember that in both follicu- 
lar and necrotic tonsillitis the white spots are usually limited to the tonsils, while 
in croupous sore throat the deposits are generally from the very first also situated 
upon the pillars of the fauces and the uvula. The white spots of the follicular 
variety can generally be recognized by their arrangement. The plugs are seen 
projecting from the follicles. In necrotic sore throat there is never a separable 
croupous membrane with its characteristic histological structure, but there is sim- 
ply a superficial necrosis of the mucous membrane and parenchyma. In doubtful 
cases the condition of the cervical lymph-glands is not unimportant; as a rule, 
they are much more affected in diphtheria than in the benign cases. Inasmuch 
as we have seen that the milder forms of tonsillitis may be serologically related 
to diphtheria, it is well in practice to make a guarded prognosis, even in cases of 
follicular and necrotic angina, particularly in children ; and we should always 
isolate the patient from other children. 

Treatment. — These troubles run so favorable a course that active treatment is 
very seldom needed. The gargle usually prescribed generally gives the patient 
more discomfort than relief. The most common prescriptions are: Solutions of 
potassic chlorate (5-10 : 300), of alum (5-10 : 500), or of borax (10 : 300) ; salt 
and water; and weak solutions of carbolic acid or of permanganate of potash. 
To paint the parts is a useless and now almost obsolete proceeding. Inhalations 
of spray are better, with alkaline solutions, diluted lime-water, alum, or tannin. 
It is beneficial to put a cold wet compress around the throat. Children must be 
kept in bed, and adults are generally forced to go to bed, if the constitutional 
symptoms are well marked. 

In parenchymatous tonsillitis with a tendency to suppuration ice will some- 



CHRONIC HYPEETEOPHY OF THE TONSILS 



399 



times alleviate the pain. Often, however, the patient can not bear it. If there 
is evident fluctuation, we can make an incision with a spear-pointed bistoury, 
after guarding a portion of the blade with sticking-plaster. The best place is 
almost always in the velum palati, corresponding to the outer boundary of the 
tonsil. Great relief follows; and even if there is no distinct abscess an incision 
will usually give relief, if there is excessive swelling, and if there is a deeply- 
seated abscess will facilitate its spontaneous discharge. Punctures of this sort 
cause scarcely any pain. 

We may add that if a person is subject to sore throat, he can lessen his liability 
to attacks by hardening his skin through the use of cold baths. [Hoffman has 
pointed out that in some cases permanent recovery can be attained by breaking 
down the partitions between the crypts of the tonsils, thus establishing thorough 
discharge of their secretions. — V.] 



CHAPTEE II 
CHRONIC HYPERTROPHY OF THE TONSILS 

Chroxic hypertrophy of the tonsils occurs not only in those who have had 
repeated attacks of tonsillitis, but also in cases in which no occasion for it can be 
found. Even in childhood there may be well-marked hypertrophy, which must 
be due to a congenital predisposition. 

The condition is at once revealed by inspection. There may be no signs what- 
ever of any acute or chronic inflammation, or there may be an accompanying 
chronic pharyngitis. The tonsils bulge out in two great lumps. They may be so 
large as to touch the uvula on each side. Histologically, there is a genuine hyper- 
trophy of the organ — that is, an increase of all its component tissues. 

In many cases, where the swelling is moderate, there is no discomfort. The 
possessor of the tonsils is not aware that they are enlarged. In other cases the 
hypertrophy proves of clinical importance, inasmuch as all forms of sore throat 
are found to occur more frequently if the tonsils are enlarged, and to cause more 
trouble when they do appear. The hypertrophied organs may also be the seat of 
a chronic catarrh, which by extension gives rise to chronic nasal catarrh, catarrh 
of the Eustachian tubes, or hoarseness. 

If the hypertrophy is considerable, the local discomfort may be quite marked. 
Swallowing is rendered difficult, if not painful. Frequently there is evident 
dyspnoea. The patient has to breathe through his mouth, and sometimes when 
asleep snores and snorts in a way to frighten one. Children are particularly apt 
to suffer in this manner. Many instances of pavor noctumus, or " night terrors," 
in children are referable to this cause. AYe have already mentioned that cases of 
bronchial asthma sometimes seem to be connected with hypertrophy of the tonsils 
(see page 182). 

Treatment. — The attempt to reduce the enlargement by applying lunar caus- 
tic, tincture of iodine, etc., usually fails. If there is much distress, if the patient 
is subject to frequent sore throats, or if the hypertrophy of the tonsils keeps up a 
chronic nasal or pharyngeal catarrh, then the simplest remedy is to remove the 
tonsils. The operation is free from any danger. The extirpation of hypertrophied 
tonsils can be accomplished either with the tonsillotome, the galvano-cautery, or 
with scissors and forceps. The latter way is the simpler, and is equally easy. 
[In adults, excision of the tonsils sometimes causes troublesome bleeding, and for 
them the galvano-caustic snare is the best means to employ. — Y.] 



400 



DISEASES OF THE DIGESTIVE OKGANS 



CHAPTER III 
CHRONIC PHARYNGITIS 

etiology. — It is not practicable to distinguish between chronic catarrh of the 
soft palate and of the pharynx, for, as a rule, the two are combined. Sometimes 
the condition is the result of repeated acute attacks; sometimes — and probably 
oftener — it is due to persistent, injurious, local influences. A large number of 
cases originate in bad habits, or in abuse incident to certain vocations. Exam- 
ples are seen in smokers, drunkards, singers, preachers, teachers, and men who 
work out-doors. In talking and singing, the soft palate is strained; or the dis- 
ease is excited by breathing cold or impure air, or by such chemical irritants as 
alcohol or tobacco. In many cases, chronic pharyngitis follows chronic rhinitis or 
chronic laryngitis. The general passive congestion due to cardiac disease or pul- 
monary emphysema may sometimes promote the development, or prolong the ex- 
istence, of a chronic pharyngitis. 

Symptoms. — The local discomfort is often slight. The patient gets used to it, 
and does not mind it except when there is some exacerbation. It becomes a more 
important matter if the calling of the patient is interfered with, as in a preacher, 
singer, or teacher. 

Deglutition is seldom impaired. There is often, however, a constant feeling 
of dryness, burning, or scratching in the throat. The patient has to clear his 
throat frequently, and often acquires an habitual, short, sudden cough, which may 
or may not be dry. The expectoration, if there is any, is almost pure mucus. 
When there are violent efforts to clear the throat, there may be a slight hemor- 
rhage from the dilated blood-vessels of the posterior wall of the pharynx, explain- 
ing the presence of small amounts of blood in the expectoration. This blood 
often has a dried-up look, as if not fresh. It sometimes leads over-anxious pa- 
tients and physicians to suspect pulmonary haemorrhage. The uvula becomes so 
long that its tip rests on the tongue or the posterior wall of the pharynx; and 
this gives rise to a peculiar and disagreeable sensation of tickling. All these 
uncomfortable feelings are temporarily increased if anything affects the throat 
unfavorably; and they are generally at their worst on rising in the morning, 
apparently because the mucous membrane has become dry? or a collection of 
tough mucus has formed during the night. Every one knows how drunkards have 
to hawk and cough in the morning, so that often they almost strangle or vomit. 

On inspection, we generally find the mucous membrane reddened. Very often 
a number of dilated and tortuous veins are visible both on the soft palate and in 
the back of the throat. Of equal frequency is the appearance of numerous small 
gray projections, corresponding usually to swollen follicles or else to hyper- 
trophied mucous glands. This is called granular pharyngitis. Small follicular 
ulcers are not infrequent. Exceptionally there are more extensive catarrhal 
ulcers. The mucous membrane of the posterior wall of the, pharynx may present 
patches of opaque or thickened epithelium, giving the surface a grayish-white 
appearance. 

Frequently chronic pharyngitis is combined with chronic laryngitis, evidenced 
by hoarseness ; or with posterior nasal catarrh, or catarrh of the Eustachian tube, 
producing deafness and ringing in the ears. 

Varieties of Chronic Pharyngitis 
1. Chronic Catarrh of the Naso-pharynx, or Chronic Posterior Nasal Ca- 
tarrh. — This has the same aetiology as the ordinary form. It is practically im- 
portant because the nose and ear are frequently involved. 



CHRONIC PHARYNGITIS 



401 



The anatomical changes are essentially those already depicted under chronic 
pharyngitis. The region affected can not be seen by direct inspection, so that 
accuracy in diagnosis requires the use of a nasal speculum (see particulars in the 
works mentioned on page 135). The ordinary examination of the throat may 
reveal a condition which is quite characteristic of posterior nasal catarrh : a col- 
lection of muco-pus, or of firmly adherent dry crusts, rests upon the posterior 
wall of the pharynx, and can be seen to extend upward toward the naso-pharynx. 

The local discomfort is somewhat similar to that experienced in chronic 
pharyngitis. There is a scratchy feeling, or a feeling as if there were a foreign 
body in the back of the throat, accompanied by a constant desire to blow the nose, 
hawk or cough. Dried and decomposing secretion often causes extremely foul 
breath. There is often also vertigo, and occipital headache. 

In many cases the nostrils are stopped up. The posterior opening of the nos- 
trils is closed in part by the swelling and hypertrophy of the mucous membrane, 
and in part by the accumulated secretions. The patient, therefore, usually has 
to breathe through the mouth. The ear is frequently involved. The catarrh 
extends into the Eustachian tubes and the tympanic cavity, or the opening of the 
tubes is occluded with the secretions. For a detailed consideration of the deaf- 
ness, tinnitus, etc., thus produced, consult works on otology. 

2. Pharyngitis Sicca, or "Dry Atrophic Catarrh of the Throat and Naso- 
pharynx." — This name is applied to an atrophic disease of the mucous membrane, 
which sometimes is spontaneous and sometimes is a sequel of chronic pharyngitis. 
The whole mucous membrane of the pharynx and the naso-pharynx (seen with the 
rhinoscope) seems pale, smooth, and perfectly dry, and has a peculiar luster, as if 
varnished. Here and there tortuous veins project from the general anaemic 
surface. 

If an opportunity is afforded to examine the mucous membrane microscopic- 
ally, it will be found that the atrophy involves all the elements of the tissue, 
though the follicles and mucous glands suffer most. 

This condition may not cause any symptoms, but, in many cases, the patient 
suffers constantly and considerably. The chief trouble is a feeling of dryness in 
the throat, rendering deglutition difficult or even painful. There is also a con- 
stant desire to clear the throat. The secretion hawked up may be scanty and 
tough or more abundant, and it is often tinged with blood. Actual coughing 
may also be due to pharyngeal trouble (" throat-cough ")• Talking is often ren- 
dered difficult, the voice grows weak and it becomes easily tired. In severe 
cases there is considerable general debility. Not infrequently pharyngitis sicca 
is associated with atrophic rhinitis (q. v.), but it occurs also where there is no 
nasal disease. 

The disease is most frequently seen in the elderly, but it also occurs in children 
and young persons. It is especially common in ill-nourished individuals or in 
those who are suffering from such diseases as tuberculosis or chronic nephritis. 

3. Hypertrophic Catarrh in the Pharynx and Naso-pharynx. — An opposite 
condition, of hypertrophy, sometimes results from chronic catarrh. The changes 
consist mainly in hyperplasia of the lymphatic tissue, and they are usually 
termed " adenoid growths." The choanse and the posterior extremity of the nasal 
septum may be almost completely hidden by these growths, as they extend down 
from the roof of the pharynx in grayish-red, uneven masses. In many cases the 
hypertrophy seems to originate chiefly in Kolliker's " pharyngeal tonsil." 

The adenoid growths are especially common in childhood. The symptoms 
consist in a change of the voice (which loses its reverberating quality and becomes 
nasal), frequent snuffling and hawking, and a tough mucous secretion, often 
tinged with blood. Not infrequently there is headache. Of greater importance 
is ear-trouble, which is often occasioned by the growths. 
26 



402 



DISEASES OE THE DIGESTIVE OKGAXS 



An accurate diagnosis requires rhinoscopy. Positive results are also often 
obtained by palpation. The index-finger, being pressed backward and bent up- 
ward, can touch the protuberances and the enlarged pharyngeal tonsil in the 
naso-pharynx. 

Prognosis. — In all varieties of chronic pharyngeal catarrh, the prognosis as 
to recovery is doubtful, for in all severe cases the process is very obstinate, and 
permanent restoration to health exceptional. It is essential for the best results 
that all injurious influences should be removed. Even if decided improvement 
occurs there is a tendency for the trouble to grow worse again, and for acute 
exacerbations to occur. 

Treatment. — Many of the milder cases never apply to a physician. The pa- 
tient uses some domestic remedy or gargle, or becomes so accustomed to the dis- 
agreeable sensations that he does not consider it necessary to do anything in 
particular about them. 

The treatment of a well-developed case requires gTeat patience and persist- 
ence on the part of all concerned. If there is some underlying disease, such as 
pulmonary or cardiac disease, that must be treated. All exciting- causes must be 
avoided. Energetic local treatment is also indispensable. This has been greatly 
elaborated by specialists, and for the many details we must refer to their writ- 
ings ; but the following remarks will meet the requirements of ordinary practice : 

Gargles are seldom satisfactory, for they never reach farther than the soft 
palate. Inhalations are better; we may use solutions of alum or tannin, or. in 
mild cases, of common salt. Still more efficient is the painting of the entire sur- 
face of the pharynx with some concentrated solution. The physician usually has 
to perforin this, although some patients learn to do it for themselves. Proper 
solutions are : Argentic nitrate, five or ten per cent. ; tannin, eight to twenty per 
cent. ; tincture of iodine, either pure or diluted : or iodized glycerine, composed 
of pure iodine, parts 0.5; iodide of potassium. 2; glycerine. 20, with the addi- 
tion, if desired, of two drops of oil of peppermint. These applications must reach 
all the diseased surface. If the naso-pharynx is involved, the brush must accord- 
ingly be bent upward, to reach that region. Eor this a mirror may be needed. 
It is very important to make the applications to the mucous membrane itself, 
freed from any interposing secretions. 

In the treatment of chronic posterior nasal catarrh the nasal douche (vide dis- 
eases of the nose) plays an important part. It should be used two or three times 
a day. It not only removes the collected secretions, but it is a means of making- 
local applications. The instrument is merely a fountain-syringe. The nozzle 
must be of a size to rill the nostril completely. The force of the current should 
always be moderate, and the patient's head should be sharply flexed forward. 
The fluid used- — the best is a one-per-cent. solution of sodic chloride or bicarbonate 
— must have about the temperature of the body. Other medicated solutions must 
be very weak, such as sulphate of zinc. 1 to 1,000. 

The insufflation of powders into the throat can be made through any small 
glass tube, three to six times a week. Alum or tannin may be used, either pure 
or mixed with equal parts of pulvis gummosus [P. G., made of gum-arabic, three 
parts; licorice-root, two parts; and sugar, one part], or 3-5 parts of nitrate of 
silver to 100 of starch. Eor the naso-pharynx, a bent tube of glass or hard 
rubber is to be introduced through the mouth. There are numerous " insuffla- 
tors " to be had at the instrument-makers. 

Many baths enjoy a great reputation for the cure of chronic pharyngitis. 
Besides Ems, there are Peichenhall. Kreuznach, Salzungen, the cold sulphur 
springs, such as Weilbach, and many others. Good results are also achieved in 
Kissingen and Marienbad, if these places are favorable to the patient's general 
constitution. 



RETROPHARYNGEAL ABSCESS 



403 



In pharyngitis sicca, the nasal douche with a one-per-cent. salt solution is to 
be recommended. It is sometimes also beneficial to paint the parts with solution 
of argentic nitrate, iodized glycerine, etc. Many irritating influences which do 
harm in common pharyngitis seem sometimes actually to benefit this form — such 
as smoking and taking snuff. 

In treating the hypertrophic forms of pharyngitis and the adenoid growths, 
cauterization with nitrate of silver suffices for the milder cases alone. A thor- 
ough and permanent cure can be achieved- only by removing the growths with the 
galvano-cautery. 

[To Hooper, of Boston, belongs the credit of showing that a radical opera- 
tion for the removal of adenoid growths of the naso-pharynx can safely be done 
under anaesthesia. The blood does not, as was feared, run into the air-passages, 
but either into the stomach or outwardly. Anaesthesia thus renders it possible 
to scrape away with the finger or tear away with forceps the hypertrophied tissue 
at one sitting, and to do it in the child before secondary changes have taken place 
in the facial expression, the jaw, the ears, or the form of the chest.] 



CHAPTEK IV 
RETROPHARYNGEAL ABSCESS 

Retropharyngeal abscess is formed by a suppurative inflammation of the 
connective tissue lying between the posterior wall of the pharynx and the spinal 
column. It is a serious disease, although a rare one. If unrecognized, it proves 
fatal in many instances; while, if a correct and timely diagnosis is made, the 
patient can usually be easily cured. It is commonest in childhood, and before 
the second year. It almost always appears as a primary, acute disease, without 
any special cause being evident. Probably the agents which excite the inflamma- 
tion penetrate into the tissue from the pharynx. The idea that the inflammation 
originates in the small lymphatic glands which lie in front of the vertebras lacks 
proof as yet. 

The disease attacks not only weakly children, but those who have been per- 
fectly healthy and vigorous. The child grows restless and fretful, and does not 
nurse well. Apparently, deglutition soon becomes painful, but one can not be 
certain about this except in older children. Generally, the respiration quickly 
takes on a peculiar stertorous character, particularly during sleep. Mucus collects 
in the mouth and throat. Upon swallowing, there is often regurgitation through 
the mouth or nose, or some of the food gets into the windpipe and causes violent 
coughing. The lymph-glands of the jaws are usually somewhat swollen, and the 
neighboring parts may seem slightly oedema tons. After a week or two the dysp- 
noea gradually increases. Respiration becomes more and more laborious, with 
loud rattling, and signs of stenosis. The jugular veins become distended, the 
lips cyanotic, and portions of the thorax are retracted during inspiration. The 
voice is feeble, and may be hoarse and indistinct. 

The correct interpretation of these symptoms, which are common to various 
disorders, requires a careful examination of the throat. It must be confessed 
that this has its difficulties in an infant. Still, we can sometimes see distinctly 
a swelling in the posterior wall of the pharynx. This may be either in the median 
line or on one side. All doubt is removed by digital examination, in making 
which, however, we must insert a wedge between the teeth, to avoid being bitten. 
The finger detects fluctuation. 



404 



DISEASES OF THE DIGESTIVE ORGANS 



The diagnosis once established, the abscess must be opened at once. We 
should not delay, even if the dyspnoea has not yet become extreme. To use the 
finger-nail for the purpose, as has been recommended, is permissible only in an 
emergency. As a rule, incision is made with a bistoury, of which all but the 
point is guarded with sticking-plaster. The left index-finger is placed upon the 
abscess, and used as a guide. Meanwhile, the child's head is kept upright, and, as 
soon as the cut is made, bent over forward. The pus pours out in abundance. It 
is advisable to syringe out the mouth repeatedly with lukewarm water. The 
threatening symptoms vanish almost instantly upon the escape of the pus. Ex- 
ceptionally, the abscess refills and requires a second incision. 

If the trouble is not correctly diagnosticated, or if the abscess is not opened 
promptly, the patient may suffocate. The abscess, however, may burst sponta- 
neously; then there is either speedy recovery, or asphyxia from the pus filling the 
larynx. In some instances, when a retropharyngeal abscess has not been properly 
treated, the pus has gravitated far down into the neck and posterior mediastinum. 
The recognition and incision of the abscess may prove very difficult if from the 
start it is situated lower down in the throat than usual. 

Analogous to this acute idiopathic abscess of which we have been speaking is 
the chronic abscess due to caries of the cervical vertebrae. This occurs in chil- 
dren as well as adults. Incision of such abscesses is indicated only when there 
is danger of suffocation. Because of their tuberculous character, the prognosis 
is, of course, much more unfavorable than in ordinary suppurative inflammation. 

Retropharyngeal abscesses sometimes occur in pyaemia or other severe acute 
infectious diseases, but they have hardly any interest except to the pathologist.* 

s 



SECTION III 

Diseases of the (Esophagus 

CHAPTER I 

INFLAMMATION AND ULCER OF THE CESOPHAGUS 

iEtiology and Pathology. — The various forms of oesophageal inflammation 
and ulceration are not of very great clinical importance. The processes are sel- 
dom of a severe grade, or, if so, they are generally a part of some complicated 
disease, to which they seldom contribute prominent symptoms. Very likely the 
milder forms of inflammation occur frequently, but the symptoms are hardly ever 
characteristic. 

A simple catarrhal inflammation of the oesophageal mucous membrane may 
be caused by swallowing substances which are injurious mechanically, chem- 
ically, or from their temperature. It may also occur in the general infectious 
diseases, such as typhoid and typhus fevers, and the acute exanthemata. Any 
inflammation of neighboring tissues may extend into the oesophagus. Chronic 
catarrh is seen in heart disease, from the passive congestion. It is also found 
in the vicinity of other chronic oesophageal diseases, particularly cancers and 
diverticula {vide infra). 



* Tuberculosis of the pharynx is spoken of in the chapter on pulmonary tuberculosis, p. 248. New 
growths in the mouth or pharynx belong to the domain of surgery. 



INFLAMMATION AND ULCER OF THE (ESOPHAGUS 405 



The acute catarrh is distinguished by not having the usual increase of secre- 
tion. The epithelium grows spongy, as a rule, and is cast off more rapidly than 
usual, so as to suggest the name of a desquamative catarrh. It is in only a few 
cases that the scanty mucous glands become swollen and look like papules upon 
the surface of the membrane; this form is called follicular catarrh. In limited 
areas the desquamation may be complete, giving rise to small catarrhal erosions. 
Likewise, the swollen follicles may break down into small follicular ulcers. 

In chronic catarrh there is a moderate increase in the secretion of mucus, and 
a marked thickening of the epithelium. In very protracted cases actual papillo- 
mata may finally be formed. In some cases ulcers are seen. 

Croupous and diphtheritic inflammations of the oesophagus are very rare. We 
have already said that the specific pharyngeal diphtheria frequently extends into 
the larynx, but only exceptionally into the gullet. Still, we have ourselves seen 
in a child a stricture in the upper third of the oesophagus, which was said to have 
been a result of a severe attack of diphtheria. Isolated cases of diphtheritic 
oesophagitis have also been seen in connection with severe infectious diseases, 
such as typhus, typhoid, small-pox, cholera, pyaemia, and pulmonary tuberculosis, 
as well as in the course of Bright's disease and cancer. In variola it is not un- 
usual for pocks to appear upon the oesophageal mucous membrane. 

A purulent, phlegmonous oesophagitis now and then attacks the submucous 
layer. It may be either diffuse or circumscribed. The mucous membrane is dis- 
sected up from the muscular layer by the pus, and pushed inward, so as to dimin- 
ish the lumen of the oesophagus more or less. Most of the cases end by the dis- 
charge of matter into the tube, when complete recovery may ensue. If the mu- 
cous membrane, however, has been extensively undermined, Zenker states that a 
fissure-like cavity may be left, even after healing has taken place. Its walls grow 
smooth, and finally acquire a layer of fresh epithelium. 

Purulent oesophagitis is caused either by the presence of foreign bodies in the 
oesophagus, or by purulent inflammation in neighboring parts, as in glandular 
abscess, vertebral abscess, or laryngeal perichondritis. It has now and then 
resulted from the action of concentrated acids and the like upon the mucous 
membrane. 

The action of corrosive poisons (corrosive oesophagitis) is to cause necrosis 
of the tissues, which in its turn produces inflammation. The inner surface of 
the oesophagus is converted into a rotten, hemorrhagic, sloughing mass, of a 
dirty gray or almost black color. The muscular layer itself may be partly de- 
stroyed. If death does not occur speedily, the necrosed portions come away, leav- 
ing extensive purulent ulcers behind. These, if they heal at all, cause large cica- 
trices and stenosis. 

Symptoms. — The milder cases, as we have stated, produce almost no distinc- 
tive symptoms. . Possibly there may be pain along the oesophagus, or at some one 
point in it, during deglutition. In a more severe case the pain may be great; 
but the other symptoms are usually too grave for this to excite special attention. 
Laborious deglutition, and the feeling* as if the food were inclined to stick in the 
throat, result from implication of the muscular layer. A diagnosis of the par- 
ticular form of oesophagitis is attainable only when the aetiology guides us to it. 

Treatment must be purely symptomatic. No solid food should be taken. The 
pain is to be allayed by bits of ice, or by morphine. 



406 



DISEASES OE THE DIGESTIVE OKGAXS 



CHAPTEE II 
DILATATION OF THE OESOPHAGUS 

1. Diffuse Dilatation 

Diffuse, spindle-shaped dilatation of the oesophagus is observed as a result of 
stricture of the cardiac orifice. At first the muscular coat hypertrophies as the 
orifice contracts, and is able to overcome the obstruction, so that there is no dila- 
tation; but as soon as the muscles are paralyzed, and food collects behind the 
stricture, the dilatation begins and keeps on increasing. The ectasis is greatest 
at the lower end of the tube, as is natural from its mode of origin, and gradually 
diminishes upward. 

There have been a very few well-substantiated instances of this diffuse spindle- 
shaped dilatation, without any demonstrable stenosis of the cardiac orifice. Their 
cause is unknown. Sometimes the walls of the oesophagus may have been ren- 
dered more yielding and less contractile by a precedent inflammation or other 
disorder. In other cases, some chance bend or distortion of the lower end of the 
oesophagus may have produced a mechanical obstruction. In some cases the ex- 
citing cause is said to be a blow on the chest, or the lifting of a heavy weight. 
Perhaps in many cases there is a congenital anomaly. 

The symptom of this condition, when well developed, is a chronic difficulty in 
deglutition, lasting perhaps for years. The patient himself feels that most of the 
food he eats does not reach the stomach, but lodges higher up. Usually the food 
is soon afterward vomited, or rather gulped up. When there is stenosis of the 
cardiac orifice, the explanation of these symptoms is easy. It is much harder 
to explain the almost equal dysphagia when there is dilatation without stenosis. 
Sometimes a localized bulging of the wall causes the food to collect in that spot, 
and thus to obstruct the lumen. As is to be expected, the partial or complete 
hindrance to the ingestion of food results in marasmus. 

If there is stenosis, it can easily be detected with the oesophageal sound, and 
all the symptoms can thus be explained. In the rare cases, however, of diffuse 
dilatation without stenosis, the use of the sound does not give us so much infor- 
mation. If the instrument passes readily into the stomach, we may safely exclude 
stricture; but. in one case of our own, we made an erroneous diagnosis of a 
diverticulum, because the sound sometimes glided readily into the stomach, and 
sometimes could not be passed. A pocket must have been formed at the lower end 
of the dilated tube, in which the sound caught. 

The treatment is directed chiefly to the satisfactory nourishment of the pa- 
tient; for the oesophageal trouble itself is dangerous only as it prevents the taking 
of food and leads to starvation. We do not speak of the initial lesion, if there be 
one, which causes the dilatation. If nourishment can be given through a stom- 
ach-tube, the patient almost invariably shows a rapid improvement, which lasts as 
long as the artificial feeding can be kept up. If, however, any cause prevents the 
introduction of the tube, we must resort either to nutrient enemata (vide infra) — 
and these will not support the system indefinitely — or we must make a gastric 
fistula. In the latter case the prognosis depends on the success of the operation 
and the nature of the original lesion. 

2. Diverticula 

^Etiology and Pathology. — Circumscribed pouches in the wall of the oesopha- 
gus are termed diverticula. They are divided into two essentially distinct varie- 



DILATATION OF THE (ESOPHAGUS 



407 



ties according to their mode of origin. Zenker has given them the names of 
pressure and traction diverticula. 

The diverticulum due to pressure is extremely rare. It is caused by pressure 
upon the mucous membrane from within, by which some abnormally weak spot 
is forced outward. All cases that have been carefully examined thus far have 
shown that, histologically, the wall of the diverticulum is not the distended but 
otherwise unchanged wall of the oesophagus, but is composed exclusively of the 
mucous membrane and the thickened submucous coat. We are therefore obliged 
to suppose that the mucous membrane is pushed out like a hernia through some 
gap in the muscular coat. It is only about the neck of the diverticulum that any 
muscular fibers are found. 

The original factor, therefore, in the occurrence of a pressure diverticulum is 
apparently to be sought in some circumscribed lesion of the muscular coat. As a 
result of several observations, it is established that a foreign body, sticking in the 
throat, may separate some of the muscular fibers and push the mucous membrane 
through the gap thus formed. Or a severe injury leads to a trifling rupture of 
the muscular coat, and then the food, as it is being swallowed, presses out the 
mucous membrane at this weakened spot. There are still many other cases in 
which the true origin of the diverticulum remains obscure. 

As soon, however, as the formation of the pouch has once begun, there are 
many influences to make it grow larger. Each successive bit of food, as it 
glides by, presses upon this yielding and inelastic spot. Gradually a little sac is 
formed, in which bits of food lodge. These exercise a constant pressure upon the 
walls of the pouch, and by their weight drag it bodily downward. The larger the 
pouch, the more it holds, and consequently the more it grows. Thus a pressure 
diverticulum of the smallest size originally may gradually attain to a diameter of 
four inches or more. The general shape of the diverticulum may approach the 
hemispherical, or it may be more cylindrical or pear-shaped. 

It is remarkable that, with very rare exceptions, these pressure diverticula are 
always situated at the beginning of the oesophagus, or rather between it and 
the pharynx, and almost invariably affect the posterior wall. The pouch hangs, 
therefore, in front of the spinal column. It pushes out through the lowest fibers 
of the inferior constrictor of the pharynx; and the feebleness of this muscle is 
apparently a potent factor in determining the precise point of origin. 

The cases thus far seen have been almost all in men, and at a rather advanced 
age. A few cases have occurred in children. 

Traction diverticula are much more common, but in most instances have little 
interest except for the pathologist. They are not infrequently found unexpected- 
ly at the autopsy. Rokitansky, and later Zenker, have given explanations of 
their occurrence : some tissue, which has formed adhesions to the oesophagus, con- 
tracts and gradually pulls out the oesophageal wall in the shape of a funnel. Bron- 
chial glands are apt to be the seat of the contractile change. These glands are 
situated near the bifurcation of the trachea, and accordingly the traction diver- 
ticula occur oftenest at this level. There may be two or three in one subject. 
They are rarely over a third of an inch in depth. Erom within, the mucous 
membrane, much wrinkled transversely, is seen to be drawn toward the apex of the 
diverticulum. The wall of the latter consists either of the mucous membrane 
alone, bulging out like a hernia, or of the mucous membrane covered by the mus- 
cular layer. Inasmuch as children quite often suffer from suppuration and case- 
ation of bronchial glands, with subsequent shrinkage, we see why traction diver- 
ticula are frequent in children. 

Clinical History. — The large pressure diverticula always cause grave symp- 
toms, for they obstruct more and more each day the passage of food. At first 
there is scarcely any disturbance. Gradually, however, deglutition is impeded. 



408 



DISEASES OF THE DIGESTIVE ORGANS 



A portion of the food lodges in the pouch, and is either wholly or in part regurgi- 
tated, though perhaps not immediately. Decomposition is apt to take place in 
the contents of the diverticulum, giving rise to foulness of the breath and to 
nausea. The danger reaches its climax when the distended sac presses sidewise 
upon the oesophagus and closes its lumen, so that no food reaches the stomach. 
After protracted strangling and vomiting, the material may be in part ejected, 
and the patient enabled once more to swallow. 

Of course the symptoms in individual cases depend upon the mechanical con- 
ditions present, and they may vary greatly. Patients contrive all sorts of manip- 
ulations, by which they manage to get at least some portion of their food down. 
Such individuals may maintain a tolerable degree of nutrition for years, although 
they scarcely ever are in a normal condition. But at last some cause or other 
renders the amount of food ingested inadequate ; whereupon a rapidly progressive 
marasmus sets in, and the patient will inevitably starve to death unless some 
relief is afforded. 

The most valuable objective evidence in these cases is gained by the use of the 
oesophageal sound. If the sound enters the sac, its passage is impeded. If it 
happens to slip by the mouth of the diverticulum, it glides readily into the 
stomach. This varying result may sometimes be obtained at one sitting by 
repeated trials, and is of the greatest importance in making the diagnosis. 

In some instances where the sac was large, a tumor in the neck has been 
observed at one side of the trachea, appearing after eating and disappearing when 
the sac emptied itself. Symptoms due to compression of the recurrent and 
phrenic nerves and of the blood-vessels have been noticed in some cases. 

Auscultation of the oesophagus during the act of swallowing has been prac- 
ticed, and, of late, attempts have been made to examine it with a speculum. 
Whether these methods of investigation will prove valuable for diagnosticating 
diverticula, experience must determine. 

The traction diverticula are usually of no clinical importance. They do not 
affect deglutition at all, and their size is too limited to permit any great accumu- 
lation of food in them. There is but one way in which they are dangerous : the 
apex of the funnel may undergo ulceration and perforation. A foreign body, such 
as some bit of food, produces necrosis of the wall, by what is probably at first a 
purely mechanical irritation. The tissue ulcerates ; and then the inflammation 
may gradually progress till it causes a severe and usually fatal illness. The most 
frequent event is perforation into a bronchus, followed by the aspiration of food 
and pulmonary gangrene; or the perforation may take place into the pleural cav- 
ity, exciting an ichorous empyema. In other cases the pericardium or a large vein 
has been perforated. Many a case of apparently spontaneous pulmonary gan- 
grene, or purulent inflammation of the anterior mediastinum, or empyema has- 
been found at the autopsy to have been brought about in the manner above indi- 
cated. These occurrences are fortunately, however, exceptional. 

Treatment. — The only possible way of treating the large pressure diverticula 
successfully would be by operation. Perhaps surgery will some day win victories 
in this domain. In the meanwhile our efforts are confined to sustaining the 
patient. If he can not swallow, we must try to feed him through a tube. As 
long as this is possible, starvation is averted. It is well to have the patient 
pass the tube himself. He will find out how best to avoid the sac and reach the 
stomach. If food can no longer be given in this way, there remain two alterna- 
tives : rectal feeding (vide infra), or making a gastric fistula. As to the latter, 
there has been thus far very little practical experience, because cases are so rare. 

The traction diverticula admit of no special treatment. If the events above 
mentioned occur, we must endeavor to meet the indications of the individual case. 



STENOSIS OF THE (ESOPHAGUS 



409 



CHAPTER ITI 
STENOSIS OF THE OESOPHAGUS 

iEtiology and Pathology. — Contractions of the oesophagus occur with such 
relatively great frequency that they are the most important of all its disorders. 
They originate in various ways. By far the commonest cause is ring-shaped car- 
cinoma of the tube. The new growth in the mucous membrane encroaches more 
and more upon the lumen of the oesophagus, until finally it fills it. Carcinoma 
will be discussed at length in the next chapter. We shall here confine our atten- 
tion to its purely mechanical action in causing stenosis. 

(Esophageal tumors other than cancer are very rare. Eibrous pedunculated 
polypi have been observed a few times. They usually originate in the lowest 
portion of the anterior wall of the phaynx, hanging down into the oesophagus, 
which they may thus obstruct. 

A second cause of stenosis is the contraction of cicatrices of the oesophageal 
wall. The most frequent occasion for this is the extensive ulceration caused by 
caustic poisons, such as concentrated acids or alkalies. If the victim escapes a 
speedy death, he is almost certain to have extensive scars formed in the wall of 
the oesophagus. These scars radiate irregularly in all directions, and, contract- 
ing, may almost completely close the tube. 

Ulcers from other causes, resulting in stenosis due to the scars they leave, are 
among the greatest rarities. Syphilis has been the well-established cause in some 
instances, and Quincke has described a few cases in which there were ulcers at the 
lower end of the oesophagus analogous to the round ulcer of the stomach, or 
" ulcer due to digestion " (vide infra). These ulcers also may eventually produce 
cicatricial stenosis. 

A third and rare cause of stenosis of the oesophagus is compression from 
tumors external to it. Such swellings may originate in the thyroid gland, or in 
the lymph-glands of the neck or the anterior mediastinum; or the swelling may 
be due to a vertebral abscess or an aortic aneurism. This form of stenosis is sel- 
dom extreme, for the portion of the tube pressed upon is usually limited. 

JSJext on the list after stenosis due to compression is usually placed what is 
called intermittent dysphagia (dysphagia lusoria). This term is applied to the 
difficulty in swallowing which is said to be caused by an anomaly in the course of 
the right subclavian artery. The artery is given off as the last branch from the 
arch of the aorta, and runs toward the right side just behind or just in front of the 
oesophagus. It seems, however, a priori improbable that the feeble pressure of 
this vessel as it pulsates should impede deglutition ; nor has it yet been proved 
to do so. It would be more natural to believe, what was indeed the original ex- 
planation of the phenomenon, that a large morsel of food passing down the oesoph- 
agus compresses the vessel and thus excites uneasiness and palpitation ; but so far 
as we know even this is extremely rare, if it ever occurs. 

Stenosis due to foreign bodies belongs to surgery. It need not be said that 
the clinical symptoms differ greatly in different cases. 'Not only the obstruction, 
but also a possible laceration and consequent inflammation are to be considered. 
Occasionally thrush has been abundant enough to cause pronounced symptoms of 
stenosis. 

Above the point of stenosis, no matter how the condition arose, if only it is 
well developed and has lasted a certain length of time, the circular fibers of the 
muscular coat are more or less hypertrophied. This hypertrophy is due to the 
increased force required to propel the ingesta downward. In many cases the tube 
is also diffusely dilated above the stenosis. 



410 



DISEASES OF THE DIGESTIVE ORGANS 



Symptoms. — The effect of every oesophageal stenosis is to render deglutition 
difficult. If the case is a mild one, the patient experiences nothing more than a 
moderate pressure in the oesophagus upon swallowing. He feels that the morsel 
is longer than usual in reaching the stomach. Very soon he notices that solid 
food and large morsels can be swallowed only with difficulty. Accordingly, he 
is gradually led to confine himself to a liquid diet, takes small mouthfuls, and 
always washes down any solid food with a swallow or two of liquid. The narrower 
the stenosis, the more he is troubled. Einally, even liquids can be taken only 
slowly and in sips. 

It must not be thought that the dysphagia just described is due exclusively to 
the mechanical obstruction of the lumen. Sometimes a patient is almost entirely 
unable to take nourishment, and yet at the autopsy no adequate mechanical 
obstruction is found. The dysphagia must therefore be due to some lesion of the 
muscular coat of the oesophagus. The impaired contractility of the muscular 
coat at the affected spot is always a potent factor in impeding deglutition. 

As soon as the dysphagia has become considerable there is usually regurgita- 
tion of food. At first only a portion of the food comes up, but at last all of it. If 
the tube has become dilated above the stenosis, food may collect for some hours, 
and then be regurgitated, mixed with an abundance of very tenacious mucus. 
We saw a case of this kind in which the patient could fill the sac above the stric- 
ture with quite a large amount of fluid without a drop reaching the stomach. If 
he bent his head sharply forward, the collected fluid would run out again through 
his mouth. It was not until the pouch was completely filled that a small amount 
of liquid would trickle through the stenosis into the stomach. 

Although the dysphagic symptoms above described generally imply oesophag- 
eal stenosis, the diagnosis can not be really established without using a sound. 
Upon introducing this, it is usually easy to detect the obstacle, which may either 
allow the instrument to pass, with a noticeable jerk, or else prevent its further 
progress. By measuring the length of the portion introduced before the stenosis 
is reached we can learn its positioii. On the average, the entire distance from the 
teeth to the cardiac sphincter is in adults sixteen inches (forty centimetres) ; 
from the teeth to the beginning of the oesophagus, six inches (fifteen centime- 
tres) ; and consequently the length of the latter is about ten inches (twenty- 
five centimetres). If we succeed in passing a smaller sound through the stric- 
ture, the feeling as we move it back and forth will give us some idea of the length 
of the stenosis, or will demonstrate the existence of several lying one below the 
other, etc. If the end of the sound can be moved about very freely above the ste- 
nosis, we may conclude that the tube is dilated there. 

Hamburger has employed auscultation of the oesophagus for diagnostic pur- 
poses. If we listen behind, to the left of the upper dorsal vertebrae during deglu- 
tition, we hear a gurgling sound, due to the act of swallowing, extending down 
the tube to the stenosis, but no farther. Then come all sorts of sounds, some of 
them caused by the fluid trickling slowly through the narrow part, and some 
caused by regurgitation. In general, the results obtained, by auscultation are 
rather variable and uncertain. 

Having established the fact of the existence of a stenosis, we have next to de- 
termine its nature, which is our chief guide to prognosis and treatment. In cer- 
tain instances the history of the case gives us the needed information. The diag- 
nosis of cicatricial stricture can hardly be made unless the patient himself tells us 
of being burned or injured by caustic poisons. The previous history is likewise of 
great importance if the stenosis be due to foreign bodies or to syphilis. If no de- 
cisive serological factor can be elicited, we must carefully examine the neck and 
thorax, with regard to the possible existence of a swelling compressing the 
oesophagus. When an aortic aneurism has acted in this way, a rhythmical 



STENOSIS OF THE (ESOPHAGUS 



411 



movement has sometimes been communicated to the free end of a sound intro- 
duced as far as the stenosis. If the physical examination does not reveal a com- 
pressing tumor, and particularly if the stenosis has developed gradually and in an 
elderly person, we are almost compelled to assume that there is cancer of the 
oesophagus. This is, after all, by far the most frequent cause of oesophageal stric- 
ture. If the new growth has ulcerated, a little portion of it may adhere to the 
end of the probe, and, On microscopic examination, render our diagnosis of carci- 
noma certain. 

The prevailing characteristic in stenosis of the oesophagus is inanition, increas- 
ing as the dysphagia increases. The patient gets to be very much emaciated, and 
so feeble that he can not leave his bed. The temperature is subnormal ; for weeks 
it keeps at 95° to 97° (35°-36° C). The pulse grows very small and slow, being 
40 to 60 per minute. The heart-sounds are soft. Respiration is superficial and 
slow; and toward the close of life short pauses occur after expiration, before 
inspiration begins. The stomach and intestines are so empty that the abdomen 
is very concave, while the abdominal walls usually feel tense and resistant. In 
all cases when the nature of the stenosis precludes the possibility of cure or 
improvement, death results from increasing exhaustion, the lamp of life gradu- 
ally flickering out. 

Prognosis and Treatment. — In prognosis the main factor is of course the 
nature of the stenosis. If it is due to foreign bodies or to cicatrices, it may be 
completely cured. In stenosis from other causes it is often possible to produce 
-considerable improvement, at least temporarily. The final result must be con- 
fessed to be usually unfavorable, as we should expect from the nature of the origi- 
nal trouble. 

The treatment is chiefly mechanical. We shall not speak of operations for 
the removal of new growths, etc. What we do refer to is a methodical and grad- 
ual dilatation of the stricture. Its results are sometimes brilliant, particularly in 
cicatricial stenosis. Other varieties, such as the stenosis from cancer, may some- 
times undergo considerable though but temporary improvement with this treat- 
ment. 

The best instrument to employ is the flexible, so-called English, oesophageal 
bougie. It is made in all sizes. If the stenosis is very narrow indeed, we may 
nave to resort to catgut at first. Whalebone bougies, with olive-shaped ivory tips 
of various sizes to screw on the end, are also good, except that, being stiffer, there 
is more danger in using them. For introduction of the bougie, the patient should 
he seated, with the head slightly extended backward. The first two fingers of the 
left hand are introduced into the throat and guide the instrument, previously 
well oiled, over the back of the tongue and the epiglottis into the oesophagus. Of 
course, no violence must be used. Otherwise a perforation might occur if there 
were a soft, broken-down cancer, or an aortic aneurism. However, such a mis- 
fortune is very exceptional. 

The use of the bougie is almost invariably beneficial if the stricture can be 
passed. The patient generally finds that he can swallow easier than before, and 
will himself request a repetition of the performance. If the patient is an intelli- 
gent person, it is advisable to have him introduce the bougie himself. Patients 
often acquire even greater skill with it than the physician has. The bougie 
should be passed regularly once a day, or, at most, twice daily; and in favorable 
•cases we shall be able gradually to increase the size. If so, the symptoms speedily 
abate, and, with the increased ingestion of food, the patient gains flesh very fast. 

If the stenosis is extreme, and, although it admits the bougie, does not allow 
of sufficient nourishment, we must pass a tube into the stomach through which 
to introduce liquid food. Milk is the best food to choose. Raw eggs, sugar, wine, 
etc., may be mixed with it. The various infant's foods and Hartenstein's " legu- 



412 



DISEASES OE THE DIGESTIVE ORGANS 



minose " are also excellent. Their consistence is favorable for the purpose, and 
they supply a considerable amount of nourishment in a small bulk. Until re- 
cently the sounds and dilators employed in stenosis of the oesophagus have been 
usually introduced by the mouth, but of late the practice has been constantly 
growing of treating stenosis through an artificial opening in the oesophagus. 
Mechanical dilatation can thus be accomplished with much greater rapidity and 
completeness. In the surgical wards here in Erlangen admirable results have 
been obtained in this manner in cicatricial stenosis ; whereas in carcinoma of the 
oesophagus the improvement is of course merely temporary, although the symp- 
toms are greatly alleviated. Further particulars with regard to oesophagotomy 
are to be sought in text-books on surgery, where a description of some other modes 
of treatment of oesophageal stenosis will be found, including the insertion of 
self -retaining canulse, and the creation of an artificial gastric fistula. 

We desire to append a few remarks as to the nourishment of patients by ene- 
mata, to which we are particularly apt to have recourse in cases of oesophageal 
disease. 

Brilliant results are never to be expected from rectal feeding. It is indeed 
probable that life may be by this means somewhat prolonged, but not indefinitely. 
The moral effect, however, is very valuable, when the patient could otherwise re- 
ceive no nourishment whatever. The sufferer feels that something is being done 
to avert absolute starvation. 

The simplest materials for the nutrient enemata are milk, eggs, and wine ; to 
which we may add pepsine and pancreatine in the hope of promoting absorption. 
Leube's pancreatic meat emulsion is still better, although more troublesome in its 
preparation. Leube's directions are as follows: About five ounces (grammes 
150) of meat, cut very thin and then minced finely, and about two ounces 
(grammes 50) of minced pancreas (from the calf) free from fat, are to be stirred 
with about three ounces (grammes 100) of lukewarm water until the mixture has 
the consistence of gruel. Before it is injected, the rectum should be cleansed by 
an enema of plain water. One such enema is to be given daily. Also, when ene- 
mata of milk and eggs are given, the rectum must invariably be first rinsed out 
with plain water. Too large an amount ought not to be given at one time, say 
about two ounces (grammes 50), and the fluid must be raised to about the tem- 
perature of the body. [The limit in quantity set by the author is smaller than 
many patients can retain. If the fluid is injected gently and slowly, four to 
eight ounces may be administered every six hours, and cases are on record of 
patients retaining even sixteen ounces. The rectum seems capable of a certain 
amount of training in this regard, so that the amount given may eventually be 
greater than at first. Unusual irritability may be diminished by adding to the 
enema about five minims of laudanum. — V.] 



CHAPTER IV 
CANCER OF THE (ESOPHAGUS 

.ZEtiology and Pathology. — Cancer is the most important and most frequent 
affection of the oesophagus. We have already mentioned in the preceding chap- 
ter that often stenosis is the result of carcinoma in the oesophageal walls. 

Little is known about the aetiology. It has been often maintained that me- 
chanical, chemical, or thermic irritation of the mucous membrane may result 
in the development of cancer; but this is not certain. It receives some support 



CANCER OF THE (ESOPHAGUS 



413 



from the remarkably frequent occurrence of oesophageal cancer in hard drinkers. 
Now and then the patient himself will allege a perfectly definite cause for his 
disease, such as the lodging of a foreign body, or the swallowing of a very large 
or very hot morsel. Still it is hardly possible in any particular case to decide 
how much value such statements have. It has been maintained that the carci- 
noma sometimes develops in the scar of an old ulcer. This is of interest when we 
recall the similar fact in regard to gastric carcinoma (vide infra). 

(Esophageal cancer follows the general rule in being most frequent in elderly 
people — somewhere between forty and sixty years of age. The male sex is de- 
cidedly more often attacked than the female. 

As we might expect from the histological character of the epithelium lining 
the oesophagus, primary cancer here is invariably composed of pavement cells. 
The new growth may be either hard, firm, and fibrous, or it may be soft, succulent, 
and but scantily supplied with connective tissue. The first variety corresponds to 
the " scirrhus " of older writers, and the second to " medullary " cancer. Usually 
the new formation encircles the entire tube like a ring, extending three to ten 
centimetres longitudinally. Exceptionally a still larger portion of the oesophagus 
is involved, sometimes almost all the mucous membrane. The tumor is usually 
seated in the lower and middle thirds of the oesophagus, being much rarer above. 

Symptoms and Complications. — In the great majority of cases the symptoms 
are those of a gradually increasing stenosis, with its results. We may therefore 
refer to the preceding chapter for most of the particulars. There are, however, 
exceptional cases in which the carcinoma is flat and entails no dysphagia, or so 
little that oesophageal trouble may not be suspected. We have repeatedly seen 
cases of extensive secondary hepatic cancer, or of pulmonary gangrene (vide 
infra), in which the real primary disease was a flat cancer of the oesophagus, 
which gave no clinical signs of its existence, and was therefore not diagnos- 
ticated. 

It is characteristic of the stenotic symptoms produced by oesophageal cancer 
that sometimes a considerable and apparently spontaneous amelioration occurs. 
This is because of an ulceration of the new growth. It crumbles away, as the 
result of superficial disintegration. The tumor is transformed into an ulcer, and 
one can easily understand how this may occasion a temporary improvement in 
deglutition. 

Important clinical symptoms may result from conditions secondary to the new 
growth. The cancer may extend to neighboring organs. Not infrequently the 
cardiac extremity of the stomach is thus involved. Sometimes such a tumor may 
be felt in the epigastrium ; but in most cases there is nothing to indicate that the 
stomach is attacked. 

The neighboring parts of the trachea or bronchi are sometimes affected, and 
important symptoms result from such a complication. If perforation occurs, an 
almost certain result is the inhalation of food or of decaying bits of the tumor, 
with consequent pulmonary gangrene, and, as a rule, speedy death. The disease 
has also been observed to attack the pleura, and end in perforation. The same 
is true of the pericardium and the aorta. A few instances are known in which the 
vertebras have been involved, the spinal cord compressed, and paraplegia thus in- 
duced. We have ourselves seen one such case. 

Quite frequently the recurrent nerve is affected, and a paralysis of the vocal 
cords is produced, which can be detected by the laryngoscope. This nerve lies 
so close to the oesophagus that it is peculiarly exposed to injury from the new 
growth itself, or from any inflammatory process which may be set up around it. 

Metastatic cancer in distant organs is not infrequent, and may give rise to 
important symptoms. It attacks most frequently the liver. The lungs, kidneys, 
pancreas, bones, and brain are also liable to it. 



414 



DISEASES OE THE DIGESTIVE ORGAXS 



Pulmonary gangrene must be mentioned as a relatively frequent complication^ 
and one which has serious consequences. We have already stated that it may 
result from perforation. A still more frequent cause is the inspiration of decay- 
ing masses vomited or regurgitated by the patient. 

Clinical History, Termination. Prognosis, and Treatment. — The disease is 
incurable. Operative removal has never been successful. The entire" duration of 
the disease seldom exceeds a year, or a year and a half. At the end of this period 
the patient dies either from lack of nourishment or as a result of some one of the 
complications above enumerated. Treatment is purely symptomatic. Temporary 
improvement may be obtained by mechanical treatment of the stenosis. The par- 
ticulars about this may be found in the preceding chapter. 



CHAPTER V 
RUPTURE OF THE (ESOPHAGUS 

Medical literature records a small number of cases which prove that the sud- 
den rupture of the oesophagus in persons previously perfectly well is possible, 
although of course very rare. The first and most famous instance was described 
by Boerhaave in 1724. 

The symptoms, according to the observations thus far reported, usually com- 
mence with sudden nausea and vomiting, during or shortly after a hearty meal. 
There is simultaneously an extreme, general collapse. There is pallor of the face 
and extremities, cold perspiration, and an extremely feeble pulse. Sometimes the 
patient feels a sudden darting pain in the chest. Almost invariably an extensive 
emphysema overspreads the neck and thorax. Death results in a few hours, or 
at latest in a few days. 

The autopsy reveals a tear in the oesophagus, invariably situated in its lower 
half. It may be five centimetres long, and it is almost always longitudinal. Food 
has usually escaped into the surrounding tissues, in which case a secondary puru- 
lent inflammation exists, if death was not immediate. 

Zenker has attempted to explain this remarkable phenomenon by a supposition 
which is really very plausible, namely, that oesophagomalacia always precedes 
these so-called spontaneous ruptures. The cause of this softening of the oesophag- 
eal walls is probably the action of gastric juice escaping into the tube and attack- 
ing a surface which, through some temporary disturbance in the circulation, has- 
lost its normal powers of resistance. 



CHAPTER VI 
NEUROSES OE THE OESOPHAGUS 

1. Spasm of the (Esophagus. — In rare instances oesophageal disturbances are 
observed, which appear to result from spasmodic contraction of its muscular coat. 
Nervous and hysterical subjects are particularly apt to present temporarily the 
symptoms of extreme stenosis, for which there can be no anatomical basis. Such 
cases are termed " spastic stenosis " of the oesophagus, or " oesophagismus." It is, 
of course, possible that there may exceptionally be some real lesion at the founda- 



EXAMINATION OF THE GASTRIC CONTENTS 415 



tion of the trouble, and that the spasm is the reflex result of an ulcer or inflamma- 
tion affecting the oesophagus. It is even affirmed that the reflex influence may 
sometimes originate in distant organs, such as the uterus; but the exact nature 
of these reflex spasms is at present exceedingly obscure. The dysphagia is usually 
attended by a painful sense of constriction in the throat and chest. The bougie 
comes upon an obstruction, which usually soon yields. This circumstance, that 
when the spasm relaxes it is possible to introduce the bougie without any diffi- 
culty, confirms the diagnosis. Other important factors are, the character of the 
symptoms as a whole and the other attendant nervous and hysterical disturbances. 
Some authors also explain the " globus hystericus " — that feeling as if a lump 
were passing up or down in the throat and chest — as a spasm of the oesophagus. 

2. Paralysis of the (Esophagus. — Of this subject we have little accurate 
knowledge. It is not improbable that an extensive bulbar paralysis, affecting the 
muscles of the pharynx and larynx, may sometimes involve the oesophagus; al- 
though such a disturbance hardly ever gives rise to prominent symptoms in this 
disease. Ziemssen asserts that sometimes the oesophagus seems to participate in 
post-diphtheritic paralysis, when extensive. 



SECTION IV 

Diseases of the Stomach 

CHAPTER I 

BRIEF PRELIMINARY REMARKS ON THE EXAMINATION OF THE 

GASTRIC CONTENTS* 

When a disease of the stomach exists, we have the subjective symptoms to 
consider, such as anorexia, eructations, vomiting, and gastric pain, together 
with the external physical signs obtained by inspection and palpation, such as 
tenderness, distention, peristaltic motion, swelling, and tumors ; and we also have 
for our guidance an examination of the stomach and the stomach contents. The 
procedure was introduced by Leube, followed by Ewalcl, Boas, Riegel, and many 
others. It is carried out by means of the stomach-tube, and is now universally 
employed among physicians, for in fact its results are so important and decisive 
with regard to diagnosis, that an examination of this sort is at the present day 
indispensable in any severe case of persistent gastric trouble. The inconvenience 
of the investigation for the patient is comparatively slight, especially now that 
a soft and yielding tube (Nelaton) is employed. This should have free aper- 
tures at its lower extremity, and it is introduced into the stomach in the follow- 
ing manner : The tube is moistened with water, put into the patient's mouth, 
and passed backward over the base of the tongue, and he is told to swallow it, as 
it were; the physician at the same time aids by pushing the tube, but he does 
not introduce his finger into the patient's mouth. In this way it is almost always 
easy to introduce the instrument into the oesophagus, and so into the stomach. 
Most patients, if the tube has to be employed frequently, soon learn to guide it 

* Complete particulars with regard to the methods of examining the gastric contents can not be given 
here, but they may be found in the following works: Ewald, Klinik der Verdauungskrankheiten ; 
Boas, Diagnostik und Therapie der Magenkrankheiten ; Leo, Diagnostik der Krankheiten der Ver- 
dauungsorgane : Kiegel. Erkrankungen des Magens, etc. 



416 



DISEASES OE THE DIGESTIVE OKGAtfS 



themselves. Formerly a wire was placed inside the tube so as to stiffen it for 
introduction, but this is ordinarily useless, if not a hindrance. 

If the tube has been introduced into the stomach, and we wish to obtain a 
portion of the contents of that organ for examination, it can, in most cases, be 
got by simple " expression." If the patient makes his abdominal muscles tense 
("presses"), or if he makes a few slight efforts to vomit, there is usually a suffi- 
cient amount of the gastric contents expressed through the tube into a beaker 
held to receive it. This portion of the gastric contents is filtered, and the filtrate 




Fig. 45.— Method of washing out the stomach. (Erlangen Medical Clinique.) 



subjected to examination. If we wish to empty the stomach completely (" rinse 
it out"), the upper end of the inserted tube is connected by means of a short 
piece of glass tubing, with a longer rubber tube connected at its other end with 
a large glass funnel, to hold about a litre of water. If warm water is poured 
into the funnel and this is alternately raised and lowered, we shall eventually 
entirely empty the stomach (see Fig. 45). It is advisable to insert a short bit of 
glass tubing in the rubber tube (fenestra), so as to observe whether the fluid 
runs well in either direction. Kussmaul originally employed a " stomach-pump " 



7 



EXAMINATION OF THE GASTKIC CONTENTS 



417 



for rinsing out the stomach, but this has been quite universally abandoned for the 
simple siphon apparatus suggested by Hegar. 

By use of the stomach-tube we are readily enabled to settle the following 
important points: First, the chemical constituents of the gastric juice, or con- 
tents ; second, the motor activity of the stomach ; and third, the size and position 
of the organ. 

1. Constituents of the Gastric Juice, particularly Free Hydrochloric Acid, 
Pepsine, and Lactic Acid. — In a healthy person the stomach is almost completely 
empty in the morning before breakfast — i. e., some ten or twelve hours after the 
preceding evening meal. If we introduce the stomach-tube we obtain, therefore, 
by expression either nothing at all or a very small amount of watery mucus, of 
neutral reaction. If this fluid contains a little hydrochloric acid, this is not neces- 
sarily anything abnormal, but if there is a large amount of acid fluid in the fast- 
ing state disease is indicated. The healthy stomach contains in the morning few 
vestiges of the food swallowed the day before. If we pour in some water, this is 
returned almost perfectly clear. If now the subject of examination eats a so- 
called test breakfast, consisting of an ordinary roll and a large cup of weak tea, 
at once the stomach begins to secrete its peculiar juice. If the stomach- tube is 
introduced an hour after a test breakfast has been taken, and a sufficient amount 
of the stomach contents is expressed and filtered, we shall obtain a fluid of acid 
reaction, and, under normal conditions, invariably containing free hydrochloric 
acid uncombined with albumen. It is the comparatively small amount of the 
test breakfast which makes it most suitable for the determination of the impor- 
tant question, whether the stomach secretes hydrochloric acid in a satisfactory 
manner. If we introduce into the stomach a larger amount of food (" test meal," 
vide infra) there will, indeed, in most cases, be free hydrochloric acid after one 
or two hours, but the amount of albuminous material present is so great that even 
under normal circumstances all the hydrochloric acid secreted is taken up by the 
albuminous substances, and consequently there is no hydrochloric acid to be 
discovered by our ordinary chemical tests. If, on the other hand, we do not 
find any free hydrochloric acid in the gastric contents, or, at any rate, merely 
doubtful traces of it, an hour after the test breakfast, this condition is termed 
anacidity, or subacidity, and it must be regarded as abnormal, particularly if re- 
peated examination leads to the same result. The term acidity in this connection 
relates to hydrochloric acid. Even if this is absent it is perfectly possible that 
there may be other organic acids in the gastric contents. 

The test for the presence of free hydrochloric acid now almost universally 
employed is one introduced by Giinzburg, who recommended a solution of 2 
parts of phloroglucine and 1 part of vanilline in 30 parts of absolute alcohol. If 
we mix a few drops of this phloroglucine-vanilline in a saucer with a few drops 
of the filtered gastric contents to be examined, and then heat the mixture cau- 
tiously so as to avoid charring, there will immediately develop on the edge of the 
fluid a beautiful red border, if free hydrochloric acid is present. Another good 
reagent for free hydrochloric acid is methyl violet. This requires an accurate 
comparison of colors, so that the weak watery solution of methyl violet is divided 
into two portions in test-tubes. If now we add to one test-tube some of the 
gastric contents containing free hydrochloric acid, the violet is immediately 
changed into a distinct blue color, which is evidently different from the original 
fluid contained in the other test-tube. For a third test what is called Congo 
paper is employed — i. e., strips of paper colored with an aqueous solution of 
Congo red. If the stomach contents contain free hydrochloric acid, the red 
color of the paper is changed to a distinct blue. There is a certain inaccuracy 
in this last-mentioned test with Congo red, as the red is colored blue by concen- 
trated solutions of other acids, particularly lactic acid; but, as a matter of fact, 
27 



418 



DISEASES OF THE DIGESTIVE OKGANS 



the other acids are scarcely ever present in the stomach in sufficient amounts to 
invalidate the test; so that in actual practice, if the Congo paper changes to 
a distinct blue, we may almost always infer that free hydrochloric acid is pres- 
ent. Still, it is advisable in every case to carry out the two other tests also, 
which are almost as simple and entirely unambiguous. There is a reagent often 
employed which indicates the presence of free acids in general, including free 
lactic acid. It consists of an alcoholic (or aqueous) solution of " tropseoline 00." 
The yellow color of tropseoline is changed to a beautiful red by even small amounts 
of acid, but still more readily by hydrochloric acid than by the organic acids. 
Blue litmus paper, as is well known, is colored red by free acids as well as by 
acid salts. If the examination of the contents of the stomach an hour after the 
test breakfast shows the presence of free hydrochloric acid, an experienced ob- 
server will often be able to estimate from the degree of the qualitative reaction 
whether he is dealing with a small or considerable amount of hydrochloric acid. 
An accurate quantitative estimation is possible by titration of the stomach con- 
tents with a decinormal soda solution, for which a few drops of phenol-phthaleine 
solution serve as index.* The amount of acid determined by this process is of 
course the sum total of free acids, and not exclusively the free hydrochloric acid. 
Still, provided there is an abundant amount of hydrochloric acid in the gastric 
contents, the results obtained may be ascribed without great error to hydro- 
chloric acid alone; for experience has shown that, when there is a considerable 
amount of hydrochloric acid in the gastric contents, there is scarcely ever any 
considerable amount of organic acids (vide infra). The degree of acidity of the 
gastric fluid is usually expressed in the number of cubic centimetres of soda solu- 
tion which are necessary, as shown by the titration, to neutralize 100 cubic centi- 
metres of the gastric fluid ; for example, if we have required 6 cubic centimetres of 
soda solution to neutralize 10 cubic centimetres of the gastric contents, the acid- 
ity is reckoned at 60. In terms of hydrochloric acid we would have 60 multiplied 
by 3.65, equal to 19 milligrammes of hydrochloric acid — that is, 0.22 per cent. 
The degree of acidity which is found in the gastric contents of healthy persons 
after the test breakfast is usually 55-65; amounts of 70-80 indicate hyper- 
acidity. If the gastric juice contains an abundance or an excess of hydrochloric 
acid, the further question, and often an important one, arises whether there is 
a hypersecretion, or, more correctly, a continuous secretion of gastric juice. As 
we have already mentioned, the normal stomach does not ordinarily secrete except 
when its mucous membrane is affected by food swallowed, or by other stimulating 
influences. The fasting stomach does not, as a rule, contain any hydrochloric 
acid, and when the stomach has passed the food on into the duodenum, its secre- 
tion immediately ceases. In order, then, to determine the existence of hyper- 
secretion or continuous secretion, we must examine the contents of the fasting 
stomach at least six or seven hours after the last meal. If we then find fluid in 
the stomach, with distinct or abundant amounts of hydrochloric acid contained 
in it, we are justified in assuming that there is an abnormal hypersecretion on 
the part of the stomach. ( 

Physiology teaches us that not only hydrochloric acid but pepsine in associa- 
tion with it, is necessary for the peptonizing of albuminoids. The demonstra- 
tion of pepsine in the gastric contents is, therefore, essential to a determination 
of the peptic function of the stomach. Experience has shown, however, that 
pepsine is rarely absent from the gastric juice, and if there is a distinct secretion 
of hydrochloric acid we may almost always assume that pepsine is secreted, with- 
out making any special examination. Even in cases of anacidity pepsine often 
continues to be secreted. Still, there are cases when the direct demonstration 



* We scarcely need to describe this simple process more fully. 



EXAMINATION OF THE GASTKIC CONTENTS 



419 



of the presence or absence of pepsine in the gastric juice is desirable. The 
process is simple. We obtain some gastric contents in the ordinary way after 
a test breakfast, and put into it a square shaving of the white of a hard-boiled 
egg. Normal gastric juice containing hydrochloric acid and pepsine, if kept at 
a temperature of 98.6° (37° C.) in an incubator, will dissolve the flake of albu- 
men completely in from thirty to sixty minutes. If the gastric juice contains no 
hydrochloric acid but only pepsine, the albumen will be dissolved if we add a few 
drops of dilute hydrochloric acid. If, however, pepsine also is absent from the 
gastric juice, the bit of albumen will swell up but will not be actually dissolved, 
.unless we add artificial pepsine. 

Besides hydrochloric acid there are also some organic acids in the gastric 
juice; the most important of these is lactic acid. At present the universal belief 
is that the lactic acid is not a product of the gastric mucous membrane, but the 
result of lactic-acid fermentation of the carbohydrates in the gastric contents, 
except for small amounts which may be directly introduced with the food. If 
we test the gastric contents a short time (fifteen to thirty minutes) after a test 
breakfast, we can often find some lactic acid present, but as yet no hydrochloric 
acid. This corresponds to the amylolytic stage of gastric digestion. Later, when 
the secretion of hydrochloric acid has begun, the lactic-acid fermentation prompt- 
ly ceases, so that under normal conditions, as we have said, we find hydrochloric 
acid distinctly, present an hour after the test breakfast, but usually no lactic acid. 
If we do find lactic acid it is always an indication of an impaired production of 
hydrochloric acid. There is a condition which is especially favorable for the 
formation and collection of large amounts of lactic acid in the stomach. This 
is when the absence of hydrochloric acid is associated with a stagnation of the 
ingesta in the stomach. This combination is especially frequent in the case of 
carcinoma of the pylorus (q. v). Under these conditions the lactic-acid fermenta- 
tion may go on unchecked, and we find an abundance of that acid in the stomach 
at whatever time we make a test. 

The qualitative test for lactic acid is by means of Uffelmann's reagent : by 
adding a drop of ferric-chloride solution to a three- or four-per-cent. solution of 
carbolic acid, we obtain a liquid of a beautiful steel-blue color. Upon adding to a 
portion of this blue fluid, contained in a test-tube, gastric contents in which there 
is lactic acid, the blue color changes to a distinct yellow, or yellowish-green. 
The test should not be regarded as positive unless there is a distinct yellow color. 
We may first agitate the gastric fluid with ether, and then make the test with the 
ether extract, as ether takes up the lactic acid. The quantitative estimation of 
lactic acid is tedious, and not very important in practice. 

The fatty acids and acetic acid are not found in the gastric contents unless 
there is marked fermentation, and their presence therefore indicates a stagna- 
tion of the gastric contents (vide infra), and the absence of hydrochloric acid, 
which acts as an antiseptic. In practice we form an opinion as to the presence 
of these acids by the sense of smell, since their demonstration by direct chemical 
means is far from simple. 

2. Determination of the Motor Activity of the Stomach. — The employment 
of the stomach-tube also enables us to form with ease a satisfactory estimate of 
the motor function of the stomach, and this is an extremely important matter. 
As physiology teaches us, the pylorus remains firmly closed during the first part 
of gastric digestion. It does not open until the food is sufficiently prepared, 
and then the chyme is discharged by successive jets into the duodenum. For 
practical purposes it is sufficient to know that the examination of healthy per- 
sons has shown the stomach to be completely empty again about two hours after 
the ingestion of a small amount of food — e. g., after the test breakfast (vide 
supra). If, then, we rinse out the stomach two hours after a test breakfast we 



420 



DISEASES OE THE DIGESTIVE ORGANS 



ought not, under ordinary circumstances, to find any large amount of bread in 
the wash water. But it is a comparatively easy task for the stomach to make 
away with the test breakfast ; so it is more suitable, if we desire to test its motor 
powers, to administer what is called a test meal, consisting of a plate of broth, 
150 grammes (5 ounces) of underdone broiled steak (minced), 50 grammes (2 
ounces) of potato puree, and a roll. A meal of this sort disappears from the stom- 
ach often in three or four hours, but at the latest, under normal conditions, in 
seven hours. If we wash out the stomach seven hours after a test meal and still 
find any considerable amount of food, it is sure proof of an unsatisfactory dis- 
charge of the stomach contents, whether as a result of impaired motor power or, 
as is most frequently the case, of a mechanical stenosis of the pylorus. If we 
really wish to know how long portions may be retained in the stomach, we may 
add to the meal a few cranberries or green-colored beans, and the like. Such 
easily recognizable things may sometimes be found again in rinsing out the stom- 
ach several days after their ingestion. 

It is of course understood that the gastric contents which we obtain a shorter 
or longer time after a test meal are examined with regard to the presence of 
hydrochloric and lactic acids, and also with regard to other characteristics, such 
as the presence of mucus and blood, and microscopic appearances. Many impor- 
tant details in regard to these matters will be brought up in later chapters. 

In this connection, however, we may make brief mention of another method 
originated by Ewald, with this same object of determining the motor efficiency of 
the stomach. The patient is given, early in the morning, a gelatine capsule 
containing fifteen grains (gramme 1) of salol. Salol is not broken up until it 
reaches the intestine, when it separates into carbolic and salicylic acids. The 
salicylic acid is then immediately excreted in the urine, and readily detected 
by chloride of iron. If the stomach does not empty itself in a normal manner, 
the salicylic reaction is often to be detected in the urine even after twenty- 
four or thirty hours, at which time it would have vanished under normal condi- 
tions. This test has not been adopted very generally in practice, because it is 
uncertain. 

3. Estimation of the Size and Position of the Stomach. — The position and 
size of the stomach are liable to great variations, and with regard to pathological 
conditions it is important to determine these points about the organ. An expe- 
rienced eye may sometimes recognize the position of the stomach by mere observa- 
tion of the abdomen, but often this is negative or misleading. By percussion we 
may distinguish the limits of the deep tympanitic resonance of the stomach from 
the usually higher tympanitic resonance of the surrounding intestines ; or we may 
mark the lower limit of dullness when the organ is full, so that we can some- 
times form a tolerably certain opinion as to the lower border of the stomach. 
In general, these results are deceptive and uncertain. 

With the aid of the stomach-tube the matter is very simple. It is accom- 
plished by blowing up the stomach with air, in the manner first elaborated by 
Buneberg. This is done by means of the ordinary double rubber bulb [such as is 
employed with the Paquelin cautery; or with a simple Davidson syringe]. The 
method used by us in our wards almost every day is as follows: The patient is 
either fasting or has had his stomach thoroughly rinsed out, and lies as nearly 
horizontal as possible upon his back. The stomach-tube, being introduced, is con- 
nected with the bulb at its upper end, and air is pumped in. As the pylorus is 
almost always firmly closed, the contours of the stomach become visible very 
shortly. We should then not only mark the position of the greater curvature but 
also that of the lesser curvature, if visible. If the stomach is normal in position 
and size, the protuberance occupies the epigastrium above the navel. If the stom- 
ach is dilated, the greater curvature reaches below the navel; while if the stomach 



EXAMINATION OF THE GASTKIC CONTENTS 



421 



as a whole is displaced downward {vide infra, gastroptosis), the smaller curvature 
also falls to the neighborhood of the navel or below it. 

As soon as we disconnect the bulb the air escapes, and the distended stomach 
collapses. We can, if a certain degree of caution is used, repeat the procedure 
more than once, so as to make sure of our results. Of course, inflation should 
be interrupted immediately if the distention of the stomach becomes painful; 
and we should abstain from the procedure altogether whenever there is suspicion 
of an ulcer, because the artificial distention of the stomach in this case might do 
harm. In some cases, direct inflation does not render the contours of the stomach 
distinctly prominent, probably because of insufficiency of the pylorus. In such 
cases, and in such only, we should employ a rubber bag (condom) fastened on 
the lower end of the tube, having previously tested its distensibility. When this 
is introduced into the empty stomach and blown up, we can usually discern it 
through the abdominal walls and determine the position, but of course not the 
size, of the stomach. For ordinary eases the first-described method is not only 
simpler but more satisfactory, and, so far as the patient is concerned, less dis- 
agreeable. If the abdominal walls are thick with fat the method fails, but such 
a condition is very rare when there is severe gastric disease. 

The simple method just described seems to us to have rendered entirely super- 
fluous most of the other more or less complicated procedures for the determina- 
tion of the size and position of the stomach, especially as no better results are 
obtained by them. This last statement applies especially to electric transillumi- 
nation of the stomach and anterior abdominal walls by means of an incandescent 
light introduced with a tube. A practiced specialist can obtain valuable results 
in this way, but it is often very misleading". 

In ordinary practice where the introduction of the stomach-tube is not always 
practicable, the old method recommended by Frerich may be employed. For car- 
rying this out it is best to have the patient fasting-, and in a horizontal position. 
Seventy-five to one hundred and fifty grains (grammes 5-10) of tartaric acid are 
given, and immediately after an equal amount of bicarbonate of soda, each drug- 
being dissolved in half a glass of water. At once there is an abundant production 
of carbonic dioxide. The stomach is blown up and its outlines become sometimes 
very distinct, both for observation and for percussion. The great advantage of 
the previously-described method of pumping in air consists, however, in the fact 
that we have the degree of distention under far better control, and that we can 
repeat the process several times in succession. 

To sum up briefly all that has been said, a careful examination of the stom- 
ach should proceed in the following manner: First, rinsing out of the empty 
stomach early in the morning, to determine whether there may be stagnation (as 
indicated by lactic acid) or hypersecretion. We should also notice whether 
there is any collection of mucus in the stomach when fasting ; and we determine 
the position and size of the stomach by inflation. Secondly, the stomach being- 
empty we administer a test breakfast ; an hour later we examine the contents for 
hydrochloric or lactic acid. Thirdly, at noon we give a test meal, and seven 
hours later wash out the stomach, to determine its motor efficiency. If there 
is stagnation of the gastric contents, we test again for hydrochloric and lactic 
acids. 

4. Testing the Absorptive Powers of the Stomach. — Brief mention should be 
made of Penzoldt's method of determining the absorptive powers of the stomach. 
A gelatine capsule filled with iodide of potassium, if swallowed by a healthy person 
fasting, will give rise at the end of ten or fifteen minutes to a reaction for iodine 
in the saliva and in the urine (by adding sulphuric acid and shaking with sul- 
phide of carbon). In severe diseases of the stomach the time required is often 
much longer. In practice, however, the method has not been highly approved, 



422 DISEASES OF THE DIGESTIVE ORGANS 

because we can not draw any certain conclusions from it as to the absorption of 
food — a matter about which, in general, we possess little knowledge. 

5. Demonstration of Blood in the Gastric Contents— Any admixture of blood 
with the contents of the stomach is of great importance in the diagnosis of cer- 
tain gastric diseases, particularly ulcer and carcinoma. If there is fresh blood 
mixed with the vomitus or with the gastric contents obtained by washing out 
the stomach, it is often directly recognizable from its characteristic appearance, 
but if the blood is already decomposed or intimately mixed with the food, or 
present in very small amounts, we need special methods for its certain recogni- 
tion. Microscopic examination alone is insufficient, for the red corpuscles are 
soon destroyed in the stomach. The method of spectrum analysis requires a 
special spectroscope. We search for the characteristic bands of haematine in an 
ethereal extract, made by shaking up a portion of the gastric contents, to which a 
few drops of glacial-acetic acid have been added, with ether. For medical prac- 
tice the most useful and simple method is Van Deen's test, with fresh tincture 
of guaiac and turpentine. A mixture of equal portions of these two liquids is 
poured into a test-tube upon a portion of the gastric contents. If blood is pres- 
ent there at once appears an intense blue color, but certain other matters con- 
tained in the food may cause this same color reaction, so that it is more satis- 
factory to decompose the gastric contents with a few drops of glacial-acetic acid, 
then extract with ether and perform the guaiac-turpentine test with the ether 
extract. This test is especially distinct if there are organic acids present, as in 
case of carcinoma, in which disease the stomach contains blood in association 
with lactic acid but no hydrochloric acid. On the other 
^ ^ ^ hand, in our experience, the test is often uncertain in the 

^ ^Jb^ case °^ u l cer > because the presence of hydrochloric acid is a 
i ^ < ^ hindrance. Another common method is to see if we can 
f ^ ^ produce Teichmann's hsemine crystals from the gastric 

^ ^ ^ ^ contents. The test is not always successful, but if success- 
0^ j==? ^ ^ ful it indicates the presence of blood. We put a small por- 
jL^ yf* tion of the suspected gastric contents upon an object-glass 

M g ^ with a trace of common salt, and a few drops of glacial- 

™ acetic acid. If we now evaporate slowly to dryness there 

Fig. 46.— Haemine crystals, are formed small, brown, rhombic hsemine crystals (see 
Fig. 46), which can be seen by the microscope. Of course, 
whenever we examine the contents of the stomach for blood, we should bear in 
mind that, if found, the blood may be due to the ingestion of underdone meat, 
preparations of haemoglobin, or similar substances. Finally, we scarcely need to 
repeat that in all important cases one ought not to be satisfied with a single ex- 
amination of the stomach, but he should make certain of his results by repeated 
tests. 



CHAPTEK II 

ACUTE GASTRIC CATARRH 

(Acute Gastritis) 

etiology and Pathological Anatomy. — The mucous membrane of the stom- 
ach not being open to direct examination," as is that of the mouth and throat, 
and acute gastric disease being seldom fatal so as to render an autopsy possible. 



* The examination of the mucous membrane of the stomach by means of the stomach mirror and 
the electric light involves such technical difficulties that it has not as yet been adopted in practice. 



ACUTE GASTRIC CATARRH 



423 



the existence of acute gastritis is mainly a matter of inference from our observa- 
tions of other mucous membranes. When some harmful agency acts in a direct 
manner upon the mucous membrane of the stomach, we shall usually be right in 
supposing that there is a greater or less degree of genuine inflammation of the 
lining of the stomach, unless the organ in a simply functional way at once rids 
itself of the irritant — for example, by vomiting when the stomach has been 
" overloaded." If some noxious material acts long and continuously upon the 
mucous membrane, there will be abnormal changes not only in the blood-vessels 
and the interstitial tissue, but also in the cellular elements of the mucous mem- 
brane and,, its glands. As yet, we know little about the minute degenerative 
changes in the specific secreting cells. The microscopic inflammatory lesions, 
which we may with great certainty assume to be present, are hyperemia and 
swelling of the mucous membrane, perhaps associated with an increase in the 
secretion of mucus, and with small haemorrhages here and there. If the irritant 
is insignificant the lesions will be mild and superficial (mild catarrhal gastritis). 
If the noxious agent is more powerful (for example, corrosive poison) it will 
give rise to a deeper parenchymatous inflammation, with peeling off of the 
mucous membrane and similar effects (severe toxic gastritis). 

The mild catarrhal forms of gastritis are caused by simple chemical and me- 
chanical influences, and perhaps by thermic irritation. They are most often the 
result of errors in diet, such as the ingestion of too large an amount of food, or 
of food that is difficult to digest, unsuitable, highly spiced, or very acid. In the 
same class belong the acute indigestion following excess in alcohol, and the fre- 
quent derangement of the stomach from taking medicines; and also cases due 
to the accidental or willful ingestion of all sorts of injurious and poisonous sub- 
stances. The severe cases of toxic gastritis are most often caused by the action 
of concentrated mineral acids and alkalies. In this class comes poisoning from 
sulphuric acid, nitric acid, hydrochloric acid, caustic potash, and caustic soda. 

A special importance attaches to the ingestion of decaying substances. The 
incautious use of tainted meat or fish may be followed by relatively severe forms 
of acute gastric catarrh. The products of decomposition act as chemical irri- 
tants upon the mucous membrane; and the ferments and putrefactive agents 
likewise continue in activity after reaching the stomach, and thus contribute to 
produce the inflammation. The reason that this sort of gastric catarrh is not 
much more frequent than it is, is undoubtedly the presence of hydrochloric acid 
as a constituent of the gastric juice, because it has an antiseptic action. 

It is universally assumed that a chill of the outer surface of the body may 
excite gastric catarrh, but there seems to be actual proof of this in but few cases. 
On the other hand, there can be no doubt that many cases of acute gastric ca- 
tarrh, of apparently primary origin, are referable to infection. Infectious 
catarrh of the stomach may occur at times, particularly in summer, with especial 
frequency. As to the precise nature of the pathogenic germ we do not as yet 
possess any certain knowledge. 

The predisposition of certain individuals to gastric catarrh differs greatly. 
Some persons always have a " weak " stomach, and the disease is prone to attack 
feeble children, anaemic persons, fever patients, and convalescents from severe 
diseases, as well as chronic invalids who are ill-nourished. Enfeebled persons of 
this sort sometimes fall sick when vigorous and healthy individuals would entirely 
escape. In many of these cases of unusual predisposition to gastric disease, we 
may surmise that the secretion of hydrochloric acid is scanty, and that there 
may be a diminution in the motor power of the stomach. Each of these factors 
would of course render ingested irritants more harmful. 

Symptoms. — The most constant subjective symptom is anorexia. In many 
cases the very thought of food excites disgust. What the patient does eat tastes 



424 



DISEASES OF THE DIGESTIVE OKGANS 



flat, and lie is therefore very eager for piquant dishes, highly spiced or sour. 
Thirst is often present, and a feeling of dryness in the mouth. 

The subjective gastric sensations are seldom those of marked pain; but 
sometimes there are attacks of pain which are in all probability due to cramplike 
contractions of the muscular coat. The usual complaint is of constant pressure 
and fullness. Sometimes the patient is conscious of the peristaltic movements 
of the stomach. He has " rumbling " of the bowels. 

There is nausea, and often vomiting. In severe cases everything swallowed 
is at once rejected. The vomitus consists for the most part of undigested food 
(often ill-smelling), with which mucus, and sometimes bile, is mingled. Eructa- 
tions of gas or liquid are frequent. 

Physical external examination reveals little. The epigastrium may be some- 
what prominent as a whole, and may be tender on pressure. The tongue is almost 
always thickly coated and dry. The breath is usually disagreeable, and there is 
a persistent flat or bitter taste in the mouth. In ordinary cases of acute gastritis 
examination of the gastric contents is hardly necessary, but in severe cases we 
find a marked diminution in, or entire absence of, the hydrochloric-acid reaction, 
and distinct delay in the motor activity of the stomach. Sometimes lactic acid 
and the fatty acids are present in large amounts. 

In severe cases there is always considerable constitutional disturbance. The 
patient feels languid, and disinclined for any exertion; the pulse is moderately 
rapid, although it may exceptionally be slower than normal; the urine is usually 
somewhat concentrated, often it gives a marked indican reaction. There may 
be no fever, but not infrequently there is a moderate elevation of temperature 
with sensations of chilliness or heat. In rare cases we may observe an approach 
to the typhoid condition, with such nervous symptoms as headache, vertigo, and 
dullness. These cases were formerly termed " gastric fever," and they are prob- 
ably most of them infectious, but yet the constitutional symptoms are probably 
only in part referable to coincident constitutional infection. It is more probable 
that toxic influences are exerted by the abnormal products of the fermenta- 
tion which takes place in the stomach. Eor example, Senator mentions sulphur- 
etted hydrogen as thus generated ; and Litten has described several cases in which 
at first there were such dyspeptic symptoms as nausea, vomiting, flatulence, and a 
coated tongue, but which soon gave evidence, by restlessness, headache, great mus- 
cular weakness, and a gradual lapse into somnolence, of rather severe nervous dis- 
turbance in addition. The breath had a marked "fruity" odor; and, on adding 
chloride of iron to the urine, a strong reddish color was developed, as in the so- 
called acetone-reaction; so that it seems probable that an auto-intoxication had 
occurred, somewhat resembling diabetic coma. 

Chief among complications are the intestinal symptoms, which are frequently 
coincident with the gastric disorder. Constipation is the rule. There may be 
diarrhoea. The gastric catarrh may by extension involve the duodenum, and give 
rise to jaundice. Sometimes herpes appears upon the skin. This fact argues for 
the infectious nature of many cases of gastric catarrh. 

It is evident from what has been said that acute gastric catarrh is by no 
means uniform in its aetiology, and the general course of the disease is also sub- 
ject to great variations. Sometimes there are mild dyspeptic symptoms which 
vanish in the brief time of one or two days, while in other cases we have a rather 
severe disease associated with considerable constitutional disturbance, and last- 
ing three to ten days. There is also great variation in the intensity of the vari- 
ous symptoms, particularly the vomiting. The progress of the case may be irreg- 
ular and there may be relapses, but still, the prognosis of primary acute gastritis 
is entirely favorable. The diagnosis is usually easy, although we should never 
omit to make an unprejudiced and careful examination into the general condition. 



CHRONIC GASTEITIS 



425 



If there is fever we should bear in mind the possibility of a mild typhoid (see 
typhoid fever). 

Treatment. — If, at the beginning* of the disease, there is reason to suppose 
that the stomach is loaded with undigested food, an emetic is indicated. If it is 
desired to avoid the irritative action of an emetic upon the gastric mucous mem- 
brane, a subcutaneous injection of one sixth of a grain (gramme 0.01) of apo- 
morphine may be given. Still more efficient, although disagreeable for the pa- 
tient, is a washing out of the stomach by means of the stomach-tube, particularly 
in severe cases of toxic or infectious origin; but of course, when the gastric walls 
may have been weakened by corrosive poisons, the stomach-tube is contraindi- 
cated. 

In most cases, however, emetics and lavage may be dispensed with. The 
treatment in such cases consists mainly in a strict regulation of the diet, allow- 
ing for a time nothing whatever, and then such food as milk porridge, iced milk, 
and toast. Of internal remedies, ten to fifteen drops of dilute hydrochloric acid 
in half a wine-glass of water sometimes seems beneficial; while in other cases, 
in which there are sour eructations and vomiting, alkalies are to be given. We 
may order as much bicarbonate of soda or as much Carlsbad salts as will rest on 
the point of a pen-knife, or Ems water. The so-called stomachics and bitters are 
also often prescribed, for example, compound tincture of gentian or tincture of 
rhubarb. Another favorite remedy is resorcine, of which four grains dissolved in 
some aromatic water may be given every two hours. If the vomiting is obstinate, 
relief may be got from bits of ice or sips of cold Seltzer water. In severer cases 
we must resort to narcotics, such as opium, cocaine, and chloroform, administered 
internally. 

If there is decided constipation, an enema must be employed, or such laxatives 
as calomel, Epsom salts, or rhubarb. 



CHAPTER III 

CHRONIC GASTRITIS— CHRONIC CATARRH OF THE STOMACH 

etiology. — The same causes which excite acute gastric catarrh, if often re- 
peated, lead at last to chronic catarrh of the stomach; but, at least in adults, 
infectious influences are seldom prominent in the causation of the disease. In 
many cases it is due chiefly to the chemical and mechanical irritation of an un- 
suitable diet long continued. By far the most frequent — indeed, to speak more 
correctly, the only frequent — form of chronic gastric catarrh in adults, is due to 
hard drinking. The habitual use of distilled liquors is more influential in this re- 
gard than excess in wine or beer. The harm done by alcohol may be re-enforced 
by other dietetic causes. We have often met with genuine chronic gastritis in 
extremely destitute persons, who for a long time had to eat food that was insuf- 
ficient, bad, or even decayed. It should also be pointed out that abnormal condi- 
tions of the mouth, and particularly dirty or carious teeth, may occasion dyspep- 
tic and catarrhal conditions. Habitual excess in smoking is also said sometimes 
to occasion chronic gastritis; and finally, it is probable that the bad habit of 
rapid eating with imperfect mastication leads at last to gastric disturbance. As 
is the case with all external irritants of this sort, the results are influenced by 
individual differences in the resisting powers of the affected organ, and personal 
predisposition to disease plays a certain part in the development of chronic gas- 
tric catarrh. Often, as we have already noted, this predisposition seems, to a 
certain extent, a matter of family and heredity. 



426 



DISEASES OF THE DIGESTIVE ORGANS 



Chronic gastric catarrh is not always a primary affection. It may be sec- 
ondary to some other disease. In particular, all diseases associated with portal 
congestion are apt to lead to secondary catarrh of the stomach. This includes 
hepatic cirrhosis and hepatic syphilis. Again, the gastric catarrh associated with 
chronic cardiac, pulmonary, or renal disease is in part to be regarded as due to 
congestion. On the other hand, however, we should always consider how manifold 
are the other conditions, associated with all sorts of chronic diseases, which may 
lead to chronic gastric disturbance. We may mention, for instance, anseraia, 
muscular insufficiency, and auto-intoxication. 

Pathology. — The macroscopic changes in the gastric mucous membrane are in 
most cases very moderate. Usually it is thickened and coated with a layer of 
tough, grayish-white mucus, in which is suspended a greater or less amount of 
detached epithelium. The membrane is brownish red, unless rendered gray by 
excessive pigmentation. Under the microscope we find a well-marked infiltration 
of the interstitial tissue with fine cells, and well-marked parenchymatous 
changes, particularly extensive degeneration of the glandular cells. All these 
changes are especially marked in the pyloric portion of the stomach. If the 
catarrh has lasted a long time there may be still further changes in the mucous 
membrane. In many cases it appears smooth and atrophic. The glandular 
layer of the stomach may at last be almost destroyed, and the muscular and sub- 
mucous coats share in the atrophy, while the organ as a whole is usually dilated. 
In other less frequent cases there is a marked growth of interstitial connective 
tissue, with resultant contraction. In this variety, also, the glandular layer atro- 
phies, the stomach walls grow firmer, and the whole organ shrivels (cirrhosis of 
the stomach). Contrasting with these forms which lead to atrophy or sclerosis, 
there are others which occasion a hyperplasia of the mucous membrane. Its 
inner layer is thickened and mammillated (etat mamelonne) , and there may be 
actual polypi formed. The hyperplasia in these cases affects mainly the gland- 
tubes of the mucous membrane, but there is also a considerable thickening of the 
submucous coat. 

Symptoms on the Part of the Stomach. — The symptoms of chronic gastric 
catarrh are the same dyspeptic symptoms which we meet in various combination 
and degree in all diseases of the stomach. They include disturbance of the 
appetite; pressure or pain in the region of the stomach; a bad taste in the mouth; 
abnormal sensations in the throat; and finally, motor phenomena, including 
rumbling, eructations, and vomiting. 

The appetite is usually impaired in chronic gastric catarrh. There is some- 
times a moderate appetite, but it is soon changed to a feeling of repletion upon 
the ingestion of even a slight amount of food. In other cases there is actual 
dislike for any form of nourishment; the patient eats little, and prefers highly 
spiced, piquant dishes. There is often a persistent bitter, flat, offensive, or other- 
wise abnormal taste in the mouth. 

Subjective sensations in the region of the stomach are rarely entirely absent. 
As a rule, there is' a feeling of fullness or pressure and of dull pain. These trou- 
bles may either be constant, or occur after meals. Sometimes, especially after 
errors in diet, there may be actual pain. This is termed cardialgia or gastralgia, 
and is probably due in most cases to cramp-like contractions of the muscles ; but 
in general, habitual and severe pain does not belong to the clinical picture of 
simple catarrh. A very frequent and annoying symptom, which is particularly 
apt to come ori after eating, is the eructation of gas, usually air, but sometimes 
gases which are formed in the stomach by the processes of decomposition. Such 
gases have a disagreeable odor. The eructations may bring up, also, some of the 
fluid contents of the stomach. If there is a bitter taste associated with it this 
is usually occasioned by peptones, but sometimes perhaps by bile (vide infra). 



CHRONIC GASTRITIS 



427 



Acid eructations indicate excessive acidity of the gastric contents, ordinarily 
due to hydrochloric acid but exceptionally to lactic acid (vide infra), or to the 
fatty acids, which are recognizable by their odor. The burning feeling in the 
pharynx and lower down, which is occasioned by acid eructations and which is 
usually termed heartburn, is almost always caused by an excess of hydrochloric 
acid in the gastric contents, and consequently is not a frequent symptom of 
genuine chronic gastric catarrh (vide infra). 

In many cases the feeling of nausea increases, especially after eating, to 
actual vomiting, but in chronic gastric catarrh vomiting is not very frequent, 
and if it occurs it is the result of some special cause, such as errors in diet. There 
is this exception, that in the chronic gastric catarrh of drunkards a peculiar form 
of vomiting is very common. This is called morning vomiting. By this is 
understood a fairly regular occurrence of vomiting in the morning before break- 
fast, with the ejection of considerable amounts of watery mucus, usually alkaline. 
This vomiting is due not only to the chronic catarrh of the stomach, but also 
to the chronic catarrh of the pharynx, which latter occasions a great tendency 
to gagging — e. g., when rinsing out the mouth. The vomitus consists not only of 
mucus from the stomach but in large part, also, of a mixture of saliva and mucus 
from the mouth and throat. In the other forms of chronic gastric catarrh the 
vomitus consists often of ill-digested food and more or less mucus. If there are 
vigorous efforts at vomiting and retching, the vomitus may contain also some bile 
and small amounts of blood, which have no serious significance. 

The external examination of a patient with chronic gastritis shows little 
unusual. The general nutrition, of course, is often impaired, although in drunk- 
ards and gourmands an abundant fat layer persists for a long time. The tongue 
is usually coated, especially in its center, while its sides and tip are red. A 
thickly coated tongue and salivation are both of them due rather to accompany- 
ing stomatitis and pharyngitis — complications which are present in the case of 
most drunkards, and sometimes also in excessive smokers. Examination of the 
epigastrium shows often a considerable prominence of the stomach and tender- 
ness on pressure, but the only means of obtaining an actual insight into the abnor- 
mal process is a careful investigation, by means of the stomach-tube. This 
should not be omitted in any case of chronic gastritis of any severity, especially as 
the results of it furnish the only true guide for a rational treatment of the 
disease. If we examine the gastric juice after the manner already described, we 
shall find that free hydrochloric acid in chronic gastritis is scanty (below 0.1 per 
cent.), or even absent. Its complete absence is particularly common in chronic 
alcoholic catarrh, and also in cases of chronic gastritis in which there is atrophy 
of the mucous membrane. In the latter case pepsine, also, is often absent. With 
regard to abnormal acids, we may find lactic acid, but seldom in large amounts, 
because in simple chronic catarrh there is scarcely ever much stagnation of the 
gastric contents. If there are abnormal processes of decomposition, we find 
acetic acid, butyric acid, and volatile fatty acids, but these are very rarely 
present. 

The demonstration of an excessive production of mucus in the stomach is of 
great diagnostic importance. We have mentioned that sometimes the vomitus 
contains a distinct admixture of mucus, but the only way of forming an accurate 
opinion with regard to the amount of mucus in catarrh of the stomach is by 
siphonage, especially in cases in which vomiting is absent or infrequent. If we 
examine the stomach when fasting we shall, in many cases, find at every trial an 
abundance of mucous fluid with scarcely any other ingredients. In other cases 
there is more apt to be an abundance of mucus after a meal — either in a viscid, 
ropy fluid, or in separate transparent masses of varying size. Excess of mucus 
in the stomach is usually associated with anacidity, but there are a few excep- 



42S 



DISEASES OE THE DIGESTIVE ORGANS 



tional cases in which it is associated with increased secretion of hydrochloric acid 
(gastritis acida; acid catarrh of the stomach. Boas, Kiegel, and others). We 
must avoid confounding secretion from the mouth and pharynx that has been 
swallowed with mucus produced in the stomach. The latter is intimately mixed 
with the food, if there be any. 

The motor function of the stomach is seldom much disturbed in chronic gas- 
tritis. Often it is surprising how rapidly the stomach empties itself; but there 
may be delay, partly because digestion is impaired and partly because there is a 
gradual development of weakness and atrophy of the muscular coat of the stom- 
ach, analogous to the weakness of the muscles of the vocal cords in chronic laryn- 
gitis. If food is long retained in the stomach, there is probably some other disease 
than simple catarrh. The size of the stomach in chronic catarrh may be some- 
what increased, but this has no special importance. 

Symptoms on the Part of other Organs. — Course of the Disease. — Of the 
other organs, the intestine most frequently suffers in chronic gastric catarrh. In 
almost all cases of chronic gastric catarrh the bowels are irregular. Habitual 
constipation is the rule, but sometimes there is diarrhoea. If much gas is gen- 
erated in the stomach, the intestinal canal often becomes implicated, and tym- 
panites and flatulence develop. There may be catarrh of the duodenum leading 
to jaundice. 

The urine is often only feebly acid in reaction, and therefore frequently depos- 
its a large amount of phosphates. "We must be cautious, however, in the inter- 
pretation of this sign and the value we lay upon it, since the reaction of the 
urine is influenced by a great variety of conditions, including food, drugs, and 
the loss of acid by vomiting. 

It is often asserted that chronic cutaneous diseases and, in particular, certain 
forms of eczema, are due to catarrh of the stomach, but this is not certain, though 
not impossible. 

There has been great stress laid, particularly in recent times, upon the fre- 
quent occurrence of nervous disturbance in association with chronic catarrh of 
the stomach. This takes the form of hypochondriasis and depression of spirits 
in association with all sorts of other nervous symptoms, including pressure in the 
head, headache, dullness of mind, and dizziness (vertigo e stomacho laeso) ; but, 
while we may admit that the disease of an organ which, for many human beings, 
is the main source of happiness, may well put the patient out of sorts, yet there 
is no doubt that many earlier reports about nervous disturbances were due to a 
confusion of chronic gastric catarrh with nervous dyspepsia (vide infra). Genu- 
ine chronic catarrh of the stomach, as such, has no peculiar relation to nervous 
disease, except in the rare cases in which certain unusual symptoms develop, not 
improbably from the absorption of toxines. 

When the catarrh is of any duration and severity, the general nutrition is apt 
to be seriously impaired. The diminished appetite and the imperfect digestion 
and absorption of what is eaten contribute to produce a gradual and considerable 
loss of weight. The fatty and muscular tissues atrophy. The skin grows dry and 
harsh, and usually has a dirty-pale color. In rare cases of extreme atrophy of the 
mucous membrane (probably almost always combined with atrophy of the intes- 
tinal mucous membrane) there are developed symptoms like those of progressive 
pernicious anaemia (q.v.). 

Individual cases differ greatly in the combination of symptoms they present 
and in their course. The anorexia, gastric oppression, eructations, vomiting, and 
other important disturbances already mentioned, exhibit the greatest diversity in 
their intensity and their grouping. In the milder cases, loss of appetite and mod- 
erate local uneasiness may be the only symptoms. Erequent vomiting is con- 
fined to the severer cases. The disease often lasts for years, especially if the 



CHRONIC GASTRITIS 



429 



patient neglects himself. In most cases there are frequent remissions and exacer- 
bations, usually dependent upon external causes. 

The disease is not intrinsically fatal except in the above-mentioned rare cases 
of complete atrophy of the mucous membrane, but the general debility conse- 
quent upon it may indirectly shorten life. 

Diagnosis. — If we except the self-evident cases of chronic alcoholic catarrh, 
the only proper way of making a diagnosis of chronic gastritis is by means of a 
careful examination with the stomach-tube, along with a consideration of the 
associated conditions. If a patient has for some time been suffering from the 
ordinary gastric symptoms of anorexia, gastric oppression, eructations, and 
vomiting, we must first determine whether we have to deal with a primary dis- 
ease of the stomach, or with a secondary disturbance referable to such condi- 
tions as cardiac disease, renal disease, or pulmonary tuberculosis. If the indi- 
gestion is not symptomatic we must then consider in order each of the primary 
diseases of the stomach. If there is no indication of ulcer or carcinoma, we have 
remaining actual gastritis, nervous dyspepsia (q.v), and a dislocation of 
the organ (gastroptosis). One important factor is the general condition of the 
patient — for instance, if there is neurasthenia or the like. No actual conclusion 
can be reached, however, except by examining the contents of the stomach. We 
can not assume that there is a chronic gastritis unless there are direct objective 
changes to be demonstrated, chief among which is an abnormal production of 
mucus, associated with a change in the amount of hydrochloric acid in the gas- 
tric juice. This change is in most cases a diminution, but exceptionally an in- 
crease of the amount secreted. We wish, in this connection, to emphasize once 
more the statement that genuine chronic gastritis, except in drunkards, is by no 
means a common disease and is much less frequent than nervous dyspepsia. 

Treatment. — If the disease seems to be merely symptomatic — the result, for 
instance, of venous stasis due to chronic cardiac, pulmonary, or hepatic dis- 
ease — our efforts must, of course, be directed chiefly to the relief of the original 
trouble. We must also take into consideration all other causative influences, 
such as neglected or decayed teeth, improper mode of life, and unhealthy occu- 
pation. 

The direct treatment of chronic gastric catarrh must always begin with a 
regulation of the diet. Such vague injunctions as " to be cautious " or " to avoid 
indigestible articles of food" are useless. The patient must have a perfectly 
definite bill of fare prescribed for him; nor can any universal one, suitable for 
all cases, be drawn up. In each individual instance the individual circumstances 
must be considered. The personal experiences of the patient himself are by no 
means to be disregarded. One man may be quite unable to digest what is well 
borne by others, and vice versa. 

In the first place, certain foods must be utterly forbidden to such patients as 
do not themselves avoid whatever disagrees with them. All articles must be 
prohibited which may irritate the mucous membrane, either mechanically or 
chemically. This includes all the coarser sorts of vegetables or fruits, containing 
a large proportion of indigestible cellulose; and all dishes that are very sour, 
strongly salted, or highly smced. Potatoes, farinaceous food, and all substances 
composed mainly of hydrocarbons, must also be interdicted; because almost all 
the abnormal fermentative processes, the evil consequences of which have already 
been considered, are promoted by the hydrocarbons. Fat is also harmful. It im- 
pedes digestion by protecting the contents of the stomach from the action of the 
gastric juice, in a purely mechanical way; and then, being changed into the fat 
acids, it causes sour eructations and pyrosis. Yet we must not go too far in 
forbidding starches and fats. Particularly if the patient is emaciated it is 
advisable to give such fatty substances as good butter and cream in cautious 



430 



DISEASES OF THE DIGESTIVE OBGAXS 



amounts, and often the result is satisfactory. In general, we should not forget 
that with regard to diet the skill of the physician often lies more in what he 
permits than in what he forbids. The limitation or withholding of alcoholic 
beverages is an important point. As we have already mentioned, the great 
majority of cases of chronic catarrh are the direct result of excess in alcohol — 
the most important factors being chemical irritation and mechanical distention 
of the mucous membrane. Moreover, the experiments of Fleischer and others 
have shown that alcohol prolongs and hinders the process of digestion. In every 
severe case it is better to forbid alcoholic beverages entirely, and ordinarily such 
an injunction is much better obeyed than advice to use them sparingly. In mild 
cases we admit that small portions of beer and wine may be permitted unhesi- 
tatingly, especially if the patient himself experiences no feeling of discomfort 
from them, but rather an improvement in his appetite. 

In determining what the patient may be allowed to eat, we are to consider, as 
already mentioned, his own personal experience as well as our more general 
knowledge. An intelligent patient will often be himself the best judge of what 
agrees or disagrees with him. The following foods are very easy to digest : milk, 
soft-boiled or raw eggs, broths (especially veal and chicken broths), and certain 
artificial preparations, chief among which stand the Leube-Eosenthal meat solu- 
tion and the meat juice and peptones which have been lately put upon the 
market. It must be confessed that patients soon tire of these last. The brain 
and sweetbread of calves are easily digestible ; also birds, such as pigeons, chick- 
ens, and partridges, thin shavings of raw beef or raw ham, rice, potato puree, etc. 
Gradually we may proceed to somewhat heartier food — veal, game, roast beef, 
trout, and light farinaceous dishes. The worse the symptoms are in any case, 
the more strict must we be in regard to diet. For drink, besides water or Seltzer 
water, very weak tea, cocoa, chocolate, and water reddened with claret are allow- 
able. — Shall we permit coffee ? This is often a question of great interest to the 
patient: it must be answered according to his individual experience. Coarse 
bread is to be forbidden. Ordinary white bread, toasted, if it seems desirable, 
may be allowed in moderate amount, also rusks. 

Solid articles of diet must be finely cut up and well chewed before being 
swallowed. The food must not be very hot or very cold. It is sometimes advan- 
tageous to take more than three meals a day, each one being proportionally 
smaller. Other patients relish their food better if the intervals between eating 
are prolonged. It should be added that excessive smoking, also, is harmful in 
chronic dyspepsia. 

There are other special indications to be met. In all severe cases by far the 
most efficient mode of treatment consists in methodical washing out of the stom- 
ach. This is especially true when there is excessive production of mucus, or a 
tendency to decomposition of food in the stomach. In this way we prevent the 
accumulation of any great amount of undigested food. We remove the excreted 
mucus and the products of abnormal fermentation and decomposition, and more- 
over, we may perhaps exert a direct and favorable influence upon the mucous 
membrane. In such cases, we are accustomed to rinse out the stomach daily, and 
the best time for this is in the morning before the patient has had breakfast. 
Fresh fluid must be poured in and emptied out rapidly, until the stomach is freed 
from all foreign material, especially mucus. We use for the rinsing fluid a weak 
solution of hydrochloric acid (one to two per mille), or a one-per-cent. solution of 
either common salt or bicarbonate of soda ; and, if there is much mucus, a favor- 
ite remedy is very dilute lime-water, two to four tablespoonfuls of liquor calcis to 
a litre (quart) of water. If fermentation is going on, we employ weak solutions 
of hydrochloric, boric, or salicylic acids, or resorcine. It has also been recom- 
mended to spray or douche the mucous membrane of the stomach, for which pur- 



CHROXIC GASTEITIS 



431 



pose stomach-tubes are employed with numerous small openings, and such fluids 
are chosen as weak solutions of alum, tannin, and condurango. 

If we now turn to a consideration of the internal remedies used in chronic 
gastric catarrh, it is possible to decide with regard to their employment in a much 
more intelligent fashion than heretofore, because in all severer cases we make a 
more accurate investigation of the digestive process. If the examination of the 
gastric juice shows a diminution of hydrochloric acid, this may be artificially sup- 
plied. We prescribe, thirty to sixty minutes after each meal, ten to fifteen drops 
of dilute hydrochloric acid in half a glass of water. The benefit to be thus 
derived must not be overestimated. In appropriate cases, however, its influence 
is favorable. If there is no pepsine in the gastric juice we may prescribe pepsine 
as well as hydrochloric acid. Pancreatine and papaine are also recommended, but 
their usefulness is very doubtful. The popular wines of pepsine are not to be 
recommended, because of the alcohol in them. 

Alkalies have long been employed as well as hydrochloric acid, and often with 
good results, although the mGst common form of chronic gastric catarrh has a 
less than normal secretion of hydrochloric acid, and consequently the use of 
alkalies would seem to be contra-indicated; yet experience shows them to be 
useful. Probably their beneficial effect is that they neutralize the abnormal 
acids, promote the emptying of the stomach into the duodenum, dissolve the 
mucus, and finally stimulate the secretion of the gastric juice. This has been 
experimentally demonstrated with regard to carbonate of soda, common salt, and 
carbonic acid. Prom what has been said it is evident that in chronic gastric 
catarrh alkalies are not usually given during digestion, but when the stomach is 
empty and before meals. As is well known, the alkalies are prescribed more espe- 
cially in the form of alkaline mineral waters, which the patient drinks at home, 
or at the various health-resorts. The springs of Carlsbad possess the greatest 
reputation. Those at Ems, Kissingen, Tarasp. and Vichy also deserve to be 
mentioned as health-resorts for patients with gastric trouble. A good portion 
of the benefit at these places is, to be sure, dependent upon the fact that many 
patients are much more apt to follow a strict regimen when they make use of a 
particular " cure " than when they remain at home. It is self-evident that large 
doses of bicarbonate of soda are indicated in that form of chronic gastritis which 
is associated with hypersecretion. 

If the character of the vomitus, or gastric contents obtained by rinsing, indi- 
cates abnormal fermentation, we may not only wash out the stomach (vide supra), 
but also try certain antifercnentative remedies. Pirst among these is hydro- 
chloric acid in rather large doses, and we also give salicylic acid (in powders, 
containing 8 grains, gramme 0.5) ; creasote (two or three half -grain pills daily, 
gramme 0.03) ; benzine ('20 drops in capsules or in milk) : and similar drugs. As 
a rule, however, the last-named remedies are seldom employed. 

The best drugs to stimulate the secretion of gastric juice are the bitters. It is 
this property which has earned them the name of stomachic tonics. Compound 
tincture of gentian, tincture of nux vomica, tinctura amara, and tinctura calami, 
P. G., quassia and Colombo — these are much employed. In general, however, 
they are not very efficient. An excellent tonic in many of these cases is condu- 
rango bark. A decoction may be made (15 parts to 200 of water) ; or we may 
employ the fluid extract, giving a teaspoonful in water two or three times a day. 

A few remedies remain to be mentioned, which are said to exert a direct bene- 
ficial influence upon the catarrh, and which many physicians extol highly. 
Their efficacy, however, is somewhat problematical. VTe refer chiefly to subni- 
trate of bismuth, sulphate of zinc, and nitrate of silver. 

Certain symptoms may demand especial treatment, such as vomiting. It will 
usually yield to regular and persistent washing out of the stomach. Other reme- 



432 



DISEASES OE THE DIGESTIVE OKGASTS 



dies are small bits of ice, and minute doses of opium or chloral. Potassic bro- 
mide and chloroform, internally administered, may also be tried. 

Violent gastralgia requires narcotics, such as morphine and opium. The best 
external applications are poultices or wet compresses. " Sour stomach " may be 
relieved by a pinch of bicarbonate of soda, or of calcined magnesia. Persistent 
anorexia may yield to the bitters mentioned above, or to small doses of quinine 
or compound tincture of cinchona. If the bad taste in the mouth is annoying, 
the mouth should be frequently rinsed out with Seltzer water, a one-per-cent. 
solution of carbolic acid, or five drops of tincture of myrrh to a glass of water. 
Eor habitual constipation, enemata, or the various mineral waters, are good; 
also Carlsbad salts. In obstinate cases pills of rhubarb or aloes may be em- 
ployed. Still, we ought never to forget that the infrequency of the stools is often 
merely a natural consequence of the scanty diet, and that it is therefore possible 
to do harm with our purgatives. Iron is often prescribed for the concomitant 
anaemia ; but it should be employed cautiously, for it is often ill borne in gastric 
disease. 



CHAPTER IV 

PHLEGMONOUS GASTRITIS 

{Purulent Inflammation of the Stomach) 

Purulent inflammation of the stomach is very rare, and little is yet known 
about it. In most cases no special causes for it have been ascertainable. It is 
occasionally one of the symptoms of grave pyaemic or puerperal inflammation. 
We have seen one case in which suppuration of the pharynx led to an acute 
phlegmonous inflammation of the submucous coat of the oesophagus, also involv- 
ing a large portion of the stomach, with a fatal termination. 

Two forms are distinguished — a diffuse and a limited variety. The latter is 
equivalent to gastric abscess. The submucous layer is almost invariably the 
chief seat of suppuration. Erom this starting-point the process invades the mus- 
cular and serous coats on the one hand, and the mucous membrane itself on the 
other — the usual result being multiple sievelike perforations inward or outward. 

The usual symptoms are violent gastric derangement, with pain and vomiting, 
high fever, and the indications of constitutional infection, namely, headache, 
delirium, and general prostration. Sometimes the disease is quickly fatal, some- 
times it runs a more chronic course. The few cases in which recovery has been 
reported are somewhat obscure. 

The disease can never be diagnosticated with absolute certainty. Treatment 
must be purely symptomatic. Ice, both internally and externally, and the nar- 
cotics, are chiefly employed. 



CHAPTER V 

GASTRIC ULCER 

{Simple or Round Ulcer of the Stomach) 

etiology. — Since Cruveilhier gave the first accurate description of gastric 
ulcer, numerous explanations of its occurrence have been propounded. Even yet 
there is no universally accepted view. We may, in general, hold to the assertion 



GASTRIC ULCER 



433 



that the development of an nicer is preceded by a local disturbance of nutrition, 
or necrosis of the gastric mucous membrane, and that then the enfeebled or 
necrotic tissue is dissolved by the gastric juice — i.e., digested ("peptic ulcer"). 
But it is not known what are the special causes which occasion the primary dam- 
age to the tissue, nor why the loss of substance when it occurs is not at once 
healed, but extends in width and depth. There is, indeed, no lack of theories to 
solve these questions, and pathologists have made many experiments with regard 
to the pathogenesis of gastric ulcer. 

The explanation of the fact that the normal gastric mucous membrane is not 
attacked by gastric juice lies probably not so much in the presence of the alkaline 
blood flowing through the membrane as in the intrinsic vital resisting powers of 
the normal living cells. If the cells are in any way damaged there occurs at once 
an auto-digestion at that spot. Damage of this sort may be produced experi- 
mentally in different ways; for example, by artificially produced embolism of 
the smaller arteries of the stomach, and by wounds, including bruising, burning, 
and cauterization of limited portions of the mucous membrane. In all such cases 
a peptic ulcer is formed, but almost invariably this promptly heals, or, at any 
rate, it shows no tendency at all to extension. If, as a symptom of severe gas- 
tritis or portal congestion, there are small hemorrhages into the mucous mem- 
brane, they result in so-called hasmorrhagic erosions ; but these again are limited 
to the small spot destroyed by the haemorrhage. 

Virchow assumed that ordinary round ulcer of the stomach in man is, in most 
cases, the result of the plugging of the small vessels with a thrombus or embolus, 
because of various diseased conditions of their walls, but this supposition remains 
entirely without proof. One fact that tends to contradict this view is the appear- 
ance of ulcer in young individuals without any signs of cardiac or vascular dis- 
ease. Other investigators thought of the possibility of accidental injuries, and, 
perhaps in some few cases, even, of external trauma. Such suppositions are per- 
fectly possible, although they, again, in most cases are incapable of demonstra- 
tion. Then we have still to meet the second above-mentioned question : Why, in 
all such cases, the little erosions, if they are formed, do not immediately heal, as 
the experimentally produced ulcers almost invariably do. Lately the attempt has 
been made to settle this difficulty by pointing out that in ulcer of the stomach 
the acidity of the gastric juice is shown to be abnormally great. This hyper- 
acidity is assumed to exist even before the development of the ulcer, and in a cer- 
tain degTee to cause a predisposition for its development, as well as to explain 
the unwillingness of the ulcer to heal and its proneness in many cases to extend 
farther, to spread. If a gastric ulcer is artificially produced, the process of heal- 
ing may be considerably delayed by introducing solutions of hydrochloric acid 
into the stomach. It is very possible that hyperacidity of the gastric juice is a 
factor in the aetiology of ulcer, but the whole matter is by no means easily intel- 
ligible. We remain uncertain as to what is the primary cause of the ulcer, and it 
has not yet been proved that hypersecretion and hyperacidity exist before the for- 
mation of the ulcer. We might also believe that the excessive acidity is secondary 
to the sensory irritation occasioned by the raw spot. In a word, our present 
knowledge of the development and extension of gastric ulcer is very limited. 

Gastric ulcer occurs but seldom in childhood. It is most often seen between 
the ages of eighteen and thirty. The cicatricial stenosis of the pylorus and other 
sequelse are often seen in still older individuals, between thirty and forty-five 
years; but in most of these cases the disease probably originated much earlier. 
In still later life gastric ulcer is rare. In general, the disease seems to be more 
frequent in the female sex than in the male ; but if we count only the absolutely 
demonstrated cases, the difference is not a very great one. The view that ulcer 
of the stomach attacks by preference anaemic and chlorotic girls is very general, 
28 



434 



DISEASES OF THE DIGESTIVE ORGANS 



but to the author seems much exaggerated. The probable explanation is that 
gastric disturbances in chlorotic persons are often ascribed to gastric ulcer with- 
out sufficient reason. Taking into consideration only the absolutely certain 
cases, the author's experience does not show any especially close connection 
between chlorosis and gastric ulcer. Yet it must of course be confessed that 
indubitable cases of gastric ulcer occur in chlorotic girls. 

Pathological Anatomy. — The ulcer is usually approximately round or oval. 
Its borders are sharp ; the walls often slope inward, giving the ulcer the form of a 
shallow funnel. The base of the ulcer is almost always perfectly clean, so that in 
microscopic sections we see the ends of the gland tubes remaining unchanged, and 
reaching out into the surface of the ulcer. After an ulcer has lasted some time, a 
reactive inflammation develops around the necrotic area, leading to the formation 
of connective tissue and cicatrization. If superficial, it does not extend farther 
than to the muscular coat, but it may be deep enough to expose the serous mem- 
brane, or even to perforate it (vide infra). The size varies greatly. Some are 
hardly as large as a pea; others may measure ten to fifteen centimetres in their 
greatest diameter. As to position, most of them are found near the pylorus. They 
attack the posterior wall of the stomach, particularly the neighborhood of the 
lesser curvature, far more frequently than the anterior wall, but the greater 
curvature is not infrequently the seat of an ulcer. As a rule, we find but a single 
ulcer, although exceptions to this statement are not very rare. 

If an ulcer of any size heals, a scar is formed, with radiating lines and often of 
considerable size; smaller superficial ulcers heal with a smooth scar. Cicatricial 
contraction may alter the shape of the stomach considerably. If a deep con- 
striction is formed around the middle of the stomach, we have what is called the 
hour-glass shape. Scars of pyloric ulcers are of the greatest clinical impor- 
tance, because they lead to cicatricial stricture of the pylorus, with resultant 
dilatation of the stomach. 

If the gastric ulcer extends to the serous membrane, the final result may be 
perforation into the abdominal cavity, and general peritonitis, unless the stom- 
ach previously becomes attached at the point threatened to some neighboring 
organ, because of adhesive inflammation. The ulcers being usually on the pos- 
terior wall of the stomach, it is oftenest the pancreas to which the stomach be- 
comes adherent. In other instances it is the liver, transverse colon, diaphragm, 
or spleen. If adhesions are formed before the perforation of a gastric ulcer, 
there may be circumscribed peritoneal abscesses. These are situated with com- 
parative frequency between the upper surface of the liver and the diaphragm, or 
between the stomach and the diaphragm (subphrenic abscess). Again, after such 
adhesions there may be perforation into the pleural cavity, the transverse colon, 
the pericardium, or the lungs. 

The ulcer may cause erosion of a blood-vessel, and thus give rise to one of the 
most important symptoms of the disease, namely, gastric hsemorrhage. 

Clinical History. — There may be absolutely no symptoms. It is not a rare 
thing to find at autopsies a still active ulcer of the stomachy or the cicatrix left by 
one, in subjects who never had during life any gastric disturbances whatever. 
ISTor is it very exceptional for a person suddenly to exhibit grave symptoms, such as 
gastric haemorrhage, or peritonitis due to perforation, when there has been no 
reason previously to apprehend the existence of an ulcer. 

In other instances the ulcer does, indeed, give rise to symptoms, but they are 
not sufficiently characteristic to point to the correct diagnosis. Usually the gas- 
tric symptoms are long continued, but comparatively slight. They consist, for 
instance, of a sense of oppression or slight pain in the epigastrium, eructations, 
and occasional vomiting. In these cases, also, grave symptoms consequent upon 
the ulceration may suddenly arise. 



GASTRIC ULCER 



435 



In a third class of cases there are symptoms which are to a certain extent 
characteristic, and lead with more or less definiteness to the true diagnosis. 
These " symptoms of ulcer " are chiefly a peculiar epigastric pain, which is usu- 
ally intermittent, and vomiting, or, what is yet more distinctive, the vomiting of 
blood, or haematemesis ; also the signs of an increased secretion of hydrochloric 
acid in the gastric juice (hyperchlorhydria and hypersecretion). These symp- 
toms and their diagnostic value we must now consider in detail. 

Pain in the stomach is one of the most frequent symptoms of round ulcer. Its 
forms are very diverse. Often the patient complains only of a diffuse, painful 
sensation of pressure referred to the entire region of the stomach. This may be 
uninterrupted, or it may occur only after meals, or after excessive exertion, or as 
the result of some other special cause. This sort of pain is the least diagnostic of 
any, inasmuch as exactly similar sensations may be caused by other chronic dis- 
orders of the stomach. More characteristic of ulcer is a decided cardialgia, or, 
more correctly, gastralgia — that is, a very violent pain, coming on at intervals 
like neuralgia. It is described as " cutting," " tearing," " boring," and the like. 
These attacks of pain occur at various times, but oftenest after eating, and par- 
ticularly after the ingestion of a large amount of food, or of food of a rather 
coarse sort. Often they occur with tolerable regularity a definite time after 
eating, say half an hour or an hour. This is partly to be explained by the begin- 
ning of the expulsion of food through the pylorus, and partly by the acme of the 
secretion of acid being due at this time. The pain is felt chiefly in the epigas- 
trium, but not infrequently it extends toward the umbilicus, backward toward the 
vertebrae, into the thorax, or even into the upper extremities. In many instances 
a marked sensation of thoracic oppression accompanies it. A change of position 
may sometimes affect the severity of the pain. It is sometimes observed that 
the patient, when lying upon his right side, feels violent pain, which is at once 
relieved by changing to the left side, probably because the ulcer is located near 
the pylorus. An attack of cardialgia may last for a few minutes or for several 
hours. A third variety of pain may be observed in gastric ulcer. The suffering 
may be localized in a very limited area. Such pain is thought to be due to irrita- 
tion of the floor of the ulcer by food, or to its edges being pulled upon during the 
movements of the organ. It generally comes on after eating, and ceases if the 
stomach is perfectly quiet. In position, this pain is generally epigastric, but 
sometimes it is umbilical, or even, now and then, more toward the back. In many 
cases of gastric ulcer there is also tenderness on pressure in a quite sharply de- 
fined area and at one particular spot. Most authors regard the accurately local- 
ized pain as the most nearly pathognomonic ; but it must be said that it is decid- 
edly the least frequently exhibited of any. Transitional forms and combinations 
of the various kinds of pain are often observed. Two things may be said to be 
characteristic in all the sorts of pain connected with ulcer of the stomach: the 
localization of the pain each time in the same spot ; and the relation of the pain 
to the ingestion of food. Complete , bodily rest is beneficial; external pressure 
upon the epigastrium usually increases the pain. 

Vomiting is a frequent symptom in gastric ulcer, although it may exception- 
ally be absent or nearly so. Ordinarily, vomiting occurs, like the cardialgic at- 
tacks, after eating, and particularly after partaking of indigestible dishes. The 
vomitus in such cases consists mainly of partially digested food. It usually has 
a strongly acid reaction. If there is hypersecretion there may sometimes occur 
vomiting of a strongly acid fluid, not containing much that has been swallowed. 
If the ulcer has led to stenosis of the pylorus, the way in which the vomiting 
occurs is very characteristic. We shall describe this form of vomiting later, in 
detail. Vomiting is of the greatest diagnostic importance when blood appears. 
This may be intermixed in greater or less amount with the other contents of the 



DISEASES OF THE DIGESTIVE OKGAXS 



stomach, or it may be vomited as pure blood (haematemesis). A gastric haemor- 
rhage demonstrated by the vomiting of blood is the most valuable diagnostic 
sign of gastric ulcer. If there is no haemorrhage at all, the recognition of gastric 
ulcer is almost always rather difficult and uncertain. 

Haernatemesis is frequently the symptom which first leads the patient to apply 
to a physician. Up to this time he may have felt perfectly well. or. although 
there may have been some gastric derangement, he has not thought anything' of 
it. The patient suddenly becomes faint, perhaps while he is pursuing his regular 
occupation, or it may be at night. He feels dizzy, and everything looks black. 
Then he has nausea, and finally is obliged to vomit. The vomitus is either pure 
blood, or a mixture of blood and food. It is partly coagulated, and often has 
a rather dark or blackish color, like tar. This change in color, as well as the 
coagulation, is due to the action of the gastric juice. The haemoglobine is trans- 
formed by the action of the hydrochloric acid into haematine. If the blood, before 
it is vomited, has remained for some time in the stomach, the vomitus has the 
appearance of " coffee grounds," and no longer contains unchanged red blood-cor- 
puscles (for the chemical demonstration of blood, vide supra, page 422). The 
amount varies greatly in different cases : there may be a quart or more. Some- 
times there is a single haemorrhage, but not infrequently blood is repeatedly vom- 
ited either at short intervals or on successive days. Part of the blood escapes 
through the pylorus, so that, after a profuse gastric haemorrhage, blood is sure to 
be found in the stools. In them it is black and tarry. Exceptionally it happens 
that all the blood, beyond what is "absorbed from the intestinal canal, passes off 
per anum. so that none whatever is vomited. In such cases it is often a difficult 
matter to locate the haemorrhage. If there is a sudden faintness with pallor, and 
without vomiting, but followed by black faecal discharges, we should always think 
of the possibility of a gastric haemorrhage. 

The consequences of gastric haemorrhage depend, of course, chiefly on the 
amount of blood lost. Sometimes, although fortunately rarely, a large blood- 
vessel is eroded and the patient dies. This event may be sudden, or it may occur 
more gradually under the influence of repeated haemorrhages and after a few 
days, during which all the symptoms of acute anaemia are exhibited. On the 
other hand, the loss of blood may be so insignificant as to produce no especial 
symptoms. In most instances life is not actually threatened, but yet the signs 
and results of a more or less marked general anaemia are clearly visible. 

In such cases the patient feels extremely exhausted, and at once takes to his 
bed. He has also all the subjective symptoms of cerebral anaemia. There are 
vertigo, tinnitus aurium. specks before the eyes, frequent gaping, and sometimes 
headache. To assume an erect posture aggravates the disturbance. There is usu- 
ally excessive thirst. Xow and then a temporary amaurosis has followed an ex- 
cessive haemorrhage. 

Objectively, we notice at once the excessive pallor of the skin, particularly of 
the face. The lips and conjunctivae are also blanched. The pulse is rapid, and 
often ill sustained. For some days there may be anaemic murmurs over the heart, 
and there is a distinct sound to be heard in the femoral arteries. A moderate rise 
of temperature is very common, probably due to the absorption of the blood 
decomposing in the intestines. This is known as anaemic fever. The urine 
is pale, and usually rather abundant. Its specific gravity is not infrequently 
relatively high, namely. 1015 to 1020. All these symptoms are directly referable 
to the loss of blood, and they will be discussed with greater detail in the section 
on anaemia. 

If the haemorrhage is not repeated, the patient gradually regains his strength. 
To be sure, the pallor usually persists for a long time, but the disagreeable symp- 
toms gradually abate. When gastric discomfort has existed previously to the 



GASTRIC ULCER 



437 



haemorrhage, it often disappears entirely after it — a circumstance which is prob- 
ably due in part to the excessive caution of the patient thereafter. At the end of 
a few weeks the patient often feels perfectly well again ; and, indeed, recovery is 
not infrequently complete and permanent. In other cases, however, the symp- 
toms of ulcer return, sooner or later. 

The third group of symptoms in ulcer of the stomach is furnished by an ex- 
amination of the gastric contents, with the aid of the stomach-tube. These are 
of extreme importance. Earlier, when the soft tube now universally employed 
was not in use, we feared to introduce a tube into the stomach in case of ulcer, 
and even now we should not do it, in case of hsematemesis, if it can be avoided, 
until some weeks have elapsed; but with this exception abundant experience has 
shown that we do not need to be at all timid about the introduction of the stom- 
ach-tube ; and particularly if there is doubt about diagnosis we should never fail 
to avail ourselves of it. The most important fact which the investigations of 
the gastric contents in patients with ulcer has taught us is that there are almost 
invariably present hyperacidity and hypersecretion of the gastric juice. If the 
stomach is examined when fasting, we shall find a fluid containing a large 
amount of hydrochloric acid, and if we examine it an hour after a test breakfast, 
we shall find an extreme amount of acid (vide supra, page 417). This fact was 
discovered by Riegel, and we have found it true in all uncomplicated cases of ulcer 
of the stomach, indeed it seems to be so much the rule that if anacidity were found 
it would render any previous suspicion of ulcer extremely improbable. If, how- 
ever, the ulcer has led to stenosis of the pylorus, and so to extreme stagnation of 
the gastric contents, there may be temporary subacidity or anacidity (vide 
infra). Likewise — and this is a point of great practical importance — hydro- 
chloric acid may be absent if a gastric carcinoma has developed on the base of a 
former gastric ulcer (vide infra). Lactic acid is invariably absent when there is 
hyperacidity from hydrochloric acid; or, at most, if there is great stagnation of 
the gastric contents, there may be a moderate formation of lactic acid. It is also 
very important in cases in which there is no vomiting at all, to examine the gastric 
contents obtained by rinsing out the stomach, with regard to the possible pres- 
ence of blood. Small admixtures of blood in association with hyperacidity are 
strong evidence of gastric ulcer. 

The motor efficiency of the stomach in ulcer is at first normal or even some- 
what exaggerated, because the digestion of albumen is very energetic owing to 
the excess of hydrochloric acid in the stomach. But if the ulcer is located in the 
pyloric region and leads to a cicatricial stenosis, the emptying of the stomach 
is delayed and a greater or less amount of food will be found seven or eight hours 
after the test meal. We shall later describe the symptoms of well-marked ob- 
struction of the pylorus. If there is suspicion of an ulcer, the stomach is usually 
not inflated at all, or if so only by means of the condom (see page 421). If, how- 
ever, there is a cicatricial stenosis of the pylorus, or an hour-glass contraction of 
the stomach, our best means of determining the form and size of the organ are by 
the introduction of air. 

There are no other symptoms in gastric ulcer so important as those already 
described. The appetite in many cases is well maintained, and if the patient 
takes little food it is only because he dreads the ensuing pain. Eructations 
may be absent or there may be sour eructations and heartburn, symptoms refer- 
able to the existence of hypersecretion and hyperacidity. The tongue is seldom 
coated, being usually smooth and red; the bowels are apt to be somewhat consti- 
pated ; the urine is often very faintly acid, so that there is a tendency to a deposit 
of phosphates. 

The general nutrition of the patient often remains good, but there may be 
marked emaciation if there is a long-continued diminution in the amount of food 



438 



DISEASES OE THE DIGESTIVE ORGANS 



taken, or if there is obstinate vomiting 1 . Sometimes, but by no means invariably, 
the patients display great anaemia. This may precede the nicer (vide supra, 
aetiology), or it may develop in association with the symptoms of nicer, and even 
without any severe haemorrhage to explain it ; but that after severe haematemesis 
there should be a severe anaemia is a matter of course, and has already been 
alluded to. 

An event which has been already mentioned under pathology — namely, perfo- 
ration due to the ulcer — is of great clinical importance. It would be impossible to 
particularize here all the possibilities incident to it. We shall confine ourselves 
to the two most important because most frequent varieties of perforation: (1) 
into the peritoneal cavity, causing peritonitis, and (2) into the left pleura, or 
left lung. 

Perforation into the peritoneal cavity leads almost invariably to a quickly 
fatal peritonitis. When the ulcer has previously caused few symptoms, if any, 
the excruciating abdominal pain, tympanites, vomiting, collapse, and sudden 
death of peritonitis may abruptly supervene upon a state of apparently perfect 
health. In other cases in which there has been a previous formation of adhe- 
sions, we have an encapsulated abscess, either subphrenic, between the stomach 
and the diaphragm, or elsewhere in the abdomen. The subphrenic abscess may 
contain air as well as pus, and is then termed pyo-pneumothorax subphrenicus. 
In making a diagnosis of any subphrenic abscess, we should consider the direct 
and constitutional symptoms, and also the thoracic signs, for the respiration and 
the inspiratory expansion of the lungs should be normal. If there is perforation 
outward or into a coil of intestine, recovery may result. More often, however, the 
termination is fatal, unless surgical intervention is successful. 

Perforation into the left pleural cavity we have observed repeatedly. It 
causes a purulent or septic pleurisy on that side, and pulmonary gangrene may 
develop at the same time or later, as a result of perforation into the lung. When- 
ever we meet a case of apparently spontaneous, left-sided empyema, we should 
at any rate always think of the possibility of gastric ulcer. 

In many cases of ulcer we observe signs of threatening perforation — that is, 
localized pain due to peritonitis, vomiting, and similar symptoms, and yet the 
case finally clears up. Probably in most such instances there is a limited peri- 
tonitis resulting in adhesions. 

The general course of round ulcer of the stomach varies greatly, as we can see, 
in different cases. Complete recovery is by no means rare. In other cases the 
symptoms persist for years with varying intensity. We have already spoken of 
the haemorrhage and perforation which may suddenly intervene, and of their 
significance. Relapses are not infrequent, even after apparent recovery. If the 
ulcer cicatrizes, the scar itself may give rise to persistent disturbances : there may 
be obstinate cardialgia, or, if the scar is at the pylorus, dilatation of the stomach 
(vide infra) may gradually be developed. This extremely important sequel of 
gastric ulcer deserves special consideration. 

The cicatrization and contraction of a gastric ulcer whjlch result in stenosis 
of the pylorus may be complete, but it is by no means exceptional for the ulcera- 
tive process to persist in other places while there is a scar at the pylorus, so that 
we may have the symptoms of stenosis combined with all the other symptoms 
of ulcer, such as pain, hyperacidity, haemorrhage, and perforation. When there 
is an obstruction of the pyloric orifice as a result of interstitial thickening and 
scar formation at that place, a group of extremely characteristic symptoms is 
superimposed upon the ordinary symptoms of ulcer. Perhaps one cause of the 
change in the pylorus is the destruction of the muscular coat at that point. 

The first and most important- result of pyloric stenosis is prolonged retention 
of the gastric contents. So long as the muscular coat of the stomach is able by 



GASTEIC ULCEE 



139 



increased effort to overcome the increased resistance, there is no disturbance to 
be noticed. It is proper to speak of a compensated pyloric stenosis, just as we 
speak of a compensated valvular disease of the heart ; but if the stenosis becomes 
greater, so that even the hypertrophied muscular coat ceases to be able to dis- 
charge the chyme into the intestine, there is a gradually increasing collection of 
food in the stomach, and the only way for the organ to relieve itself is by vomit- 
ing. The vomiting, in case of pyloric stenosis, is somewhat characteristic. It 
occurs from time to time, perhaps at intervals of two or three days, and is very 
profuse. Then, the stomach being partially emptied, new collections may form 
until their large amount leads to vomiting again. The vomitus in cases of 
stenosis due to ulcer is usually very acid and contains much free hydrochloric 
acid, and sometimes blood. The stomach itself becomes gradually and increas- 
ingly dilated, because of the stagnation of its contents. Usually this secondary 
dilatation of the stomach may be recognized by mere external examination. We 
can feel the stomach as a great limp, flabby bag; and from time to time we can see 
its walls bulge out from muscular contraction. We can often distinctly recog- 
nize the peristaltic waves passing from the fundus to the pylorus. In the region 
of the pylorus we may sometimes, though by no means invariably, make out a 
distinct resistance on palpation, suggesting a tumor and corresponding to the 
thickening of the gastric walls from scar formation. In such cases it is often 
especially difficult to distinguish between the scar of an ulcer and a carcinoma. 
Even if we can feel no tumor, visible contractions of the stomach with distinct 
peristalsis are almost invariably pathognomonic of pyloric stenosis. In such 
cases there is usually a cramplike, painful sensation, associated with every marked 
contraction of the muscular coat. During these contractions of the stomach 
its contour is often so evident that we can obtain a perfectly distinct idea 
of its size, extent (often reaching below the navel), and position. But we must 
especially emphasize the fact that the size of the stomach, its dilatation, is not 
the essential point. The main thing is the stenosis of the pylorus, and, above all, 
the degree of consequent motor inefficiency. With regard to the latter, we can 
reach no complete conclusions without using the stomach-tube. With its aid 
we can determine the amount the stomach contains, and recover ingesta, such as 
cranberries and green-colored vegetables, which have been eaten many days before. 
If we empty the stomach completely and give a test meal, we can gauge more 
accurately the degree of motor insufficiency. We may also determine precisely 
the position, form, and size of the stomach when emptied, by means of inflation. 
In exceptional cases there is a large amount of bile mingled with the gastric 
contents. The author surmises that in such cases the cicatricial process has 
changed the pylorus into a rigid, though narrow, tube, which can neither be 
opened nor closed. Thus we have an " insufficiency " associated with the steno- 
sis of the pylorus, so that no obstacle is opposed to the entrance of bile into the 
stomach. 

When there is a well-marked uncompensated stenosis of the pylorus, there is 
always a decided impairment of the general health. ^Nutrition grows more and 
more imperfect because of the persistent vomiting, and there may be extreme 
emaciation. Still, many patients with stenosis due to ulcer may maintain a 
tolerable condition of health for many years, if they take proper care of them- 
selves by regular washing of the stomach and by eating proper food (vide infra) ; 
but finally, even in such individuals, the symptoms grow worse, or a new trouble 
develops, one of which there is always danger in any case of stenosis due to ulcer. 
We refer to the secondary development of carcinoma at the seat of the former 
ulcer. This happens not infrequently, and is to be considered at length in the 
next chapter. There remain to be mentioned some special symptoms, associated 
with ulcers of the pylorus when they lead to stenosis. There is usually a de- 



440 DISEASES OF THE DIGESTIVE OKGANS 

cided tendency to constipation; the urine is faintly acid and often has an abun- 
dant deposit of phosphates ; the pulse is often remarkably infrequent ; and final- 
ly, there are sometimes attacks of tetany. 

Diagnosis. — The diagnosis can be made only when the above-mentioned char- 
acteristic symptoms are present. Of these, haematemesis is by far the most sig- 
nificant, for it is with very few exceptions the result of gastric ulcer. Particu- 
larly is this true of individuals under middle age. — But how shall we determine 
whether the blood ejected did not come from the nose or the lungs, rather than 
the stomach? The answer is not always easy. If an epistaxis occurs at night, 
a part of the blood often flows back into the naso-pharynx, and, being swallowed, 
excites vomiting, so that a gastric haemorrhage is suggested. 

In doubtful cases we must, therefore, make an accurate examination of the 
nose. It is also very important for the physician to remember that blood may 
be " vomited " in hysterical cases. If there is also nervous cardialgia, one might 
easily be misled to assume the existence of a gastric ulcer. Usually, however, we 
can make sure of the diagnosis by means of the other symptoms of hysteria (see 
the chapter on hysteria), and by examining the "vomited" blood. The latter 
does not come from the stomach at all, but from the gums, the pharynx, or the 
naso-pharynx, and consequently it is almost always comparatively bright red, 
rather fluid, and mixed with mucus and saliva ; and on microscopic examination 
it shows pavement epithelium and micro-organisms from the mouth. 

The diagnosis between gastric and pulmonary haemorrhage in doubtful cases 
depends ' on the following factors : 1. The previous condition of the patient — 
whether he has had cough, expectoration, and other pulmonary symptoms, or, on 
the other hand, gastric pain and vomiting. 2. On the character of the haemor- 
rhage, whether accompanied by vomiting or by cough. But there may have been 
both. Violent vomiting may excite a cough; and, on the other hand, blood 
which has been coughed up may be in part swallowed and induce vomiting. 3. 
On the character of the blood: if from the lungs, it is usually bright -red and 
frothy, containing bubbles of air, with few clots, and of alkaline reaction. In 
gastric haemorrhage it is usually dark, mixed with food, partly clotted, and acid 
in reaction from admixture with the gastric juice. 4. On the results of physical 
examination. In this, of course, we must be extremely cautious after a haemor- 
rhage, lest the movements of the patient excite fresh bleeding; and yet we may 
be able to perceive from the general condition of the patient, or from dullness at 
the apices, or moist rales, that pulmonary disease is probable. If the blood came 
from the stomach, we usually detect nothing but the signs of anaemia. 5. The 
subsequent symptoms. In cases of pulmonary haemorrhage there is almost sure 
to be an expectoration, for the next few days, either of pure blood or of matter 
stained with blood; and, in gastric haemorrhage, the next dejection will almost 
certainly be black, from the presence of decomposed blood. In doubtful cases, 
the appearance of blood in the stools almost invariably settles the question in 
favor of gastric haemorrhage. The best way of testing for blood in the faeces is 
by means of guaiac and turpentine (vide supra). 

If no gastric haemorrhage has ever occurred in the course of the disease, vio- 
lent and persistent gastralgia of the peculiar character above described is that 
symptom which would first arouse suspicion of an ulcer, particularly if the pain 
is from time to time associated with vomiting. If hyperacidity or hypersecretion 
has been demonstrated, this condition in association with other symptoms may 
greatly strengthen the diagnosis. Severe gastric pain, combined with hyper- 
secretion, makes the diagnosis of gastric ulcer very probable. To make an abso- 
lutely certain distinction between ulcer and nervous hypersecretion (q. v.) is 
impossible, if there is no haematemesis. In general, we must remember that it 
is often possible to observe more or less distinct " symptoms of ulcer," without 



GASTRIC ULCER 



being absolutely certain that an ulcer exists. Often we are obliged to await the 
further course of the disease, and particularly the results of treatment, in order 
to settle our doubts. 

The two diseases which it is most difficult to distinguish from ulcer are nerv- 
ous dyspepsia with nervous gastralgia, and carcinoma. When we consider these 
diseases we shall discuss at greater length the differential diagnosis between them 
and ulcer of the stomach. Chlorotic patients, also, often have gastric symptoms 
(see the chapter on chlorosis) which excite suspicion of an ulcer, especially as 
hypersecretion of the gastric juice is often associated with chlorosis. Frequently 
it is impossible to make an absolute diagnosis in these cases, but the results of 
treatment may be decisive. Preparations of iron, particularly Blaud's pills, are 
ill borne in ulcer, while in case of genuine chlorosis they usually cause rapid im- 
provement in the gastric symptoms, as well as in the general condition. 

Prognosis. — The chief dangers in ulcer of the stomach, haemorrhage and per- 
foration, have already been spoken of. Whether these complications will actually 
occur in any individual case, and when, we can not determine. 

There can be no doubt that a large number of ulcers heal perfectly; but, as we 
have already said, even the resulting scar may eause trouble. We must remem- 
ber the possibility of persistent gastric disturbance, particularly cardialgia, and 
also the development of a cicatricial stenosis with its consequences. Finally, we 
have the danger, already mentioned, of the eventual development of carcinoma 
in the scar of an old ulcer. 

Treatment. — If the diagnosis of gastric ulcer is evident, or if the symptoms 
are of such a nature that there is a justifiable suspicion of an ulcer, the patient 
should be urgently advised to submit himself to careful and methodical treat- 
ment ; for it is only by means of a sufficiently persistent and properly conducted 
treatment that we can hope for good therapeutic results in ulcer of the stomach. 

One essential condition is, that the patient should keep his bed for the first 
part of the treatment, at least for three or four weeks. Complete bodily rest is 
certainly important in promoting healing' of the ulcer. The patient should also 
have moist compresses, or, still better, as Leube has advised, warm poultices 
applied all day long to the epigastrium. These applications are very good for 
the pain, and they also have a certain psychological importance, for they reconcile 
the patient to keeping quiet in bed. Thirdly, and this is probably the most impor- 
tant point, the patient must keep strictly to a prescribed diet. This diet we 
are about to describe at length. The main consideration in determining the pa- 
tient's diet is that all mechanical and chemical irritation of the floor of the 
ulcer must be avoided. Fourthly, we should have regard to the almost in- 
variable existence of hyperacidity of the gastric juice. We, therefore, give to 
patients alkaline carbonates, either in the form of Carlsbad water (on waking 
a large glassful of the lliihlbrunnen warmed to about 98.6° F., 37° C; then, in 
the forenoon, between ten and eleven, as much more), or, what we consider in 
many ways still better, bicarbonate of soda (either alone or combined with sub- 
nitrate of bismuth). Of the soda we should give as much as is held upon the 
point of a knife, every hour, so as to keep the gastric juice constantly neutralized. 
With regard to the dietetic treatment of gastric ulcer, the best way is to follow 
Leube's example, and have four diet lists. Beginning with the first, we gradually 
go on at definite intervals of time to the second, third, and fourth. For the 
first ten days of treatment the patient follows the first diet list. This contains 
boiled milk; broth; unsweetened rusks, softened by soaking; to this we may add 
the artificial solutions of meat, particularly that of Leube-Rosenthal. Then, 
during the next week, we have the second diet list, comprising gruel, soft-boiled 
rice and oatmeal, eggs, boiled calf's brain and sweetbread, boiled pigeon and 
chicken. From the eighteenth to the twenty-fourth day of treatment we have, in 



U2 



DISEASES OE THE DIGESTIVE OKGANS 



addition, the third diet, with shavings of raw beef and beefsteak, potato puree, 
boiled calf's feet, and for beverage some tea or weak coffee. Erom the twenty- 
fourth to the thirtieth day the patient has the fourth diet list — that is, broiled 
fowl or pigeon, partridge, venison, roast beef, tenderloin, finely chopped maca- 
roni, and bread. It is understood that with each advance in diet the previous 
diet lists are also permitted. In general, the patient has about five meals a 
day, the amount of each being determined by the appetite and symptoms of the 
patient. If everything goes favorably, the gastric pain will wholly cease after 
a few days of this diet, under the other regulations above enumerated. The pa- 
tient then proceeds toward recovery without any discomfort, except possibly 
hunger. If the transition to a more advanced diet causes pain, we must resort 
for a few days to the simpler foods. In general, the above suggestions must be 
regarded as an outline from which certain variations may be made to suit the 
individual case, yet we may be well assured that the results are better and more 
certain the more strict and methodical the treatment is. If the patient has borne 
the articles of the fourth diet list for about a week without any discomfort he may 
go on by slow degrees to other simple dishes, such as veal, pike, trout, porridge, 
vegetables, and other similar articles, and so to an ordinary diet. Of course, cau- 
tion in eating and drinking is necessary for a long time. 

With the mode of treatment just described, we shall in most cases accomplish 
as much as possible; but if, despite this regimen, the symptoms do not cease, 
there are two other remedies which deserve to be tried — viz., subnitrate of bis- 
muth and nitrate of silver. These are specially employed, also, in treating poor 
persons whose circumstances often render it impossible to carry out strict dietary 
rules. The subnitrate of bismuth is almost always given in combination with 
bicarbonate of soda: of a mixture containing 3 to 5 parts of bismuth and 30 
parts of soda we give several times a day a generous " knife-point full " before 
meals. In severe and obstinate cases of ulcer, we can from our own experience 
recommend also "injections" of bismuth (Fleiner). The patient's stomach is 
washed out in the morning before breakfast, and then 3 iv-v (grm. 15-20) of 
the subnitrate of bismuth suspended in a glass of warm water is poured slowly 
into the stomach-tube; the patient should at the same time lie on his right side, 
and so remain for at least half an hour. The heavy bismuth powder is expected 
to deposit itself upon the surface of the ulcer (which is probably in the pyloric 
portion of the stomach), and thus in a mechanical way protect it from irritation 
and promote its healing. The symptomatic results of this method are sometimes 
excellent. Often, also, favorable results are obtained from nitrate of silver. This 
may be partly explained by its neutralization of the hydrochloric acid, and the 
formation of chloride of silver. The drug is prescribed in a solution of six grains 
to four ounces of water (gram. 0.3-120), to be kept in opaque glass, and of this a 
teaspoonful should be given three or four times a day before meals. 

Sometimes the violent pain does not abate under the ordinary treatment, and 
demands symptomatic remedies. Of course, morphine is the most efficient, given 
internally or subcutaneously. Chloroform may also be triced: we give a table- 
spoonful of a mixture containing 1 part to 120 of water. Gerhardt recommends 
for the gastric pain 3 or 4 drops of the solution of perchloride of iron in a wine- 
glass of water. 

Excessive vomiting and persistent nausea are likewise to be combated by the 
narcotics. Opium is the best; morphine, cocaine, chloral, and bromide of potas- 
sium may also be tried. At the first appearance of blood in the vomitus the great- 
est bodily quiet and most careful dieting is absolutely indispensable. For the first 
day or two it is best to allow nothing except ice-cold milk and bits of ice in the 
mouth to appease the burning thirst. In severe cases we may try giving water 
and milk by the rectum, so as to afford the stomach complete rest. The patient 



GASTKIC ULCER 



443 



must lie as quietly as he can. A flat ice-bag, not too heavy, should be placed on 
the epigastrium. In case of persistent nausea or eructations, small doses of 
opium or morphine are to be prescribed. If the haemorrhage is obstinate we may 
try the subcutaneous injection of ergotine, or, by mouth, acetate of lead or chlo- 
ride of iron. We must wait four or five days after a haamorrhage before we can 
give a little more food by the mouth, and this must be allowed cautiously and in a 
liquid form. 

If peritonitis appears as the result of perforation, the best means to try are 
the outward application of ice to the epigastrium and the internal use of opium 
in large amounts — that is, half a grain to a grain (grm. 0.03-0.05) every two or 
three hours, or twenty to thirty drops of laudanum. Unfortunately, however, 
the cases are exceptional in which the peritonitis does not become general. The 
only remaining hope lies in surgical interference, although the results even of 
laparotomy are dubious. 

If the symptoms of pyloric stenosis are growing more and more distinct — ■ 
that is, if the hypertrophied muscular coat of the stomach is no longer vigorous 
enough to prevent the stagnation of food, with consequent dilatation of the stom- 
ach and vomiting, we can perhaps restore the patient to a comfortable condi- 
tion by means of regular washing out of the stomach, combined with a suitable 
diet. This irrigation prevents any great and burdensome accumulation of food 
in the stomach. Moreover, it rids the patient, for a time at least, of the large 
amount of strongly acid gastric juice which is usually present. These beneficial 
and agreeable effects are soon so noticeable that often the patient learns to rinse 
out his stomach himself, or even, by bending over and pressing, to empty out the 
gastric contents through the tube. As a rule, in cases of gastrectasia resulting 
from pyloric stenosis, we wash out the stomach every morning before breakfast. 
Ordinary lukewarm water suffices, but if there is an excessive secretion of hydro- 
chloric acid it is satisfactory to employ 1- or 2-per-cent. solutions of bicarbonate 
or borate of sodium. In severe cases the operation may be repeated in the even- 
ing before supper. 

The diet in stenosis following ulcer should consist of such articles of food 
only as can pass with comparative ease through the narrow pylorus, being at the 
same time highly nutritious. Most suitable are milk, eggs, soups with the addi- 
tion of meat-juice, somatose, oatmeal, rice, or flour; gruel made from rice, oat- 
meal, or preparations like Mellin's food; and finally, finely chopped meat of all 
sorts. The meals should not be too large, but should rather be frequently re- 
peated — a little food often. 

In this way it is often possible to give the patient considerable relief for 
many years, and even to make him gain weight. Other methods of treatment 
— by applying electricity to the stomach, by cautious massage of the organ, or by 
the administration of strychnine — may be employed now and then in practice, but 
they have no special value in actual stenosis. 

It may well be questioned whether the existence of such patients, who are 
preserved from excessive discomfort only by means of daily lavage and a monot- 
onous and limited diet, is really bearable ;- and, still further, what are we to do 
when, in spite of the most skillful treatment by the method described, the symp- 
toms persist and the nutrition and strength of the patient grow gradually more 
and more impaired? For such there is still the possibility of actual and com- 
plete recovery. We refer to surgical intervention. In no other severe disease 
of the stomach do operative procedures offer so great a prospect of favorable 
result as in stenosis of the pylorus following ulcer, and therefore it has been our 
rule for a series of years, in every severe case of this sort, to urge the patient 
strongly to an operation. Moreover, we should not delay too long, if the patient 
is already enfeebled, or if there is reason to suspect that carcinoma is developing. 



4M 



DISEASES OF THE DIGESTIVE ORGANS 



The operation is usually gastroenterostomy, or sometimes pyloroplasty; but we 
can not enter here into particulars. Certainly we ought not to conceal from 
the patient that we have to do with a serious operation, which is not absolutely 
without danger; yet in the great majority of cases the results of treatment are 
excellent. After a successful operation the patient is freed from all discomfort, 
he regains the appearance of health, and sometimes even the dilatation of the 
stomach completely disappears. It is true that later, perhaps years later, re- 
lapses may occur, whether because of special mechanical conditions or from the 
development of secondary carcinoma; but even then perhaps assistance will be 
given by a second operation. 

[In cases of recent haemorrhage or markedly painful digestion, the editor has 
pursued the following plan of treatment with apparently good results : The most 
powerful agent in the promotion of cicatrization is rest. Absolute rest in bed is 
therefore enjoined, with the secondary end in view of reducing the demands of 
the system. The patient is then fed exclusively by the rectum for at least one 
week, generally for two weeks, nothing but a little water being given by the 
mouth. A simple cleansing enema is given once daily; and at six-hour intervals 
a nutrient enema, six to eight ounces in bulk,, and composed of one or two raw 
eggs, an ounce of expressed beef juice, and fully peptonized milk, is administered. 
Tolerance by the rectum is promoted by the addition to the enema of a few drops 
of laudanum. After one or two weeks small quantities of milk at frequent inter- 
vals are given by the mouth, and the rectal alimentation is gradually diminished 
as that of the stomach is increased. Pain usually ceases immediately on the 
cessation of gastric ingestion, and the loss of weight during a fortnight of rectal 
feeding is surprisingly small.] 



CHAPTER VI 
CANCER OF THE STOMACH 

Etiology. — We can not here discuss the aetiology of carcinoma in general, 
and we shall therefore merely enumerate the factors which experience has shown 
to favor the development of cancer in the stomach. 

Age has a remarkable influence. Gastric cancer is decidedly most frequent 
late in life, between the fortieth and sixtieth year. Still it is occasionally seen 
in younger persons. We have ourselves seen several cases in persons between 
twenty-two and twenty-five years of age. 

Sex is of no importance. 

Heredity has a slight but undeniable influence. The most famous example of 
the transmission of cancer is presented by the family of Napoleon. 

The relations of gastric cancer to previous disease of the stomach is very 
important. It is not probable that the tendency to cancer is increased by fre- 
quent errors in diet, indulgence in alcohol, or similar causes, Most of those who 
are attacked by gastric cancer have previously lived in a perfectly temperate man- 
ner, and report that they have thus far always enjoyed a good digestion. The 
exception is to discover that there has been any special injury or trauma, such as 
scalding or corrosive poisoning, and if there is a history of them they are to be 
regarded as merely contributory causes. Far more important, however, is the fact 
which the investigations of Hauser have lately confirmed, that gastric carcinoma 
is not infrequently developed in the cicatrized edges of a previous gastric ulcer. 
We have ourselves had a considerable number of cases in which both the clinical 
course of the disease and the results of the autopsy illustrated this mode of devel- 
opment. 



CANCEK OF THE STOMACH 



445 



Pathology.- — The stomach is a favorite seat for cancer. About a third of all 
cases of cancer are gastric. The parts of the organ most often attacked are the 
pyloric end and the lesser curvature. Less frequently the cardiac end and the 
fundus suffer. 

The new growth takes the form either of a circumscribed tumor or of a diffuse 
infiltration, thickening the walls. The disease invariably originates in the mu- 
cous layer, extending thence into the submucous, muscular, and serous coats. 
Often the cancer extends by way of the lymph-channels, or sometimes the veins. 
The lymph-glands and the omentum are frequently attacked by the new growth. 
Moreover, we find metastases in the peritoneum, and also with particular fre- 
quency and abundance in the liver, whither cancerous cells are carried by the 
branches of the portal vein. The connective and muscular tissues in the neigh- 
borhood of the cancer are quite often considerably hypertrophied. 

Histologically, gastric cancer is of the cylindrical-cell variety, starting from 
the glandular epithelium. The soft tumors are termed medullary; the firm and 
hard, scirrhous or fibroid. The medullary cancers are particularly apt to be 
quite extensively broken down on their exposed internal surface, thus forming 
what are known as cancerous ulcers. This seems to be mainly the result of the 
gastric juice acting on the superficial and insufficiently vascularized portion of 
the tumor. The base of these ulcers is usually clean, as we should expect from 
the mode of their production. In many cases of rather young subjects, and some- 
times in others, we find colloid cancer. This form also may appear either in nod- 
ules or as a diffuse growth, infiltrating the tissues. It is peculiarly apt to involve 
the peritoneum extensively, with consequent ascites. 

Clinical History. — Most cases of gastric cancer exhibit a combination of 
grave digestive disturbances with a relatively rapid loss of flesh and strength. 
Now and then the gastric symptoms assume less prominence. The chief sign of 
disease is a constantly progressive marasmus or ansemia, the true cause of which 
is either entirely latent or not unmistakably recognizable till late in the illness. 

Some of the gastric symptoms are not very characteristic. They merely show 
that digestion is disordered. The tongue is usually thickly coated and dry. 
There is loss of appetite and distress after meals. The patient complains of a 
disagreeable sensation of pressure in the epigastrium, increased by food. Some- 
times this amounts to actual cardialgia. Many patients are annoyed by eructa- 
tions. Occasionally vomiting is troublesome ; in other instances there is scarcely 
any. The constant recurrence of vomiting is an almost sure sign that the cancer 
is situated in the pyloric region and obstructs the orifice. The vomitus may con- 
tain nothing but mucus and ingesta; or it may assume, from the admixture of 
blood, a very characteristic and somewhat pathognomonic appearance. 

Free gastric haemorrhage and consequent hsematemesis is exceptional, or at 
least it is much less frequent than in ulcer of the stomach ; but the vomitus often 
contains decomposed blood, and in many cases this will be for a time almost a 
constant appearance. Most of the ulcerated cancers bleed frequently, a little at 
a time. When it reaches the stomach the blood is decomposed and gives that 
well-known " coffee-grounds," or " chocolate-colored " appearance to the vomitus, 
or to the gastric contents obtained by means of a stomach-tube, which is so im- 
portant a symptom for the diagnosis of cancer of the stomach. In such cases 
the best means for demonstrating the presence of blood, in the brownish or black- 
ish fluid, is the guaiac-turpentine test (vide supra, page 422). This gives an 
extremely distinct reaction in the case of carcinoma of the stomach, because 
lactic acid also is usually present. We should mention that in the case of ulcer- 
ating carcinoma ventriculi the vomitus may have so foul an odor that it may 
even be regarded as stercoraceous. 

Immediate microscopic examination of the vomitus may reveal red blood- 



U6 



DISEASES OF THE DIGESTIVE ORGANS 



globules. Further, the vomittis consists of partially digested food, and also con- 
tains an abundance of micro-organisms. Sarcinse are found much less often in 
carcinoma than in ulcer of the stomach, but we frequently see under the micro- 
scope an abundance of yeast cells, and of long threadlike bacilli which perhaps 
have a relation to lactic-acid fermentation. It is extremely rare to find in the 
vomitus characteristic particles of cancer. It is somewhat less unusual to find 
little pieces of the growth attached to the stomach-tube, when the carcinoma is at 
the cardiac end or in the fundus of the stomach. These, if obtained, are of 
course to be submitted to microscopic examination. 

The external examination of the stomach should always be made when the 
patient is lying flat on his back. Sometimes we can clearly recognize by mere 
inspection the position and size of the organ, any peristaltic motions (vide 
infra) that there may be, and even in some cases the presence of a tumor. Pal- 
pation is, however, more important. In a great many cases the new growth can 
be felt with distinctness through the abdominal wall as a hard irregular tumor. 
Its situation is, in a majority of cases, the epigastrium. Carcinoma of the 
pylorus, which is the most common, is usually felt in the right half of the epi- 
gastrium; carcinoma of the greater curvature somewhere in the level of the 
navel. But it should be considered that the position of the stomach may be con- 
siderably altered by the presence of a growth — for example, we have seen a case 
of pyloric cancer with secondary dilatation of the stomach, in which the pylorus 
had sunk so low that the tumor could be felt about a hand's breadth above the 
symphysis. In some cases the tumor varies its position (vide infra) according 
to the degree of distention of the stomach. The influence of respiration upon the 
tumor is various. As a rule, cancer of the pylorus does not change its place 
much with respiration, unless it is adherent to the liver. Carcinomata of the 
lesser and greater curvatures usually do move with respiration; and when dis- 
placed downward they may be held in that position with the hand, returning to 
their ordinary location when the hand is removed. Tumors of the liver and 
cancers of the stomach which are adherent to the liver can not be thus held down. 
When the carcinoma is situated high up, in the lesser curvature or near the 
oesophagus, it may not be felt at all except during inspiration. 

In a minority of the cases no tumor can be felt at any time. This is true in 
most instances of diffuse cancerous infiltration of the walls of the stomach. "Under 
such circumstances the diagnosis can not often be definitely established. The 
tumor is undiscoverable, first, in most cases of diffuse cancerous infiltration of 
the stomach-walls. We may, indeed, notice an increased sense of resistance and 
hardness in the epigastrium, but we can not refer this condition with certainty to 
a new growth. Secondly, the new growth may extend chiefly inward, toward the 
cavity of the organ, and may thus escape detection. And, finally, the tumor 
may be so concealed by the liver or the edge of the ribs that it is inaccessible to 
the touch. Such cancers as attack the cardiac extremity, the posterior wall, or 
the lesser curvature of the stomach, are particularly apt to be out of reach of 
palpation. 

Percussion of the cancer rarely gives flatness, but instead a muffled tym- 
panitic resonance. This is sometimes an influential factor in the differential 
diagnosis from cancer of the liver. In a few cases, upon auscultation in the 
neighborhood of the tumor, we may hear a soft systolic murmur, probably clue 
to compression of a rather large artery. 

The examination of the gastric contents is of the greatest diagnostic impor- 
tance. While introducing the stomach-tube, or perhaps, if need be, a less flex- 
ible instrument, we should notice whether the tube enters the stomach with 
ease. Carcinoma at the cardia is not infrequently the cause of a sensible resist- 
ance to the tube when it passes the lower end of the oesophagus. With regard 



CAISTCEE OF THE STOMACH 



to the examination of the gastric contents, the chief point is about free hydro- 
chloric acid. Yon der Yelden first pointed out what numerous investigations 
have since confirmed, that in almost all cases of gastric carcinoma there is no 
free hydrochloric acid, so that the phloroglucine-vanilline reaction an hour after 
the test breakfast is negative. Associated with other symptoms this is an ex- 
tremely important diagnostic sign (vide infra). The cause of this almost invari- 
able absence of free hydrochloric acid in carcinoma of the stomach has not yet 
been determined, especially as this symptom has often been observed very early in 
the course of the disease. The associated catarrh of the gastric mucous mem- 
brane and its secondary atrophy may have some influence, but probably there 
are also other unknown causes at work. An examination for pepsine may be 
omitted in practice: it also often turns out negative. Far greater importance 
attaches to the fact that the gastric contents in carcinoma are very apt to show 
a surprising amount of lactic acid. This is almost invariably so when the car- 
cinoma obstructs the pylorus. The explanation of this is very simple. There is 
no hydrochloric acid to exert an antiseptic action, and the food is stagnant in 
the stomach, so that there is an especially favorable opportunity for the develop- 
ment of a vigorous lactic-acid fermentation. There is, then, nothing specific 
about the presence of lactic acid in the gastric contents in cases of carcinoma, 
only it is a very frequent and therefore not unimportant symptom. 

The motor efficiency of the stomach is impaired in most cases of carcinoma, 
except in cancer affecting the cardia, or in small cancers on the fundus. When- 
ever there is an extensive development of carcinoma of the stomach, the muscu- 
lar coat of the organ is sufficiently damaged to embarrass its motor activity; 
but of course the hindrance to the discharge of its contents is greatest when the 
new growth is at the pylorus. In this case, besides the direct destruction of the 
muscular tissue, we have the purely mechanical stenosis, and this may at last 
become extreme. For this reason, if we find a marked stagnation of the ingesta 
we can usually infer that the seat of the carcinoma is the pylorus (vide infra). 
We should not omit to inflate the stomach when it is possible. We can thus 
determine not only the size and position of the stomach, but also its relations to 
any tumor that may be felt ; and finally, it should be added that a test for blood 
(vide infra) should be made with the fluid obtained by washing out the stomach. 

Certain peculiarities in the clinical picture of gastric carcinoma are occa- 
sioned by its special location ; if at the cardia, the symptoms are similar to those 
of cancer of the oesophagus. As soon as the cardia is narrowed, the patient 
himself feels that it is difficult for food to enter the stomach, and speedily there 
appears vomiting, or, more accurately, regurgitation of food, so that the patient 
can take nothing but liquid nourishment. The diagnosis of carcinoma at the 
cardia is usually easy. We feel the resistance at the cardia with the stomach- 
tube some 16 to 18 inches (40-45 centimetres) from the front teeth. Externally 
the growth can not be felt until it invades the lesser curvature of the stomach. 
Then we often feel the tumor in the epigastric angle, especially on deep inspira- 
tion. In carcinoma of the fundus the symptoms may be indefinite for a long- 
time. The pylorus remaining permeable, there may be no vomiting at all. In 
late stages the tumor which may be felt is often very large, particularly if there is 
involvement of the omentum, which changes it into a great cancerous mass. 

When cancer at the pylorus leads to stenosis, the clinical picture is especially 
important as well as very common and very characteristic. As soon as there is 
a hindrance to the emptying of the stomach, whether because the muscular coat 
is impaired by infiltration with carcinoma or because there is the direct mechan- 
ical obstacle of stenosis, there result retention and accumulation of food in the 
stomach, with exaggerated peristalsis, and finally gastric dilatation. The cir- 
cumstances are precisely similar to those depicted in the preceding chapter when 



us 



DISEASES OF THE DIGESTIVE OKGANS 



speaking of cicatricial stenosis (cf. page 438). In advanced cases the contours 
of the dilated organ are clearly seen through the emaciated and collapsed abdom- 
inal walls. From time to time a contraction occurs, and we see the peristaltic 
wave slowly travel toward the pylorus. Very often the carcinomatous growth 
near the pylorus is distinctly palpable, and even visible. Often it moves with 
respiration. Washing out the stomach will demonstrate the stagnation of its 
contents, and by inflation we determine its size and position. If the stomach 
is not emptied artificially, from time to time very large amounts are vomited, the 
vomitus being invariably devoid of hydrochloric acid but containing much lactic 
acid, and sometimes also showing fermentation. If we let some of the gastric 
contents, obtained by vomiting or through the tube, stand in a glass vessel, it 
divides into layers. If fermentation has set in, a foamy layer is formed on top. 

We have now enumerated the symptoms of gastric cancer, referable to the 
stomach itself. The greatest attention should also be paid to the general dis- 
turbance of nutrition occasioned by this gastric disease. Loss of flesh is not 
rarely the very first symptom which calls the patient's attention to his disease. 
This wasting is observed earliest in cases which are attended with anorexia and 
vomiting-. The patient also gradually takes on that familiar sallow cachectic 
look which is characteristic of most cases of cancer. Some patients- become ex- 
cessively anaemic. The skin acquires a waxy pallor, and there are all the symp- 
toms which result from gTeat anaemia, such as cerebral disturbances and func- 
tional cardiac murmurs. Sometimes the blood itself presents decided peculiar- 
ities in such cases. Thus we may find microcytes and poikilocytes in it. Gas- 
tric cancer and pernicious anaemia (q. v.) have been repeatedly confounded. 
In one such case we made the interesting discovery of extremely abundant meta- 
static cancer in the bones. As the bone marrow is known to have something to 
do with the production of the blood, it may be that the anaemia was due to this 
abnormal condition. At any rate, the grave anaemia which results from cancer 
can not be regarded in just the same light as the loss of flesh and the cachexia. 
We often find extreme anaemia in patients who are tolerably well nourished, 
while, on the other hand, many patients with carcinoma, though emaciated 
to a skeleton, do not display this peculiar anaemic pallor. The anaemia 
must, therefore, depend upon some special circumstances. Probably it is most 
frequently caused by continued though small haemorrhages, due to ulceration of 
the new growth. 

Special derangements of other organs are relatively infrequent. Metastatic 
cancer is of importance. It attacks the liver chiefly. If the hepatic new growth 
is considerable, it may quite overshadow the primary cancer — there being jaun- 
dice and a greatly enlarged, nodular, and tender liver. Secondary carcinosis 
of the peritonaeum is also apt to cause marked symptoms, such as ascites and 
abdominal pain. Secondary cancer may also involve the mesenteric and retro- 
peritoneal lymph-glands, the lungs, and other organs, but it does not usually give 
rise to striking symptoms when so situated, although the discovery of even small 
metastases by palpation may have great diagnostic significance. Older plrysi- 
cians frequently mention the occurrence of swollen lymph-glands above the left 
clavicle, but we have scarcely ever found them there, although we have paid 
special attention to this point. Swelling of the inguinal glands is more impor- 
tant. We have seen small metastases in them several times. Finally, we would 
like to call special attention to the appearance of small secondary nodules at the 
navel, a fact which we have repeatedly noticed. The discovery of such a growth 
is of great diagnostic value when no primary tumor can be made out by palpation. 

Direct extension of the new growth into neighboring organs is not very fre- 
quent. We will venture to mention one case which we saw, on account of its 
great rarity. The new growth caused adhesion of the anterior wall of the stom- 



CANCER OF THE STOMACH 



449 



ach to the abdominal wells, and then, penetrating through them and the skin of 
the epigastrium, finally appeared as a tumor, of about the size of one's fist, pro- 
jecting outward. If a cancer ulcerates, it may destroy all the layers of the 
stomach, and result in perforation and secondary peritonitis; or, if previous 
adhesions have been formed, the perforation may open up an abnormal communi- 
cation between the stomach and some neighboring part of the intestine. The 
transverse colon is the part usually perforated; less often the small intestine. 

As to the bowels, constipation is the rule. Diarrhoea is rare. The urine is 
usually pale and but slightly acid. Its amount is diminished, as we should expect 
from the slight amount of nourishment taken, and from the vomiting. Over the 
heart we may sometimes hear soft anaemic murmurs. The pulse is usually accel- 
erated, although, if there be extreme marasmus, it may be sloWo 

The temperature is often normal. If the patient is greatly emaciated it is 
not infrequently subnormal, but, on the other hand, if the thermometer is care- 
fully used we shall very often find occasional irregular elevations of temperature, 
100.5°-102° (38°-39° C), or even a persistent or intermittent fever. The cause 
of these elevations, exclusive of complications, is probably, in most cases, the 
absorption of septic material from the ulcerated surface of the carcinoma. If 
there are haemorrhages, another factor may be the absorption of the decomposed 
blood (fibrine ferment). Not infrequently, in advanced stages of the disease 
there is more or less oedema of the ankles, hands, and other parts. The explana- 
tion of this is the same as in most cases of oedema in cachectic and anaemic 
patients — viz., the impaired nutrition of the vascular walls, the hydraemia, and 
the associated cardiac weakness. Sometimes there also occur marked pains in 
the arms and legs. The temperature is normal, or even subnormal. If there is 
some inflammatory complication, or if the anaemia is extreme, fever may occur. 

The entire duration of the disease may be one or two years. It is excep- 
tional for it to last longer, except when the cancer develops in the floor of a pre- 
existing ulcer. In this case the symptoms of gastric ulcer pass into those of 
carcinoma. The change may be gradual, but there may be an intervening period 
of apparent health. We have by careful questioning repeatedly been able to 
make the diagnosis of this transformation during the life of the patient, in cases 
later confirmed by autopsy. In individual instances the disease, of course, exhib- 
its many variations and departures from the typical course. Sometimes the con- 
stitutional symptoms of weakness and emaciation are more prominent, and some- 
times the distinctively gastric disturbances. 

The fatal termination is usually preceded by the symptoms of constantly in- 
creasing weakness. It may be hastened by complications, such as perforative 
peritonitis. Now and then grave nervous symptoms appear, often quite sud- 
denly. The patient falls into a condition resembling that of diabetic coma 
(q. v.), he is somnolent, and has a peculiar dyspnoea, with deep and labored res- 
pirations. Such an attack is probably due to auto-intoxication, and almost 
always ends fatally. Recovery from cancer of the stomach is unknown. 

Diagnosis. — Gastric cancer is a comparatively frequent disease, and in every 
case in which there are well-marked gastric symptoms, particularly in an elderly 
person, the physician should think of the possibility of this grave disease. The 
suspicion is all the more justified when the symptoms occur in a previously 
healthy individual without known cause, and if they are associated from the 
start with a cachectic look and a feeling of weakness and languor, as well as 
with marked emaciation. If now, having such suspicions, we wish to reach a 
diagnosis, the first requirement is a thorough investigation of the stomach. 
External examination should be particularly directed to the discovery of a pal- 
pable tumor, if any exists. We should examine while the patient is lying on his 
back or on his side. If possible, the stomach should be empty and we should 
29 



450 



DISEASES OE THE DIGESTIVE OBGANS 



palpate while the patient is breathing quietly, and also while he is taking deep 
inspirations. If a tumor can be felt, the next question is whether it actually 
arises from the stomach, or from some other organ. In most cases the other 
clinical symptoms, such as vomiting, have already indicated the stomach as tho 
seat of the disease, and thus we know the origin of the tumor. On the other 
hand, however, there may be great obscurity, and many cases of gastric tumor 
have been confounded with carcinoma of the left lobe of the liver, the pancreas, 
the omentum, the transverse colon, and other parts. It is difficult to lay down 
special rules for diagnosis, because the difficult cases almost invariably have their 
own special peculiarities. Of importance in every case are an accurate local 
examination, a mapping out of the neighboring organs, inflation of the stomach 
and perhaps also of the colon, determining whether the mass moves with respira- 
tion, and a consideration of all the other factors. Among these last the most 
important is the result of an examination with the stomach-tube. The main 
question in every case is the presence or absence of free hydrochloric acid in the 
gastric juice. If it is absent on repeated examination our suspicion of carcinoma 
is confirmed, provided the other symptoms point in the same direction ; but if they 
do not, the absence of free hydrochloric acid is by no means so grave a matter, for 
it is absent often enough under other circumstances. It is, however, a fact of 
great practical importance that when free hydrochloric acid has been distinctly 
and repeatedly demonstrated in the gastric juice, we can usually absolutely 
exclude gastric cancer, even if other symptoms point to it. If there is no free 
hydrochloric acid, but lactic acid, and also impaired motor efficiency, the cir- 
cumstances are different. In such a case, even if no tumor can be felt, there 
is great probability of a gastric carcinoma, probably involving the pylorus. An- 
other very important point is the demonstration of blood in the gastric con- 
tents (vide supra, page 422). If we have distinct "coffee-ground" vomitus, and 
at the same time achlorhydria, these factors alone almost establish the diagno- 
sis, but even smaller amounts of blood obtained by lavage are important. Final- 
ly, we should bear in mind that when no gastric tumor is made out there may 
be metastatic growths which can be felt — for example, in the lymph-glands — and 
thus a diagnosis of cancer confirmed. 

In case of symptoms which indicate stenosis of the pylorus, with subsequent 
gastrectasia, it is of great practical importance to determine whether they are 
due to cancer or to the scar of an ulcer. In this instance, even if we feel a 
tumor, that fact is not decisive, for the cicatricial hyperplasia of gastric ulcer 
may cause a distinct tumor; but, as a rule, it is not difficult to reach a decision. 
Suggesting a scar from ulcer would be : long duration of the disease (two years, 
sometimes four or five years, and longer) ; youth of the patient ; comparatively 
healthy appearance; distinct history of ulcer; cardialgia; profuse hsematemesis ; 
and finally, as a decisive factor, the demonstration of an abundance of hydro- 
chloric acid and hypersecretion in the stomach. Under these circumstances the 
differentiation of stenosis from ulcer is absolutely certain. On the other hand, 
there is complete certainty of a cancerous stenosis if the disease has developed in a 
comparatively brief time — in one or two years ; if it has attacked an elderly per- 
son; if there is distinct cachexia; and, most important of all, if hydrochloric 
acid is never demonstrable in the gastric contents, while there is an abundance 
of lactic acid. Other cases occur which are not typical and of easy diagnosis. 
Age, duration of the disease, and previous symptoms may suggest a stenosis due 
to ulcer, and yet on washing out the stomach we find no hydrochloric acid at all, 
or, at most a faint trace. In these cases we are usually justified in assuming 
that carcinoma has developed secondarily on the floor of a former ulcer. It 
must be confessed that in simple stenosis following ulcer, when there is an 
excessive stagnation of the gastric contents, there may be temporarily a com- 



CANCER OF THE STOMACH 



451 



plete combination of all the hydrochloric acid with albumen, and consequently 
no reaction for free hydrochloric acid; but if the stomach is washed out a few 
times we soon find an abundance of free hydrochloric acid. On the other hand, 
when a stenosis due to ulcer has lasted for a long time, our suspicions should be 
aroused if the reaction for hydrochloric acid is persistently feeble or at times 
absent, and in its place or along with it lactic acid appears in the gastric con- 
tents. We have ourselves repeatedly seen this gradual transition of simple 
stenosis, due to ulcer with hypersecretion, into carcinomatous stenosis with 
achlorhydria. Finally, it should be remarked that there is also a stenosis of the 
pylorus due to simple hypertrophy of its walls, without any ulcer or carcinoma. 
We have ourselves seen a few cases of this sort, which presented the ordinary 
symptoms of pyloric stenosis with great dilatation, and ended fatally. The 
pathogenesis of this rare condition has not yet been explained. We venture to 
suggest that perhaps it may be due to congenital anomalies. As yet, unfortu- 
nately, no particulars are known as to the constituents of the gastric juice in 
these cases, and for the present it is scarcely possible to make a diagnosis of 
them with certainty. 

Treatment. — If once the diagnosis of gastric carcinoma has been settled, the 
question arises whether there is any definite prospect of success from surgical 
treatment. If not, our treatment can be merely symptomatic with the object 
of alleviating the patient's suffering, and preserving his strength as long as 
possible. 

The first point in symptomatic treatment is a regulation of the diet. In gen- 
eral, we advise mainly liquids and soft foods, including milk, gruel, rice, sago, 
delicate vegetables, potato puree, softened zwieback, toast, or water-crackers, 
and delicate puddings. We may also permit finely chopped or scraped meat, or, 
still better, fowl; and fish, such as trout, pike, and perch-pike. Such artificial 
foods as somatose, neutrose, beef peptone and beef juice, and infants' foods, do 
good service for a time. If the appetite fails we order stomachics — for exam- 
ple, compound tincture of cinchona. The fluid extract of condurango deserves a 
special mention, and has been a favorite prescription in gastric carcinoma since 
condurango bark was recommended by Friedreich. We usually prescribe hydro- 
chloric acid after meals (15 to 20 drops of the dilute acid in water) in the hope 
of making up for the achlorhydria. Pain is alleviated by narcotics, such as mor- 
phine, opium, codeine, belladonna, and chloroform, and by moist warm or cold 
applications. Warm poultices on the epigastrium for several hours a day are 
usually beneficial. To combat obstinate vomiting we may give the narcotics 
just named or bits of ice, but the best remedy is rinsing out the stomach, pro- 
vided the patient is not too feeble. If there are sour or offensive eructations, 
we prescribe bicarbonate of soda, magnesia, or powdered charcoal. If the pyloric 
cancer is leading to stenosis with stagnation of food in the stomach, the daily 
washing out of that organ is an excellent means of relieving the patient for a 
time, at least, of a great part of his discomfort. If this is practiced regularly 
with either pure water or a 1- or 2-per-cent. solution of hydrochloric acid, and 
if the diet is suitable, there may be a great temporary improvement in the condi- 
tion and even a not inconsiderable gain in weight. But, despite all our efforts, 
the symptoms may become worse and worse till, finally, the subcutaneous injec- 
tion of morphine may be indispensable. Then our whole object is to alleviate 
the patient's sufferings, and to give him moral support and encouragement. 

When the vigor of the patient is such as to permit the consideration of surgi- 
cal interference, the more promptly the operation is undertaken the more chance 
is there of eradicating the disease and obtaining permanent recovery. It is, 
therefore, permissible when there is incipient disease and the diagnosis is not 
yet fully established, although somewhat probable, to propose to the patient an 



452 



DISEASES OF THE DIGESTIVE ORGANS 



exploratory laparotomy, to be immediately followed by a regular operation, pro- 
vided the case turns out to be a suitable one. The results of operations on car- 
cinoma of the stomach have not been very brilliant. Still, in many cases the 
surgeon is fully justified in endeavoring to combat an otherwise absolutely hope- 
less disease, since there is some prospect of recovery. Although there have been 
many failures, surgeons have obtained a number of extremely satisfactory recov- 
eries under these circumstances. If there is a stenosis of the pylorus and yet 
it is no longer possible, or at least no longer wise, to extirpate the tumor, gastro- 
enterostomy may give very great relief. If the patient survives the operation, 
the suffering is much diminished and nutrition may decidedly improve. For the 
particulars we refer to surgical treatises. 



CHAPTER VII 

ANOMALIES OF THE SECRETION" OF GASTRIC JUICE 

{Achylia Gastrica and Hypersecretion of the Gastric Juice) 

In the present chapter are to be considered those dyspeptic conditions which 
are associated with a change — that is, either a diminution or an increase — in the 
secretion of the gastric juice, independently, at least in most cases, of any defi- 
nite anatomical lesion. We have here to consider, therefore, no marked catar- 
rhal condition or new growth of the stomach, nor gastric ulcer with hypersecre- 
tion. The cause of the change in secretion in the cases here considered must 
rather be sought in the disturbances of the activity of the cells, the special occa- 
sion of which is as yet almost entirely unknown. Many clinical observations, it 
is true, indicate that abnormal nervous influences are important in this con- 
nection, but, on the other hand, it is possible that the explanation lies in primary 
changes in the minute structure and chemistry of the secreting cells themselves. 
Besides this uncertainty of aetiology, there is also an absolute lack of thorough 
anatomical investigations in this regard, so that it is at present a very difficult 
matter to map out and depict accurately these abnormal conditions. We must, 
therefore, limit ourselves preliminarily to a simple statement of the clinical facts 
thus far known, and present, as well as we can, the leading points of view for 
the interpretation and treatment of these groups of symptoms. 

1. Anacidity of the Stomach (Achlorhydria). — Achylia Gastrica. — Fen- 
wick was the first to observe that there are cases of chronic and complete ab- 
sence of any demonstrable secretion of gastric juice, independently of chronic 
gastritis or gastric carcinoma, but associated with an almost complete atrophy 
of the glandular apparatus of the gastric mucous membrane. The clinical pic- 
ture in these cases displayed scarcely any marked gastric symptoms. Anorexia 
and moderate oppression after eating were almost the only indications of dys- 
pepsia; but there were observed gradually progressive anaemia and emaciation, 
so that finally the general weakness, independent of any other local symptoms, 
resulted in death. Since then we have learned, particularly from the investiga- 
tions of Martius, that the grave symptoms of these cases can not possibly be 
caused by an atrophy and cessation of function of the gastric glands alone, but 
occur only when there is also present an atrophy of the intestinal mucous mem- 
brane. 

It has been shown, and we have ourselves repeatedly found, that it is possible 
to have an achylia gastrica — that is, persistent absence of hydrochloric acid 
(and pepsine, vide infra), without any noticeable disturbance of nutrition, and 



ANOMALIES OF THE SECKETION OF GASTKIC JUICE 453 



with only slight and fugitive dyspeptic symptoms, or even with no gastric symp- 
toms whatever. In all these cases it is wholly probable that the digestion and 
absorption by the intestines are perfectly normal, and completely replace the 
digestive function of the stomach. It is only requisite that the intestines should 
preserve their normal function, and that the motor power of the stomach should 
be unimpaired. In such cases the stomach serves to a certain degree merely as a 
reservoir for the ingested food, which it duly passes on to the intestines; in 
them are present in abundance all the reagents, bile, pancreatic juice, and intes- 
tinal juice, requisite for the further absorption of the ingesta. There is only 
one defect in these persons with achylia gastrica : there is no disinfection of the 
gastric contents by means of the hydrochloric acid of the gastric juice. Ordi- 
narily this lack is unimportant, but if any hurtful material reaches the stomach 
it is more likely to lead to disturbance than under normal conditions. This 
explains why those persons with achylia gastrica have a " sensitive " stomach and 
are prone to suffer from temporary dyspepsia. They very often also have a 
striking tendency to diarrhoea. But if such individuals live cautiously and are 
not exposed to any especial injurious influences, they feel perfectly well and may 
be extremely well nourished. 

Is there an atrophy of the gastric mucous membrane as a foundation for 
these benign cases of achylia gastrica? It is possible, and in many cases even 
probable, that there is; but it is not certain. This is certain: that sometimes 
a long persistent absence of hydrochloric acid has been observed clinically, and 
later an autopsy has shown no anatomical explanation of the condition. Thus, 
for example, a short time ago the author had a patient under observation in 
his wards for a considerable time with diabetes mellitus, in whose gastric juice 
no trace of hydrochloric acid could be demonstrated, although repeated examina- 
tions were made. The patient died, comatose, and the stomach seemed to be 
perfectly normal, even upon microscopic examination. Here there may perhaps 
have been some toxic inhibition of the secretion. At any rate, observations like 
this prove that when there is no gastric juice secreted, we can not assert that any 
marked anatomical change will be found in the gastric mucous membrane. 

From what has been said it follows that, according to the present state of 
our knowledge, we must distinguish several forms of achylia gastrica (or of long 
persistent gastric anacidity). We should mention incidentally that in a strict 
sense the name achylia should be employed only for that condition in which there 
is a constant absence not only of hydrochloric acid, but also of pepsine, indicat- 
ing a complete drying up of the secretion of gastric juice. Those cases, in which 
free hydrochloric acid is never demonstrable but pepsine is found, should, in 
strictness, be termed anacidity, or, better, achlorhydria. In practice it is true 
that we can not always make these fine distinctions, and that even such cases 
as present not an absolute absence but a slight or occasional trace of hydro- 
chloric acid are put in this latter category. We distinguish the three follow- 
ing forms of achylia : 

1. Achylia or achlorhydria may appear as a symptom in certain other diseases 
of the stomach, particularly, as we have already seen, in severe acute and chronic 
gastritis (when there is genuine catarrh of the stomach), and also in cancer of 
the stomach. These cases are to be termed " symptomatic achylia." 

2. Achylia or achlorhydria may appear as a necessary result of marked 
atrophy (" anadenia ") of the gastric mucous membrane. Here the further point 
is to determine the causes of this distinctly characterized anatomical change in 
the gastric mucous membrane. Sometimes it seems to be the result of a previous 
catarrhal inflammation (atrophic catarrh, analogous to similar conditions of 
other mucous membranes — vide supra, page 426). How far this assumption 
agrees with the facts must be determined by further careful investigation. 



454 



DISEASES OF THE DIGESTIVE OKGANS 



Apart from this secondary or inflammatory atrophy there is also a simple pri- 
mary atrophy of the mucous membrane. The cause of this condition is most 
likely to be found in congenital peculiarities, of which we as yet possess no in- 
timate knowledge. We might see a certain analogy in progressive muscular 
atrophy. In these cases of atrophy of the gastric mucous membrane there is no 
demonstrable secretion of hydrochloric acid, nor of pepsine. The gastric contents 
obtained in the ordinary way are absolutely devoid of peptic activity, but at the 
same time the muscular efficiency of the stomach is in many cases perfectly nor- 
mal, and this explains why, although there is no secretion of gastric juice, there 
are no marked symptoms of gastric discomfort. In many cases, however, the 
atrophy of the gastric mucous membrane is coincident with an atrophy, or at 
least with marked changes of the intestinal mucous membrane. Then it is 
inevitable that severe disturbances of nutrition should gradually develop, for the 
food can not be sufficiently digested and absorbed. Such patients grow progres- 
sively thin and feeble. Often they suffer from marked intestinal symptoms, 
having persistent diarrhoea, alternating with constipation. By suitable treat- 
ment and nursing such patients may improve, or at least their symptoms may be 
checked. In a few rare cases death finally occurs. The clinical picture of per- 
nicious anaemia (q. v.) has been repeatedly presented in association with this 
sort of atrophy of the stomach and intestines. In our opinion, however, the 
nature of these cases is still unsettled, since the atrophy of the intestinal mucous 
membrane of itself might well lead to extreme inanition, but not to a specific 
anaemia. For this there must be present some special circumstances with which 
we are as yet unacquainted. 

3. The third form is simple functional achylia. Here belong the not infre- 
quent cases in which the symptoms are not usually particularly severe, consist- 
ing of anorexia, gastric oppression, nausea, and rarely vomiting. The complaint 
may have been of recent origin. On careful examination of the gastric contents, 
we find complete absence of hydrochloric acid, while pepsine may be present, or, 
again, in other cases entirely absent. The motility of the stomach is normal, as 
a rule, but it may be somewhat impaired, probably because of a coincident weak- 
ness of the muscular coat (see the following chapter). With suitable treatment 
the symptoms diminish or vanish, but there is no change with regard to the ab- 
sence, or approach to absence, of hydrochloric acid and pepsine. It can not be 
determined how long this condition has existed. Sometimes such patients say, 
as we have already mentioned, that they have been rather subject to mild dys- 
pepsia or to temporary attacks of diarrhoea. Often, however, their previous 
health has been good. Whether we should invariably assume that there is a 
marked atrophy of the gastric mucous membrane in all such cases is very ques- 
tionable. Probably we have rather to do with an impairment of the secretory 
capacity of the individual stomach from causes not at present accurately deter- 
minable. Apparently there are not a few persons with achylia of this sort. In- 
asmuch as the condition runs along without any special symptoms, it is not 
diagnosticated by the physician, and the patient is not subjected to an accu- 
rate examination until digestive disturbance arises because of some special cause 
(vide supra), and then the anomaly is detected. If such patients do suffer from 
persistent dyspepsia there will usually be found some special reason for it, such 
as motor incapacity, possibly dislocation of the stomach, or genuine " nervous " 
dyspepsia, meaning by that term dyspepsia of psychical origin. It would be an 
interesting question to investigate whether individuals with persistent achylia do 
not perhaps have a predisposition to the development of carcinoma. 

The diagnosis of achylia, whether essential or secondary, can always be easily 
made by means of a careful examination of the gastric contents (see the first 
chapter of this section). Of course, the diagnosis is not established until re- 



ANOMALIES OF THE SECRETION OE GASTRIC JUICE 455 



peated and painstaking examinations have been made at various times and 
under various circumstances, and have invariably given the same negative result. 
If achylia is demonstrated, the next question is whether it is merely symptomatic 
or essential. The presence of chronic gastritis is excluded by the absence of 
all setiological factors and of excessive mucous secretion, and by the general 
course of the disease. The suspicion of cancer will often likewise be rendered 
untenable by the general course of the disease, and the absence of a tumor. In 
cases of atrophy of the gastric and intestinal mucous membrane, with conse- 
quent emaciation, there may be very great difficulty in excluding cancer. On 
the whole, however, the course of gastro-intestinal atrophy is much slower than 
that of carcinoma. Accompanying signs of pyloric stenosis invariably indicate 
the presence of carcinoma; and if we are enabled by the absence of any severe 
disturbance of nutrition to exclude any marked atrophy of the gastric and intes- 
tinal mucous membrane, we reach at last a diagnosis of simple functional achylia 
_by exclusion. Whether in such cases there is a demonstrable anatomical change 
in the gastric mucous membrane, the present state of our knowledge does not 
enable us to determine. 

We do not need to enter upon a special discussion of the treatment of symp- 
tomatic achylia. The severe cases of achylia which occasion extreme disturb- 
ance of nutrition need the most careful dietetic management. They should have 
such food as milk, soups, eggs, and meat-peptones. Practical experience will 
usually be a better guide than any theoretical considerations. Internally we 
may try hydrochloric acid and preparations of pepsine and pancreatine, also all 
sorts of stomachics, including nux vomica and condurango. The stomach may 
be rinsed out with a 2-per-mille solution of hydrochloric acid, and galvanic elec- 
tricity may be employed. It is self-evident that when there is actual atrophy of 
the mucous membrane, the results of treatment must be very limited. The 
milder cases of achylia do not need treatment except when special dyspeptic 
symptoms appear, or when there is intestinal disturbance, such as diarrhoea ; then 
the treatment is the same as in ordinary disturbances of the stomach or bowels, 
including a suitable diet, hydrochloric acid, perhaps rinsing out the stomach a 
few times, and, in case of diarrhoea, opium. If the symptoms subside, and we 
now find there is a persistent achylia, of course we must earnestly recommend 
such individuals to exercise a certain caution with regard to diet. They should 
not take too great a quantity of food at one time, and in general should choose 
a largely vegetable diet — i. e., one containing an abundance of starches. There 
is this exception, that if the achylia is associated with a dread of eating and a 
tendency to hypochondriasis, we must encourage the patient to take a rather 
abundant amount of nourishment and employ hydrotherapy and other general 
tonics. 

2. Hypersecretion and Hyperacidity of the Gastric Juice (Acid Dyspepsia). 

— We have seen in the first chapter of this section that it may be regarded as a 
rule, that when fasting the stomach is almost completely empty, and that an hour 
after a test breakfast (vide supra, page 418) the acidity of the gastric contents 
is about 55 to 65. The investigations of late years have shown, however, that 
this rule has numerous individual exceptions not necessarily pathological. There 
are many persons who secrete scarcely any hydrochloric acid (vide supra), and 
also there are apparently still more who always have hydrochloric acid in the 
stomach even when fasting, and whose hydrochloric-acid index after a test break- 
fast is as high as 80 to 100, or even higher. Many such individuals have no 
dyspeptic disturbances whatever, so that the unusual abundance of hydrochloric 
acid can be regarded only as an individual peculiarity of secretion, and not due 
to disease. In other such cases, however, there are decided gastric symptoms, 
and these symptoms are such as to indicate very strongly their direct dependence 



456 



DISEASES OF THE DIGESTIVE OKGAXS 



upon the increased production of acid. This state is termed acid dyspepsia, by 
which we mean the abnormal excess of hydrochloric acid at the time of diges- 
tion — that is, hyperacidity as distinguished from hypersecretion, which latter 
term is applied to the continuous secretion of gastric juice even when digestion 
is not taking place, the stomach having received no food, or having discharged 
its contents into the pylorus. Hypersecretion is probably almost always associ- 
ated with hyperacidity, but not vice versa. However, we can not maintain a 
strict clinical distinction between the two in practice. 

Essential, acid dyspepsia should be sharply distinguished from symptomatic 
hyperacidity and hypersecretion, such as occur perhaps in certain forms of gas- 
tritis (page 428), and almost invariably in ulcer of the stomach. This distinc- 
tion is very important, even from a practical point of view. It must be con- 
fessed that it may be scarcely possible to make a differential diagnosis, as we 
shall soon see, between ulcer and hypersecretion; but we can. at any rate, hold 
fast to the important theoretical distinction between the two conditions. The 
term " essential " hypersecretion ought to be applied only to cases in which there 
is an increase in the secretion of hydrochloric acid, without any ulcer forma- 
tion. If we regard hypersecretion as a possible cause of ulcer (vide supra, page 
433), then ulcer can be termed merely a complication of hypersecretion. 

As to the causes of simple hyperacidity and hypersecretion we have as yet, 
unfortunately, scarcely any knowledge. Very few histological examinations 
of the mucous membrane in characteristic cases have thus far been made. It is, 
therefore, at present customary to assume that hypersecretion is a "neurosis," 
and this view is apparently confirmed by the frequent combination of hypersecre- 
tion with other nervous conditions. We must later discuss this point more fully. 
On the other hand, however, it is not impossible that functional disturbances of 
cellular activity may lead to increase in the secretion. We are ourselves in- 
clined to class many cases of hypersecretion along with the well-known cases of 
increase in the secretion of sweat (hyperidrosis of the hands and feet), of saliva, 
and of similar products. Eor such it is not at all essential that there should be 
abnormal nervous conditions. 

Having such imperfect insight into the true nature of these processes, we 
must provisionally take a purely clinical standpoint, and describe the phenomena 
seen in practice. It should be added that some of the conditions are by no means 
infrequent, but it is often difficult to interpret accurately what we observe. One 
important question is how far the symptoms which are present are actually refer- 
able to the hypersecretion as such, and how far they are due to the other anoma- 
lies which often accompany the hypersecretion, such as general nervousness, gas- 
troptosis, and chlorosis. In order to get a better comprehension of the subject 
we shall distinguish in what follows several forms of acid dyspepsia, but we wish 
to repeat that a perfect differentiation is impossible, particularly between hyper- 
acidity and hypersecretion. 

1. Dyspepsia with Hyperacidity (Hyperchlorhydria). — The conditions which 
belong in this category are most often found in young females. They are 
very often conjoined with symptoms of chlorosis, general nervousness, etc. Cer- 
tain errors in diet may also excite hyperchlorhydria, such as hot or highly spiced 
food, and particularly too strong coffee; and dyspeptic conditions with hyper- 
chlorhydria are frequently observed in excessive smokers. 

The symptoms are tolerably characteristic. They occur especially after eat- 
ing, and sometimes only after certain kinds of food, and consist first of a sense 
of oppression in the stomach, often increasing into genuine cardialgia. Usually 
the pain does not appear until two or three hours after eating — i. e., at a time 
when the stomach is already empty, although the excessive secretion of acid is 
still going on. Many patients have noticed that if they then take some more 



ANOMALIES OF THE SECKETION OF GASTRIC JUICE 457 



food or drink their pain will abate. This is easy to understand. Often there 
will be acid eructations at the time of the excessive formation of acid, and a 
distinct feeling of heartburn. The acid gastric contents may be vomited, but 
this is not especially frequent. When the stomach is completely empty, the pa- 
tient feels perfectly well again. Inasmuch as the appetite is usually unimpaired, 
nutrition remains fairly good. The general course of the disease is chronic, with 
marked variations. At many times the symptoms are aggravated, particularly 
under the influence of psychical disturbances, such as anger or excitement, or be- 
cause of an unsuitable mode of life. At other times the symptoms may entirely 
vanish. 

The diagnosis of hyperchlorhydria may be suggested by the symptoms just 
described, but it can not be established except by means of the stomach-tube. 
External examination of the stomach shows nothing special except that there 
may be a moderate diffuse tenderness on pressure. It is not surprising that 
often there is gastroptosis. If we examine the stomach when fasting, it is empty 
or almost empty, provided the case is one of pure hyperchlorhydria. The acid 
index after a test breakfast is very high, TO to 100 or over. The digestive power 
of the gastric juice is greater than normal. It is therefore natural to find, as 
we do find, that the stomach is entirely empty as a rule as soon as three or four 
hours after a test meal; which indicates also a good degree of motor power. At 
that time hydrochloric acid is still present. On the other hand, digestion of 
starch in the stomach is impeded by the abundance of hydrochloric acid. 

If we find things as above depicted, the diagnosis of hyperchlorhydria as such 
is established. But a difficult question remains to be answered — whether the 
case is one of simple functional increase of the secretion, or whether the hyper- 
acidity is symptomatic of an ulcer. If there are no characteristic symptoms of 
ulcer, such as gastric haemorrhage and localized tenderness, it is often impossible 
to answer this question with more than a certain degree of probability. It is 
characteristic of simple hyperchlorhydria that the pain is often improved upon 
taking food, while in ulcer the pain is aggravated. If there are well-marked 
symptoms present of general nervousness, this is usually decidedly in favor of 
"nervous hyperacidity." Finally, the results of treatment may aid us in diag- 
nosis (vide infra). 

The mode of treatment will be considered with that of hypersecretion. 

2. Dyspepsia ivith Hypersecretion of the Gastric Juice ("Continuous Flow 
of Gastric Juice "). — Here belong those cases of dyspepsia in which the examina- 
tion of the stomach shows the presence, even when fasting, of considerable 
amounts of fluid containing an excess of hydrochloric acid, and in which this 
hypersecretion can not be regarded as the result of an ulcer. 

The disease is much more exceptional than simple hyperchlorhydria. It ap- 
pears in men somewhat oftener than in women. ISTo special serological factors 
can be named, except long-continued mental strain and excitement ; often no 
cause can be made out. 

The symptoms, as in hyperchlorhydria, consist of cardialgia, sour eructations, 
heartburn, and not infrequently vomiting. Pain often appears when no food has 
been taken. When vomiting occurs there may be little or no food in the 
vomitus, but merely a cloudy, often bile-stained fluid, strongly acid, with a very 
sharp taste and so irritating that it causes burning pain in the pharynx. The 
appetite is generally good, and the patients have usually found out by experi- 
ence that if they drink some tea so as to dilute the gastric juice, or take some 
sort of food, they get relief. Often there is abnormal thirst ; the bowels are usu- 
ally constipated; the urine faintly acid and turbid with deposits of phosphates; 
the pulse is often slow; "in many cases there is a distinct general neurasthenic 
condition, associated with the dyspepsia. Here, again, the only method of arriv- 



458 



DISEASES OF THE DIGESTIVE OKGANS 



ing at a certain diagnosis is by examining the gastric contents. The decisive 
point is that in the morning before breakfast we should invariably find a consid- 
erable amount of fluid, containing practically no portions of food but a large 
percentage of hydrochloric acid. At the same time it should be particularly 
pointed out that it is not abnormal, now and then, to find a teaspoonful or two of 
fluid in the stomach, containing hydrochloric acid, while fasting. It is not 
proper to speak of the case as one of hypersecretion unless we can obtain from 
the fasting stomach, without special effort, some two or three ounces (50-100 
cubic centimetres) of strongly acid fluid. Along with the hypersecretion there 
is usually hyperchlorhydria, so that we find a high acid index an hour after the 
test breakfast. If we give a test meal, and examine three hours later, we shall 
find that the meat has vanished, while the digestion of starches has been decid- 
edly delayed by the hyperacidity. Some seven hours after the test meal the 
stomach is empty of food, but probably contains an abundance of acid secretion. 

If we inflate the stomach, we may find the organ dislocated downward (gas- 
troptosis). This, however, is merely a chance complication. There is never 
great dilatation. If we find the stomach much enlarged, our suspicions are at 
once directed to pyloric stenosis, and this condition is usually easily diagnosti- 
cated, one important indication being delay in the emptying of the stomach. 
Whenever the stomach in a fasting condition, or seven or eight hours after a test 
meal, is found to contain not only an abundance of hydrochloric acid, but in 
addition considerable amounts of partially digested food, the condition is not 
one of simple hypersecretion, but of hypersecretion combined with stenosis of 
the pylorus due to ulcer. This puts an entirely different aspect on the case. 

It is a much more difficult matter to distinguish hypersecretion from a gastric 
ulcer without stenosis. Indeed, sometimes an absolute decision is almost impos- 
sible. In such instances we may be enabled to form an opinion by considering 
the general course of the disease, the associated nervous symptoms, and all the 
special symptoms (vide supra). 

In general, the course of acid dyspepsia with hypersecretion is chronic, but 
variable. The prognosis is not unfavorable, and correct management, based, as 
it must be, upon an accurate examination, may bring about very satisfactory 
results. 

In the treatment of acid dyspepsia, including hypersecretion as well as sim- 
ple hyperchlorhydria, we meet with one difficulty in the fact that we can seldom 
absolutely exclude ulcer of the stomach. The physician must, therefore, deter- 
mine whether he shall begin with a course of treatment for ulcer or not. We 
believe that in all cases in which the symptoms have existed for a considerable 
time and are severe, and in which there has been no systematic treatment as yet, 
it is wise to treat the patient as if there were an ulcer. If the case is one of 
simple acid dyspepsia this can do no harm, and if it is one of ulcer it is the only 
method that can do good. In either case, the quiet, the unirritating diet, and 
the administration of alkalies are certainly appropriate. Moreover, cases are 
not infrequent in which the patients are anxious and hypochondriacal, and upon 
them a methodically conducted " cure " for ulcer often has a favorable subjective 
influence. Still, this just-mentioned combination of acid dyspepsia with de- 
cided nervous and hypochondriacal disturbances may, on the other hand, render 
the effect of a strict ulcer treatment quite unfavorable. This applies to patients 
who have long been tortured by a dread of gastric ulcer, have consequently gone 
through the appropriate treatment many times already, and have grown thin and 
feeble as the result of an excessively cautious dietary. Eor such unfortunates 
there may be no use whatever in repeating a strict course of treatment suitable to 
ulcer. Such a procedure confirms the patient in his apprehensions, and merely 
makes him more wretched. 



ANOMALIES OF THE SECRETION OF GASTRIC JUICE 459 



We see, then, how carefully we should consider the individual in the treat- 
ment of acid dyspepsia, and, above all, how much weight we should assign to the 
general condition as well as to the dyspeptic symptoms. It is often advisable to 
begin with a course of treatment for ulcer in the ordinary manner, but upon the 
prompt cessation of symptoms to make a more rapid transition than usual to 
nourishing food and other therapeutic methods. The more convinced the physi- 
cian becomes that he has to do with simple " nervous " hypersecretion and not 
with an ulcer, the less need has he to pursue a strict dietetic treatment. In 
such cases it is best to prescribe for the patient a diet list, containing an abun- 
dance of albuminoids, including meat, fish, eggs, and milk; and with this, rye 
bread and butter, and easily digested vegetables. There should be as great a 
limitation as possible of alcoholic beverages, spices, strong coffee, and sour arti- 
cles, as well as of puddings and starchy vegetables. Yet in such cases, also, one 
must be guided by the individual experiences of the patient as well as by merely 
theoretical considerations. As to drugs, of course alkalies come first. We 
should be guided by the circumstances of the particular case in prescribing, sev- 
eral times a day, particularly after meals, a knife-point full of bicarbonate of 
soda, or some similar powder, such as bicarbonate of soda and calcined magnesia, 
equal parts ; or bicarbonate of soda, 30 parts ; subnitrate of bismuth, 5 parts ; and 
similar drugs. If there is hypersecretion we like to give the patient in the morn- 
ing, before breakfast, a half litre (pint) of warm Carlsbad water, or the artificial 
Carlsbad salt, dissolved in water. In severe cases of hypersecretion regular wash- 
ing out of the stomach is advantageous. The best time to do this is in the early 
morning. We may employ a one-per-cent. solution of bicarbonate of soda. 

Atropine and the narcotics, such as morphine and codeine, have been recom- 
mended for the purpose of diminishing the secretion of the gastric glands. We 
have ceased to expect any benefit from their use, and we would warn the physician 
against their unnecessary employment. 

The simultaneous constitutional treatment is very important, particularly 
in all cases associated with neurasthenic symptoms (vide infra, the chapter on 
nervous dyspepsia). From this point of view there is much benefit in drinking 
the waters at Carlsbad, Tarasp, and similar watering places, in connection with 
the hope of constitutional improvement from the outdoor life, the baths, cold 
sponging and rubbing, and similar agencies. In treatment at home these last 
factors must always be duly considered. 

3. Periodical (Intermittent) Hypersecretion (Gastroxynsis). — In the con- 
dition here to be described, persons who at other times feel perfectly well, with- 
out any digestive disturbance, are rather suddenly attacked by violent gastric 
pain, sour eructations, and vomiting. The intervals between attacks may be 
longer or shorter, and there may be either some exciting cause or no apparent 
reason for the disturbance. The vomitus consists of large amounts of watery 
fluid containing an excess of hydrochloric acid. During these attacks the gen- 
eral condition of the patient is wretched; he looks pale, his pulse is small and 
frequent. Often there is extremely violent headache at the same time. An 
attack of this sort lasts a few hours, or even two or three days. Often it ends 
with considerable suddenness, to be followed by a period of good health which 
may last a week or even months, or longer. 

The causes of this strange disease are entirely unknown, but it certainly seems 
as if there were conditions of irritation, originating in the nervous system. It 
seems to us indubitable that there is a close relation between gastroxynsis and 
migraine (see the chapter on migraine). It is a very important fact that almost 
precisely the same group of symptoms occurs in tabes dorsalis (q. v), under 
the name of gastric crisis. In every case, therefore, the physician should exam- 
ine the tendon reflexes and the pupils ; but attacks of this sort undoubtedly occur 



460 



DISEASES OE THE DIGESTIVE OKGANS 



when tabes is absent. It may be added that in its well-marked form the condi- 
tion is quite rare. 

If possible we should examine the gastric secretion in the time between at- 
tacks, as well as during the attack. It appears that many cases of periodical 
gastroxynsis are merely acute exacerbations of a constant hypersecretion. In 
such cases there are likely to be mild dyspeptic symptoms in the intervals, and a 
careful treatment of these by lavage, alkalies, and Carlsbad water has an excel- 
lent effect upon the paroxysms. If there are coincident neurasthenic symptoms, 
of course the greatest stress must be laid upon constitutional treatment. The 
treatment of the paroxysm itself is seldom very successful. The best remedy 
is bromide of sodium in large doses. We may also try chloral, chloroform, 
belladonna, codeine, and also antipyrine. Externally, warm compresses or hot 
poultices may be applied over the stomach. If the pain is very violent a subcu- 
taneous injection of morphine may be almost indispensable, although we should 
avoid it if possible. 



CHAPTER VIII 

ABNORMALITIES IN THE SIZE AND POSITION OF THE STOMACH — 
MOTOR DISTURBANCES OF THE STOMACH 

1. Abnormalities in the Size of the Stomach. — Atony of the Stomach. — 

Like any other organ, the stomach may present considerable differences in its 
size without being pathological. These differences partly depend upon con- 
genital conditions, and partly are associated with the mode of life. It has long 
been known that certain classes of people who eat very bulky articles of diet 
(e. g., a great proportion of potatoes), and other large eaters, including many dia- 
betics, have noticeably large stomachs; but a change in size of this sort can 
not be regarded as pathological, provided the function of the stomach is not im- 
paired. The excessive distention of the organ, or the excessive demands upon the 
functional activity of the muscular coat of the stomach, may finally render it 
unequal to its task. Then we reach a pathological disturbance, a sort of over- 
strain of the stomach, a muscular insufficiency analogous to the myopathic dis- 
eases of the heart, which have been so much studied. Obviously one important 
factor here would be the original quality of the muscular fiber: if the muscles 
of the stomach are weak from the start, they will become insufficient all the 
sooner. 

We must state that in our experience well-marked cases of primary idiopathic 
dilatation of the stomach, as an expression of pure muscular insufficiency, seem 
to be far from frequent, although slight degrees of muscular weakness occur 
quite often. 

Erom what has been said, it is evident that the physician should lay little 
stress upon the mere estimation of the size of the stomach. And, indeed, its size 
varies greatly according to the amount ingested. We can form an opinion of the 
size of the organ by percussion of the empty stomach, or by percussing it alter- 
nately empty and filled with water by means of the stomach-tube, or, what is 
much simpler and more certain, by distending it with air, as above mentioned 
(page 420). In general, we can say there is dilatation of the stomach if the 
lower border of the fundus extends below the level of the navel while the lesser 
curvature is in a normal position; but, as we have said, the important question 
is not the size, but the motor ability of the organ, and it is far more important 
to determine the functional activity by means of a test meal, in the manner 



THE SIZE AKD POSITION OF THE STOMACH 461 



already explained (page 420), than to find out the mere size of the stomach. If 
the organ empties itself in a normal way, any dilatation that there may be has 
no significance. If there is some tendency to stagnation of the gastric contents 
because of muscular insufficiency, we may have mild dyspeptic symptoms, such 
as gastric oppression, eructations, or even occasional vomiting. 

If, however, we find that the stomach is dilated and that the motor efficiency 
is decidedly impaired, with actual stagnation and accumulation of ingesta in 
the stomach, we ourselves think it is always justifiable to assume that there 
is a pyloric stenosis. In such case the disease with which we have to deal is not 
a dilatation of the stomach, but an ulcer or cancer of the pylorus, which leads 
to stenosis and its results, as we have already described at length (pages 438 and 
447). It has often been maintained that in cases of primary muscular dilata- 
tion there may occur mechanical kinks in the pylorus and sacculations in the 
stomach, so as to cause a considerable hindrance to the emptying of the viscus, 
This may be possible, but we have never seen such a case, nor read a conclusive 
report of one. 

In this place a symptom may be mentioned which is often regarded as a sign 
of dilatation. We refer to splashing in the stomach when palpation is practiced 
by a sort of pushing or thrusting motion. Marked splashing is indeed very often 
audible in cases of actual dilatation due to stenosis of the pylorus, but it is very 
frequently heard in persons who have dyspepsia, and even in persons who are 
perfectly well. Children sometimes play at producing splashing sounds in their 
own stomachs, and by practice acquire great technical dexterity! And in pre- 
cisely the same way the sound is produced by nervous and hypochondriacal pa- 
tients, to whom the splashing is a source of anxiety. Splashing occurs when air 
and fluid are both present in the stomach, provided the abdominal walls as well 
as the gastric walls are not too tense. In this sense it is, therefore, correct to 
associate so-called atony of the stomach with the splashing, because it may often 
be due to a certain laxity of the muscular coat of the stomach, but we should 
never lay any special stress upon the sound, unless upon examination we find at 
the same time a distinct disturbance of the motor efficiency of the stomach. 

It follows, therefore, that mere dilatation of the stomach is not an independ- 
ent disease. For example, in practice we may unhesitatingly refer every case of 
well-marked dilatation with decided stagnation of the gastric contents to steno- 
sis of the pylorus, and of course this latter is to be regarded as the true disease, 
At the same time, however, there are slight degrees of gastric dilatation, or per- 
haps a better expression would be idiopathic motor insufficiency of the stomach 
(muscular atony of the stomach), which occur when there is no reason for be- 
lieving that there is any anatomical change at the pylorus. We may assume 
that such motor insufficiency exists when there is a slight but distinct tendency 
for food "to accumulate in the stomach. 

In treating this simple muscular atony, we should first regulate the diet. The 
separate meals must not be too large, but they should be nutritious, and per- 
haps even somewhat stimulating. Rje bread, small portions of vegetables, and 
nourishing meat dishes are by no means interdicted. Large amounts of liquid 
are to be avoided, as they needlessly dilate the stomach. In simple atony, lavage 
is seldom necessary. At the most, we might at the beginning of treatment com- 
pletely empty the stomach a few times. Other suitable measures are cold spon- 
ging and rubbing of the epigastrium, the application of electricity (particularly 
the galvanic current) to the stomach, and cautious massage of that region. 
Among internal remedies, nux vomica deserves to be employed. 

Whether there is such a thing as abnormal smallness of the stomach, giving 
rise to symptoms, is not yet known. Perhaps there may be such a condition in 
cases in which feeble and ill-nourished individuals, usually of the female sex, 



462 



DISEASES OF THE DIGESTIVE OKGANS 



can take but a few morsels before they have a feeling of fullness and satiety, and 
so never become well nourished despite every effort. We may find the stomach 
very small as a secondary result in many forms of inanition, particularly in as- 
sociation with stenosis of the oesophagus and of the cardia. 

2. Abnormal Position of the Stomach .— Gastroptosis— Kussmaul was the 
first to call attention to the great frequency of the downward dislocation of the 
stomach. Glenard has written much about it. Either the entire organ may 
sink down, or, what is more common, the right half alone, so that the organ 
takes a vertical position. The cause of this anomaly may lie partly in congenital 
conditions, but in the main it is certainly the purely mechanical result of the 
pressure of clothing. Gastroptosis is an extremely common phenomenon in grown- 
up girls and women who wear tightly-laced corsets, and fasten the bands of their 
clothing snugly about them. It also occurs in men, but far less often. Usually, 
with the gastroptosis is associated a change in the position of other organs, occur- 
ring in the same way. In particular, the right kidney becomes abnormally mov- 
able, and consequently readily palpable (see the chapter on movable kidney), and 
the transverse colon sinks down either in its right half or in its middle portion. 
Glenard has termed this condition enteroptosis, and ascribed to it an important 
role in the aetiology of nervous dyspepsia and neurasthenia. Well-marked cases of 
enteroptosis are most frequent in women who have lax abdominal walls because of 
repeated confinements. 

The experienced eye may often recognize, or at least surmise, gastroptosis 
upon external inspection of the abdomen. One is struck by the collapsed appear- 
ance of the epigastrium, where one often feels marked pulsation of the abdom- 
inal aorta. Below the navel, on the other hand, is seen a protuberance, the shape 
of which may quite distinctly suggest the contours of the stomach. At this 
spot, below the navel, distinct splashing may not infrequently be obtained by 
proper palpation. An absolute diagnosis of gastroptosis, however, requires the 
artificial inflation of the stomach (vide supra, page 420). When this is done the 
abnormal position of the stomach is immediately recognized. Of course, the 
most important point is the demonstration of a downward displacement of the 
lesser curvature. This is found halfway between the navel and the epigastric 
angle, or often even at the level of the navel. The downward displacement of 
the greater curvature alone does not establish gastroptosis, because it may be 
due to dilatation of the stomach. 

Inflation of the stomach is such a simple and reliable method of examina- 
tion that there scarcely seems any real necessity for other methods. For this 
reason Einhorn's recommendation of electric transillumination of the stomach, 
by means of an incandescent light introduced into the organ (" gastro-diaphanos- 
copy is scarcely likely to become generally adopted by physicians. It gives 
some indications of the position of the stomach, but the conclusions drawn from 
its use are by no means infallible. The displacement of the kidney, which is 
often associated with gastroptosis, can be easily recognized by means of palpa- 
tion. The position of the colon (coloptosis) can be demonstrated by distending 
the large intestine with air or water. 

The question of the clinical significance of gastroptosis is not very easy to 
answer. In the first place, it should be remarked that, if we pay attention to 
the subject, we shall find that well-developed gastroptosis is very frequent in ppr- 
sons who have not the slightest symptoms. On the other hand, there are many 
patients, especially women, who complain of such annoyances as pressure and a 
sense of fullness, attacks of gastric pain, eructations, and occasional vomiting, 
and who are found to have a distinct gastroptosis. In such a case we should 
invariably proceed to test the secretory and motor functions of the stomach. 
Very often these are perfectly normal, and such a condition scarcely justifies us 



NERVOUS DYSPEPSIA 



463 



in assuming offhand that there is a causative relation between the gastroptosis 
and the patient's symptoms. Gastroptosis is so common that the relation is more 
likely one of simple coincidence. If we make a searching examination into the 
patient's condition we shall usually discover that the gastric symptoms are asso- 
ciated with many other symptoms of a neurasthenic kind, and hence are very 
likely, for the most part, of purely psychical origin (see the following chapter). 

Still, it can not be absolutely denied that certain disagreeable sensations in 
the abdomen and along the digestive tract may be directly dependent upon gas- 
troptosis; and, furthermore, gastroptosis in some few cases seems to occasion a 
mechanical hindrance to the discharge of the stomach contents, especially be- 
cause of the vertical position of the organ, so that we have a sense of oppression 
in the stomach, eructations, and other symptoms; but this motor insufficiency 
should be proved, not assumed. As a rule, even well-marked gastroptosis is not 
associated with any disturbance of the motor function of the stomach. There is 
more likelihood that the habitual constipation, which often accompanies the 
dyspeptic symptoms of gastroptosis, is at least in part the result of an associated 
coloptosis. 

For the treatment of the dyspeptic symptoms which may be present in a 
case of gastroptosis, we have a most desirable basis in the gastroptosis itself, 
although the author at least is convinced that its main efficacy is subjective. 
If gastroptosis has been made out, we must absolutely forbid the wearing of 
tightly-laced corsets, or too snugly fitting gowns. It is often useful to apply a 
wide abdominal band above the symphysis. This in many cases fully replaces 
the more complicated " abdominal corsets " and similar apparatus. With regard 
to diet, we forbid the taking of large amounts of liquid, and prescribe nourishing 
food that is not bulky. Particularly when patients are emaciated and appre- 
hensive, we often do the greatest good by ordering a highly nutritious diet. The 
region of the stomach should be rubbed briskly once or twice a day with cold 
water or brandy. The employment of faradic and galvanic electricity or mas- 
sage is particularly indicated when constipation is present. 

Of course we must pay attention, as we have said, to the general neurasthenic 
condition, which is usually also present. In this regard great importance at- 
taches to a suitable mental treatment, in order to free the patient from her exag- 
gerated anxiety and apprehension. 



CHAPTER IX 

NERVOUS DYSPEPSIA 

( Gastric Neurasthenia) 

We have repeatedly indicated in the preceding chapter that many disturb- 
ances of the gastric functions may be due to changes in the innervation of the 
stomach, or to actual disease of its nerves; thus some have been inclined to 
refer the disturbances of the secretion of the gastric juice, such as hyperacidity 
and hypersecretion, to abnormal conditions of the secretory nerves. Many cases 
of " cardialgia " have been regarded as pure " neuralgia " of the sensory nerves 
of the stomach; and also in the domain of the muscular activity of the stom- 
ach, authors have distinguished conditions of nervous weakness (nervous atony 
of the stomach) and of nervous irritability of the muscular coat (so-called 
" peristaltic unrest " of the stomach ; constant rumbling in the stomach and 
similar symptoms). There is no doubt that in cases of severe organic disease of 



464 



DISEASES OE THE DIGESTIVE OKGANS 



the nervous system there may be well-marked gastric symptoms as direct conse- 
quences of nervous irritation — for example, we have nervous vomiting in cerebral 
tumor and meningitis, and gastric crises in tabes. It is, therefore, not impos- 
sible that there may also be primary diseases of the sensory, motor, and secre- 
tory nerves of the stomach with corresponding symptoms, but this is by no means 
proved, and it is certain that such actually " nervous " gastric diseases are very 
rare, if they occur at all. At present, clinical experience does not justify us in 
putting in this category, with any degree of certainty, any disorder except the 
state above described (page 459), in which there is periodical vomiting with gas- 
tric pain and hypersecretion. 

There are numerous cases which are at present habitually termed nervous 
dyspepsia, but in our opinion the overwhelming majority of these have an origin 
different from the one implied. Such patients assert that after every meal 
they have pressure and pain in the stomach, that after a few mouthfuls the 
stomach feels full and distended, and consequently they often have palpitation 
and a troublesome feeling of constraint in the chest. The patients frequently 
complain of eructations also, and occasionally of vomiting. These symptoms 
are all such as occur in the same way in actual diseases of the stomach, but in 
these patients there are usually certain other symptoms present, which indicate 
the nervous character of the disease. In the first place, it is noticeable that the 
above symptoms display striking variations in their severity. The same patient 
who to-day complains of great distress in his stomach after a few spoonfuls of 
soup, at another time, when he is in a happy and lively frame of mind, will eat a 
large dinner without being reminded that he has a stomach; but as soon as he 
gets angry or irritated, or, in brief, in a " sensitive " condition, the gastric symp- 
toms appear at once in an exaggerated form. On all such occasions, therefore, 
we see most clearly the influence of the imagination and of general psychical 
irritation on the behavior of the stomach. Every one knows that a violent rage 
or any experience arousing anxiety or hope — any excitement, sad or joyful — may 
immediately destroy the appetite; and very great mental disturbance not infre- 
quently also causes vomiting or similar symptoms. In the same way in sensitive 
individuals even the mildest psychical influences produce similar results; but 
in this regard there is nothing which has so unfavorable an influence as that 
state of psychical disturbance which is associated with great concern for one's 
own health — that is, a condition of hypochondriacal anxiety — anxiety lest 
something which has been eaten may do damage; constant dread that a grave 
disorder of the stomach may be developing. These mental disturbances are es- 
pecially influential in maintaining and progressively aggravating the abnor- 
mal condition. This is the explanation of that peculiar psychical hyperesthesia 
which feels the acutest " pain " in the stomach, when there is really nothing 
but a perfectly normal general sensation. And the same explanation applies 
to certain muscular contractions — half unconscious, half voluntary — which 
occasion eructations, vomiting, and similar phenomena. The patient has some 
symptoms which he feels subjectively, and some which seem to him to be actually 
objective, and they are in part the result of pure imagination (or " auto-sug- 
gestion") and in part the physiologically necessary consequence of the great 
psychical disturbance. 

What we wish to emphasize is our conviction that in the great majority of 
cases of nervous dyspepsia we are not dealing with any functional disturbance of 
the gastric nerves, but with abnormal " psychogenic " irritations of the central 
nervous system, the results of which are apparent mainly in the domain of the 
gastric functions. Nervous dyspepsia is merely one example of that great group 
of nervous diseases which owe their origin mainly to hypochondriacal disturb- 
ances of mind, and which may appear in the most diverse organs. It is properly 



NERVOUS DYSPEPSIA 



465 



nothing but a symptom of the constitutional " nervousness " or neurasthenia, and 
is therefore termed by many physicians, with absolute correctness, gastric neu- 
rasthenia. By careful clinical observation it is easy to demonstrate that almost 
all the ordinary gastric symptoms may, under favorable circumstances, be 
excited by purely psychical influences. It is evident that anorexia is often the 
result of simple mental disturbance, especially when of a hypochondriacal char- 
acter; but excessive craving for food (bulimia) is certainly in most cases also 
of purely psychical origin, arising from special imperative conceptions. There 
is no doubt that the most varied abnormal sensations, ranging from simple 
oppression to a most acute pain in the stomach, may have a purely subjective 
origin. The best proof of this lies in the often apparently miraculous effect of 
remedies which have a purely suggestive and psychical influence (simple reassur- 
ance of the patient, hypnotism, and various external and internal remedies). It 
is very important to know that in many cases also eructations and vomiting have 
a merely psychical and central origin. They are due to the influence of certain 
ideas which make the eructations or vomiting appear unavoidable, and the 
action at first is due to unconscious volition, and finally becomes a sort of dis- 
eased habit. Many nervous and hypochondriacal patients who regard them- 
selves as dyspeptics become true virtuosi in eructations and vomiting, the reflex 
process becoming easier and easier because of repetition, and being excited by 
unconscious volition. General psychical disturbance may also cause eructations 
and vomiting by direct stimulation. We know persons who are attacked with 
nausea and vomiting upon any great excitement. Even in children it is by no 
means rare to observe persistent vomiting after almost every meal, and that this 
is of a purely " nervous " character appears from the rapid beneficial effect of 
exclusively psychical treatment — e. g., if the child is strictly forbidden to vomit. 
We often see just the same condition in adolescent girls, frequently associated 
with other hysterical symptoms. In this connection it should be briefly men- 
tioned that there may be a " nervous " — that is, hysterical — hsematemesis. (For 
particulars in regard to this, the reader is referred to the chapter on hysteria; 
and, in general, the chapters on hysteria and neurasthenia should be referred to 
as supplementing what has been said here.) 

Very often other nervous symptoms are observed besides those referred to 
the stomach. There are signs of excessive mental irritability, symptoms ref- 
erable to the head, such as headache, pressure in the head, vertigo; abnormal 
sensations in the extremities, of pain, coldness, numbness, and the like. There 
are almost invariably, also, certain attendant intestinal symptoms. The patient 
complains of bloating of the abdomen, and of irregular and sluggish bowels. 

Nervous dyspepsia becomes a more serious matter when the patient is pre- 
vented from taking sufficient nourishment, by fear of committing errors in diet, 
and because of the loss of appetite which his mental uneasiness occasions. There 
are sometimes complete nervous anorexia, a constant dread of eating or an actual 
aversion toward any food, and a considerable or excessive emaciation, usually 
associated with great bodily weakness. Such patients finally take to their beds 
and give the impression of severe illness. 

Diagnosis. — In many cases the experienced physician can make an extremely 
probable diagnosis of nervous dyspepsia merely from the symptoms which the 
patient enumerates. The true condition is suggested by the general nervous- 
ness, by the prominence of anxiety and of hypochondriacal notions, the variabil- 
ity of the symptoms and their relation to psychical irritation, and the other 
attendant symptoms of a nervous character, such as headache, vertigo, palpita- 
tion, and a sense of oppression. Still, it is easy to be deceived, because the symp- 
toms seem to be so objective that the physician feels constrained to believe that 
there is some organic disease of the stomach, although none exists, and because, 
30 



466 



DISEASES OE THE DIGESTIVE ORGANS 



on the other hand, an actual disease of the stomach may be present in a very 
nervous individual and fail to be recognized, being wholly obscured by the gen- 
eral nervous phenomena. Eor this reason, even in cases which seem to be the 
most simple, we would do well to make a careful objective examination, and this 
is of course an absolute necessity in all cases which are obstinate and severe. 

Often the objective examination shows clearly normal conditions in every 
respect : the external examination is normal, and the position, secretion, and 
motility of the stomach are normal. In such a case the diagnosis is established, 
and the mere result of examination will often have a most beneficial effect upon 
the patient. For this reason a painstaking examination is often the best rem- 
edy for many patients with nervous dyspepsia. It is more difficult to reach a 
conclusion when certain abnormalities are found, although there are no signs 
of indubitable organic disease — that is, there is no tumor nor evidence of steno- 
sis of the pylorus nor genuine haemorrhage — but we do find, for example, 
distinct hyperacidity or hypersecretion : less often achlorhydria ; very frequently 
gastroptosis; and often, it is said (although, according to the author's experi- 
ence, this is rare), some slight disturbance of motility, so-called atony of the 
muscular coat of the stomach. How shall such cases be interpreted? Shall we 
always lay stress exclusively upon the objective anomalies which are discovered, 
and refer to them every one of the many symptoms the patient enumerates? In 
the author's opinion, this would often be erroneous. It has been especially 
emphasized in the preceding chapters that the conditions mentioned are frequent 
and are apt to cause no symptoms at all, so that if we find associated with well- 
marked nervous dyspepsia a gastroptosis, or a moderate hypersecretion, or achlor- 
hydria, in many cases the association is a mere chance coincidence without sig- 
nificance. We think that such conditions should not be wholly disregarded, but 
yet their clinical importance should not be overestimated; and from a therapeu- 
tic point of view, also, they should be borne in mind, but never to the neglect 
of that general psychical treatment which is usually much more important. 
Such conditions also are very useful as a handle for mental therapeutics (as we 
have already pointed out), because of the favorable effect which treatment of 
them has upon the mind of the patient. 

A most difficult question in diagnosis, in our opinion, is to distinguish be- 
tween ulcer and nervous dyspepsia when there is distinct hypersecretion without 
evident signs of ulcer (see page 458). In such a case all the separate symp- 
toms must be duly considered, and yet we may be obliged to await the further 
development of the disease and the results of treatment before arriving at a 
conclusion. Patients with nervous dyspepsia are apt to grow worse and worse 
under strict treatment for ulcer, while an opposite mode of treatment (vide 
infra) often has the most brilliant results. 

Prognosis. — The prognosis depends mainly on the outward circumstances of 
the patient. If the harmful mental influences or other ^etiological factors are 
persistently active, actual and permanent recovery is hardly to be expected ; but if 
the cause can be removed, complete recovery is not rare, even in what seem to be 
grave cases. A liability to relapses is, of course, almost always left behind, as 
most patients are constitutionally nervous. 

Treatment. — If nervous dyspepsia has once been diagnosticated, the proper 
aim of our therapeutic efforts becomes perfectly definite. We must, in the first 
place, convince the patient that he has no incurable or even dangerous gastric 
disease, but that, on the contrary, his stomach is perfectly capable of performing 
its functions in a normal manner. Xothing could be more harmful to a sufferer 
from nervous dyspepsia than to have his physician manifest great anxiety about 
treatment, and prescribe a very strict diet. The patient must rather be grad- 
ually led to use an abundance of nutritious food. It is in this way alone that 



XEEVOUS DYSPEPSIA 



407 



he regains a confidence in himself, when he sees that the hearty food does him no 
harm, that he is gaining flesh, and that the bowels are becoming regular. 

Internal remedies are best omitted altogether if the patient has already taken 
a good deal of medicine. If they are successful, it is usually because of their 
influence on the mind. It is very important to make sure that there is no abuse 
of purgatives. If we must prescribe some medicine, the bitter tonics are most 
suitable, particularly the tincture of nux vomica. For anaemic patients, we may 
order iron, quinine, or arsenic. For nervous vomiting and eructations, bro- 
mide of potassium is to be given, or antipyrine and similar remedies. Treatment 
with cold water and with electricity are often extremely beneficial, although 
probably their effect is mainly subjective, for in cases of .this sort psychical treat- 
ment is of the greatest importance. Even if we gravely command the patient 
not to yield to the impulse to vomit, but to resist it as much as possible, such an in- 
junction will often do away with the symptom, and it is not rare to find in cases 
of nervous vomiting that it will cease as soon as nourishing diet is allowed, 
although previously it has occurred invariably after the most delicate kinds of 
food. It is often very advantageous in nervous vomiting to limit, as far as pos- 
sible, the amount of liquids, such as soup and milk, and to prescribe a dry sub- 
stantial diet. In many cases the vomiting will then cease very promptly. 

If there are certain objective abnormalities present as well as the purely nerv- 
ous symptoms, we must pay a certain amount of attention to these (vide supra). 
If there is gastroptosis, we should forbid constriction of the waist by the cloth- 
ing, and should order a suitable abdominal bandage. If there is hypersecretion, 
we should employ alkalies, or possibly lavage ; if achlorhydria, hydrochloric acid. 

Those methods of treatment are of great value which are directed to the ton- 
ing up of the body in general and the nervous system in particular. The patient 
may go into the country or to the mountains or the seashore. Methodical treat- 
ment with cold water is good; in particular, sponging combined with rubbing of 
the trunk and the whole body almost always gives good results. On the other 
hand, those health-resorts which often do good in the case of organic gastric dis- 
ease are but seldom beneficial in nervous dyspepsia. Thus, we have frequently 
seen such patients, who had been sent by their physicians to Carlsbad, return 
worse rather than better. We have repeatedly found electricity valuable, al- 
though we surmise that its subjective effect may be of chief importance. Gal- 
vanism is applied along the spinal column, and also through the stomach horizon- 
tally, one large electrode being placed upon the epigastrium and the other on the 
back. It is well to reverse the current frequently. Faradization and massage 
of the abdominal walls are indicated, especially when there is constipation. 

We need hardly add that the ^etiological factors must not be overlooked. The 
patient must be warned against mental or bodily overexertion, emotional excite- 
ment, etc. The main point is to aim at a methodical moral training of the 
patient. He should learn to feel and to behave like a healthy person. He should 
regain his self-control, and not allow himself to be upset by every slight psychical 
shock, whether subjective or coming from without. It is self-evident that this 
goal is to be attained not by baths and prescriptions, but by correct moral guid- 
ance. The best proof of the correctness of our views, with regard to the true 
nature of this disease, lies in the therapeutic successes which can be obtained in 
this manner alone, although it is a pity that they are more often achieved by 
empirics and quacks than by scientifically educated physicians. It is therefore 
true of nervous dyspepsia, as of all other similar neurasthenic conditions, that 
it is to be cured not by physic but by the physician. 



468 



DISEASES OE THE DIGESTIVE ORGANS 



SECTION Y 

Diseases of the Intestines 

CHAPTER I 

INTESTINAL CATARRH 

( Catarrhal Enteritis) 

iEtiology. — Tlie majority of cases of intestinal catarrh, like gastric catarrh, 
are due to an abnormal irritation of the mucous membrane of the intestine by 
its contents. In many cases the irritants are of a mechanical or a chemical 
nature, and depend upon the quantity and quality of the food taken, which ex- 
plains why catarrh of the stomach and catarrh of the intestine are so often com- 
bined with each other. Noxious substances, taken into the system by the inges- 
tion of spoiled food, such as spoiled meat, fish, beer, etc., very often play a part in 
the origin of intestinal catarrh. 

To the intestinal catarrhs caused by improper food we may add the toxic 
catarrhs which are produced by the direct ingestion of poisonous substances into 
the digestive tract. Severe inflammations of the intestinal mucous membrane 
arise from poisoning by mineral acids and corrosive alkalies, arsenic, corrosive 
sublimate, etc. Intestinal catarrh may also arise from the imprudent use of 
certain drugs, especially active cathartics. 

A great many cases of intestinal catarrh are due to infectious influences; 
these include most of the apparently spontaneous catarrhs, and also many, if not 
all, of the catarrhs attributed to taking cold or getting wet, and, finally, those 
affections which often develop epidemically or endemically in hot weather, and 
which we term summer complaint, cholera morbus, etc. Cholera morbus is an 
especially severe form, and it will be described more fully later on. We must also 
mention here that intestinal catarrh is very often one symptom of other general 
infectious diseases, such as typhoid, dysentery, septic diseases, or severe malaria. 

In a final class of cases intestinal catarrh develops from disturbances of the 
circulation, which cause a passive hyperasmia of the intestinal mucous membrane. 
Diseases of the liver and portal vein, and also chronic diseases of the heart, kid- 
neys, and lungs, are the chief affections which produce a stasis in the portal sys- 
tem, and thus an intestinal catarrh; but here the stasis is probably, in most cases, 
only a predisposing factor in the development of the catarrh, since the action of 
all other irritants is made easier by the disturbance of the circulation. 

The great frequency of intestinal catarrh in both sexes, and at every age, is 
well known. Children, above all, have a pronounced tendency to diseases of 
the intestine, so that, by a probable estimate, almost one third of the illnesses 
of children are to be referred to the intestinal canal. We will give a special 
description of intestinal catarrh in children on account of- this fact. 

Pathological Anatomy. — The pathological changes in catarrhal inflammation 
of the intestines are essentially the same as are met with in the inflammation 
of any other mucous membrane. Redness and swelling of the mucous coat, 
increased secretion of mucus, and in severe cases purulent products on the sur- 
face of the membrane, and a cellular infiltration of the tissue itself, are the well- 
known processes characteristic of all catarrhal inflammations. The solitary and 
agminated follicles often swell in follicular catarrh, and they may finally become 
the seat of superficial follicular ulcers. We often find superficial erosions on 
the rest of the mucous membrane, and in severe cases the so-called catarrhal 
ulcers. 



INTESTIXAL CATARRH 



469 



If the catarrh has lasted a long time, we sometimes find a considerable thick- 
ening of the mucous membrane, which is due to hyperplasia of the connective 
tissue, and gives an uneven, puffy appearance to the internal surface of the 
intestine. Circumscribed hyperplasia of the connective tissue may actually lead 
to the formation of polypi. If the orifices of Lieberktihn's follicles are stopped, 
we have a cystic degeneration of the follicles from the retention of the intestinal 
juice. 

We very often find, however, a considerable atrophy of the mucous membrane, 
especially in the chronic intestinal catarrh of children. This atrophy, which has 
lately been carefully investigated, especially by ISTothnagel, affects chiefly the 
glandular layer of the mucous coat. In place of the glands, which in many parts 
may wholly disappear, we find connective tissue more or less rich in cells. The 
atrophy is usually most pronounced in the colon and the lower part of the ileum. 
The muscular coat may also take part in the atrophy. 

Certain peculiarities of catarrh affecting single portions of the intestine will 
be mentioned later on. 

Symptomatology. — The symptom by which chiefly we determine an affection 
of the intestinal canal, and which in the milder cases is often almost the only 
sigm of an intestinal catarrh, is diarrhoea — that is, abnormally frequent stools of a 
looser consistency than usual; yet, strictly speaking, we should not attribute 
every diarrhoea to a catarrh of the intestinal mucous membrane, since a large 
number of influences may directly produce an increased peristalsis and a conse- 
quent diarrhoea. Thus, for instance, it is a well-known fact that sudden terror or 
great anxiety may sometimes cause an obstinate diarrhoea in a very short time. 
In general nervous and neurasthenic conditions, we sometimes have a chronic 
diarrhoea which can be due only to abnormal processes of innervation — " nervous 
diarrhoea." The diarrhoea which may arise immediately after taking cold is also 
merely the result of abnormally great peristaltic movements excited in a reflex 
manner. Probably a number of chemical and infectious irritants may also stimu- 
late the movements of the intestines, and thus set up a diarrhoea, without causing 
at the same time a catarrh of the mucous membrane. Practically, however, we 
can not make a sharp distinction between diarrhoea and intestinal catarrh; and, 
in most of the diarrhoeas which have lasted for some time, we are certainly right 
in supposing that there are actual anatomical lesions of the intestine, as well as 
functional disturbances. 

There are two chief factors which cause diarrhoea in intestinal catarrh. In the 
first place, as has already been intimated, the same injurious substances which 
cause the catarrh also excite peristalsis. The many products of the abnormal 
processes of decomposition in the intestine also exert a like influence. Besides the 
abnormal irritants, however, we ought also to consider an abnormally great irri- 
tability of the intestinal walls in catarrh. Thus it happens that the fluid contents 
of the intestine are expelled by the vigorous peristaltic movements (which the 
patient himself often feels as a "rumbling in the abdomen"), before the normal 
consolidation of the faeces is completed by the absorption of water. The food, 
under normal conditions, passes throug'h the small intestine in two or three hours, 
and thus the consolidation of the fseces takes place, as is well known, almost ex- 
clusively in the colon. We see, therefore, why the diarrhoea owes its origin 
chiefly to the increased peristalsis of the large intestine ; although in many cases 
the peristaltic action of the small intestine is also increased. 

Besides increased peristalsis, another circumstance may perhaps contribute to 
the diarrhoea, viz., the greater fluidity of the contents of the intestine due to the 
increased secretion of mucus and the exudation caused by the catarrhal inflam- 
mation. 

In the intestinal catarrh due to passive congestion we must consider still an- 



470 



DISEASES OF THE DIGESTIVE OEGAXS 



other factor, to explain the thin and watery stools — namely, the diminished ab- 
sorption of water by the intestine from disturbance of the circulation. In other 
catarrhs this factor is quite subordinate to increased peristalsis. 

The diarrhoeal dejections show a considerable difference in regard to their 
minor characteristics. Their number varies very much. There are sometimes 
two or three, and sometimes ten or more, evacuations in the twenty-four hours. 
The consistency of the stools is pap-like, or almost wholly watery. This is due 
to the abnormal amount of water in them, amounting to ninety or ninety-five per 
cent., while the amount in normal stools is about seventy-five per cent. The 
color of the thin stools in intestinal catarrh is usually bright yellow, but they are 
sometimes greenish from the admixture of bile pigment, and sometimes slimy 
(vide infra). 

In only a part of the cases does microscopic examination give us information 
as to the extent and intensity of the catarrh. We usually find the remains of the 
food, muscular fibers, starch-granules, and fat, and also countless bacteria, and 
often triple phosphates, occasional pus-corpuscles, and cylindrical epithelium — 
chiefly the constituents which are found in normal stools. Further peculiarities 
will be mentioned below. 

Besides the diarrhoea, there is often, but by no means always, abdominal pain 
in intestinal catarrh, either continuous, or having the character of paroxysmal, 
so-called colicky pains. In catarrh of the rectum there is that constant painful 
desire to go to stool which we term tenesmus. 

Physical examination of the abdomen gives, on the whole, few important 
results. Sometimes the abdomen is flat, and sometimes there is meteorism. 
Marked peristaltic action of the intestines often causes gurgling and rumbling 
noises — borborygmi. On palpation, the abdomen is often somewhat sensitive. 
The peculiar colicky pains, however, are, as a rule, alleviated by external pressure. 
In rare cases we may detect a fluctuation on palpation, if the intestine contains 
much fluid. The results of percussion depend largely upon the contents of the 
intestines. There is dullness on percussion if the intestines are full, and also if 
they are contracted and devoid of air. 

In niany cases of simple diarrhoea the general health is practically unaffected, 
but in other cases of acute intestinal catarrh, especially in the severe infectious 
forms, the disturbance of the general health may be considerable. The patient 
feels so dull and weak that he stays in bed. TTe often see a moderate rise of tem- 
perature, between 100° and 102° (3S°-39° C). There are very often gastric 
symptoms also, especially loss of appetite and vomiting. Other organs are quite 
rarely affected, except in duodenal catarrh, when the liver is involved (ride infra). 
In acute infectious intestinal catarrhs, there is sometimes an eruption of herpes 
on the lips. We have repeatedly seen, in severe cases of acute enteritis, marked 
muscular and articular pains, and even slight but manifest swelling of the joints. 
There may also be albuminuria, casts, and even the signs of acute nephritis, as 
a sequel of enteritis. 

Different Forms of Intestinal Catarrh. — Since the intestine is an organ 
which is only slightly accessible to physical examination during life, and since 
we can only rarely make a post-mortem examination in the mild diseases of the 
intestine, our knowledge as to the different forms of enteritis is defective in many 
respects. In practice we content ourselves in most cases with diagnosticating an 
intestinal catarrh simply from the existence of diarrhoea, without laying much 
stress upon the special variety ; but in many cases some points can be obtained 
which give more accurate information as to the seat of the catarrh. The distinc- 
tion between acute and chronic intestinal catarrh is also of practical significance. 

Duodenal catarrh can be diagnosticated only if it is combined with jaundice. 
The details regarding it may be found in the chapter on catarrhal jaundice. 



INTESTINAL CATAKRH 



471 



Isolated catarrh of the small intestines, of the jejunum and ileum, is probably 
only of rare occurrence, except when the upper portions of the colon are involved. 
We can very rarely diagnosticate it with certainty, but there are a number of fac- 
tors which permit us to decide that the small intestine is chiefly affected, or at 
least that it is involved in the disease. In the first place, we may assume an affec- 
tion of the small intestine, from obvious reasons, in all those cases in which there 
are also gastric disturbances. It is evident that, in the frequent combination of 
gastric and intestinal catarrh, the portions of the intestine nearest the stomach 
will be chiefly affected. Physical examination of the abdomen also gives some 
indications, since the slight sensitiveness and swelling of the abdomen, as well as 
the visible abnormal peristaltic action, affect chiefly the middle and lower por- 
tions of the abdomen ■ in catarrh of the small intestines, while the analogous 
symptoms in catarrh of the large intestine affect the lateral and upper por- 
tions of the abdomen, corresponding to the anatomical course of the colon. We 
can not make a sharp distinction, however, in this respect. The results which 
auscultation and percussion over the abdomen give in regard to the point of origin 
of the gurgling sounds and the fullness of the loops of intestine are very rarely 
unequivocal, and hence are of little value in diagnosis. 

Careful examination of the stools gives us more information. As has already 
been said, we need not have diarrhoea in a catarrh confined to the small intestines, 
since diarrhoea is due only to the increased peristalsis of the large intestine ; hence 
diarrhoea is absent, for example, in most cases of duodenal catarrh (catarrhal 
jaundice). In more extensive catarrh of the small intestines the firm stools 
passed may, however, be regarded as pathological, because, on microscopic exami- 
nation, they appear intimately mixed with little lumps of hyaline mucus (ISToth- 
nagel). As a rule, of course, catarrh of the small intestines is combined with a 
catarrh of the upper portion of the large intestine. Then we have a diarrhoea, 
but the thin stools show some peculiarities which point to an implication of the 
small intestines. As a result of the increased peristalsis of the small intestines, 
we find certain constituents in the stools which are normally contained in the 
small intestines, but which under normal conditions are no longer to be met with 
in the faeces in the large intestine. We find here, in the first place, undigested 
constituents of the food, large masses of muscular fiber, or even fragments of meat 
which may be recognized by the naked eye, and also starch and fat. Of course 
the opposite hypothesis does not hold good, that, if we find a large amount of the 
undigested portions of the food in the stools, it must necessarily always point to a 
catarrh of the small intestines, since the digestion may be impaired by other cir- 
cumstances, and increased peristalsis of the intestines, from any cause, must re- 
sult in the same symptoms. A diarrhoea, in which the thin stools contain a very 
large amount of undigested particles of food which can be recognized by the 
naked eye, was formerly called lientery, and the term is still occasionally used. 

If the stools contain bile in addition to some portions of the food, it is to a cer- 
tain degree characteristic of catarrh of the small intestines. Under normal con- 
ditions the contents of the small intestines alone show Gmelin's test for bile-pig- 
ment, while the contents of the large intestine, and also the normal stools, do 
not. In intestinal catarrh, with increased peristalsis of the small and large intes- 
tines, there is, however, often quite a large admixture of still undecomposed bile- 
pigment. The green stools which are so often seen in the diarrhoea of children, 
and more rarely in that of adults, are also well known. Such stools usually show 
a marked color reaction with nitric acid. In other cases we find only certain con- 
stituents of the stools stained with bile — a fact to which Nothnagel has called 
special attention. Yellow pigmented bits of mucus, and cylindrical epithelium 
and round cells stained with bile, are especially characteristic of the diarrhoea of 
catarrh of the small intestines. 



472 



DISEASES OE THE DIGESTIVE ORGANS 



Catarrh of the large intestine is probably present in every diarrhoea, as has 
been repeatedly stated, inasmuch as the thin stools can be explained only by an 
increased peristalsis of the large intestine; but in a number of cases we have 
symptoms which point especially to a disease of the large intestine, particularly of 
its lower portion. 

Physical examination of the abdomen should show changes, such as swelling, 
sensitiveness to pressure, etc., chiefly in the lateral portions, corresponding to 
the course of the colon; but this is rather a theoretical hypothesis than a sign of 
practical value. We can not definitely affirm, either, that " colicky pains " are 
characteristic of catarrh of the large intestine alone. The condition of the stools, 
however, is of importance. In the first place, we may note that, if the stools con- 
tain many masses of mucus which may be recognized by the naked eye, it is of 
diagnostic significance. As we have seen above, the stools in catarrh of the small 
intestines also contain mucus, but it is intimately mixed with the other constitu- 
ents of the fseces, and hence it can usually be recognized only by the microscope. 
In catarrh of the large intestine, however, the mucus rather adheres to the out- 
side of the other constituents, and is often present in large masses visible to the 
naked eye. If the catarrh affects the lower part of the large intestine chiefly, it 
may be that the intestinal contents are already formed into firm lumps, which 
may sometimes be wholly or partly inclosed in a layer of mucus. In acute catarrh 
of the lowest part of the large intestine the evacuations are sometimes composed 
chiefly of pure mucus, with a greater or less admixture of pus, as is seen especially 
in the "catarrhal flux" (see the chapter on dysentery). The more the rectum is 
involved in the inflammation, the worse is that painful feeling of tension and 
pressure at the anus during and after the evacuation, which we term tenesmus. 

Isolated inflammation of the rectum (proctitis) is, at least in part, directly 
accessible to examination by the finger or by the speculum. Painful tenesmus 
and an admixture of mucus, and especially of pus in the stools, are the chief 
symptoms of the disease. In most cases, however, we have to do, not with a pri- 
mary disease, but with a secondary catarrh of the rectal mucous membrane, as a 
result of different morbid conditions in the vicinity of the rectum, or of new 
growths, syphilitic processes, etc., in the rectum itself. Periproctitis (ischio- 
rectal abscess) belongs to the domain of surgery, and can not be described here. 

Intestinal catarrh is divided into an acute and a chronic form. 

In the acute intestinal catarrhs, excluding the toxic inflammations, we class 
simple diarrhoea, which usually passes off in a few days, and the severe enteritis, 
which is probably usually infectious, and is attended by a marked disturbance of 
the general health, by fever, and sometimes by gastric symptoms also, as well as 
by herpes, by occasional slight albuminuria, by articular pains, etc. It lasts from 
three to ten days. Cholera morbus (vide infra) is to be regarded as a special form 
of acute infectious inflammation of the gastric and intestinal mucous membranes. 

Chronic intestinal catarrh either comes from an acute disease of the intestinal 
mucous membrane, or gradually develops independently. In adults it is by no 
means a frequent disease, at least as regards pronounced cases, and is much rarer, 
for example, than chronic gastric catarrh ; but we have already mentioned that it 
is very common in practice among children. 

In regard to the aetiology and symptomatology, much the same may be said of 
chronic catarrh which we have learned to recognize in considering acute catarrh. 
In regard to aetiology we must note, in adults, chiefly the intestinal affections 
remaining after an attack of some acute disease — e. g., dysentery, severe malaria, 
or typhoid. Among the most prominent symptoms are the abnormal evacuations, 
usually alternating between diarrhoea and constipation, due chiefly to the atrophy 
of the muscular coat and the disturbance of the nervous apparatus. We must also 
mention, as a prominent symptom, the secondary disturbances of the general 



rSTTESTLNTAL CATARRH 



473 



nutrition, such as emaciation and anaemia. In regard to peculiarities in the char- 
acter of the stools, we must refer to what has been said above. As chronic catarrh 
of the large intestine is far commoner than chronic catarrh of the small intes- 
tines, we very often find large amounts of mucus in the stools. 

Treatment. — Most of the milder cases of acute intestinal catarrh need only a 
dietetic treatment. If the patient avoids all injurious substances for a few days, 
he recovers completely. The different gruels, such as barley and oatmeal gruel, and 
also weak broths, milk, and thoroughly toasted bread, or the German zwieback, 
are generally regarded as the most suitable food. The coarser vegetables and 
fruits, fat meat and brown bread, are to be avoided as much as possible. The 
best beverage is tea, or claret diluted with water. In other respects we may 
refer to the dietetic rules laid down under the treatment of chronic gastric 
catarrh. 

It is also an important rule, confirmed by much experience, to keep the abdo- 
men warm. Children should always stay in bed, and adults should do so, at least 
in all severe cases. It is a good plan, particularly in children, to protect the abdo- 
men from cold by a flannel band. 

In many of the mild cases it is scarcely necessary to use internal remedies. 
Gum mixture (P. G.) or almond mixture is a good prescription if there is no other 
special indication, but in severe cases further medication may be proper. If 
we have reason to suspect some irritating ingesta or a collection of faeces as a 
cause of the intestinal catarrh, a cathartic acts favorably at the beginning of the 
treatment, in spite of the existence of diarrhoea. Our best cathartic in such cases 
is castor-oil or calomel. In all those cases in which many thin dejections point to 
a greatly increased peristalsis of the intestine, we use astringents, especially 
opium, which we give in the form of the simple tincture or the wine in doses of 
ten or fifteen drops, one to three times a day; or as a powder, half a grain to a 
grain (gramme 0.03 to 0.05) of opium with a grain (gramme 0.05) of sugar, two 
or three times a day. It is also well to combine the opium with some mucilagi- 
nous vehicle, as 2 parts of laudanum to 150 of gum mixture or decoction of salep 
(P. G.), a tablespoonful every two or three hours. Tannic acid and the like are 
seldom employed in acute enteritis. 

If there is severe colic, opium, or, under some circumstances, an injection of 
morphine is the best remedy. In milder cases it is sufficient to apply warmth to 
the abdomen, by warm poultices or hot towels. The colic, however, often depends 
upon the presence of old faecal masses in the intestine, when it is necessary to 
prescribe a cathartic, such as castor-oil. 

In all cases in which the symptoms point to a more intense disease of the large 
intestine, local treatment may be employed. This is chiefly of importance in the 
treatment of chronic intestinal catarrh situated mainly in the large intestine. 
We irrigate the large intestine daily with weak astringents, and sometimes with 
disinfectants. The necessary apparatus is very simple. It consists of an ordi- 
nary irrigator, to which a rubber tube, about half a metre long and with a proper 
tip, is attached. Instead of the irrigator we can use a large glass funnel, a " He- 
gar's funnel." We may very well use, for an end-piece to be introduced into 
the rectum, a long, soft, elastic oesophageal tube, which can easily be pushed 
quite high up. The fluids used for irrigation must always be warmed to about 
85° (30° C), and should be allowed to run in gradually and slowly. The amount 
of fluid used for one irrigation should be two or three pints (1-14 litre), or some- 
times more. The patient keeps on his back during the irrigation. The knee- 
elbow position, which is much more uncomfortable than the dorsal, is only occa- 
sionally necessary. The fluids most used are a one- or two-per-cent. solution of 
salicylic acid, solutions of salicylic and boracic acids combined, a one-per-cent. 
tannin solution, or a solution of acetate of lead (1 to 1,000). 



474 



DISEASES. OF THE DIGESTIVE ORGANS 



If there is painful tenesmus, it is usually relieved by suppositories of cacao 
butter containing- extract of opium. 

In chronic intestinal catarrh a careful regulation of the diet is of the greatest 
importance. To be avoided are fruits and sour or greasy dishes, indigestible vege- 
tables and puddings, coarse bread, and above all, beer; and to be recommended 
are tender lean meat (sirloin), sweetbread, fish that are not oily (such as trout 
and pike), potato puree, and particularly soft-boiled rice and sago. In regard to 
eggs and milk, individual experience must decide. Beyond this the main point is 
overcoming the chronic diarrhoea. Besides the cautious use of opium, the as- 
tringents are to be particularly borne in mind, either alone or combined with 
opium. Those most often prescribed are tannic acid, acetate of lead, columbo, 
and logwood. We have also seen excellent results in mild cases from the steady 
use of bilberry wine. The preparations of bismuth also deserve to be recom- 
mended, particularly the salicylate (8 to 15 grains several times a day, gramme 
0.5-1), and the newly introduced tannigen (acetyl-tannin) and tannalbine (albu- 
minate of tannin) in doses of eight grains or more (gramme 0.5) several times a 
day. In case the offensive odor of the discharges indicates abnormal decomposi- 
tion in the intestinal canal, we employ naphthaline in doses of 1-J to 5 grains 
(gramme 0.1-0.3) several times a day. We often have to try various remedies in 
a particular case before we find one that is efficient. Great care should be exer- 
cised that there be no long periods of constipation; if necessary, we may use in- 
jections, saline laxatives, or castor-oil. 

Good results are often obtained in chronic intestinal catarrh by drinking the 
waters at Carlsbad, Tarasp, Kissingen, Marienbad, or Homburg, particularly in 
cases with occasional constipation. 

It is of practical importance to distinguish the genuine cases of chronic in- 
testinal catarrh with an anatomical basis, from the common nervous disturbances 
of the digestive tract. Not infrequently the most diverse symptoms on the part 
of the intestine, including colic and irregularity of the bowels, appear as part of a 
general neurasthenia or nervousness (see page 1193). In such cases there is little 
benefit from internal remedies and strict diet, while appropriate general treat- 
ment with cold water, electricity, and massage is often attended with the best 
results. With regard to this compare also the chapters on nervous dyspepsia and 
on habitual constipation. 

APPENDIX 

Membranous Enteritis and Mucous Colic. — The name of membranous enter- 
itis or mucous colic is applied to a condition which is not very common, but yet 
of great practical importance. It is characterized chiefly by the habitual dis- 
charge with the faeces of a great abundance of mucus, in the form of membranes. 
The disease is observed especially in women, but, in rare cases, also in men. It is 
noticeable that the patient is almost always a nervous, hysterical, or hypochon- 
driacal individual. 

In many cases a discharge of the membranes takes place in separate attacks, 
which occur either daily or at longer intervals, and are associated with severe 
colic ("mucous colic ")• The membranes are gray or reddish gray, and often cy- 
lindrical or rolled up in a ball. They consist mainly of mucine — sometimes, it is 
said, of albuminoid matters also — and examined under a microscope they are 
usually found to contain an unusual amount of desquamated cylindrical epithe- 
lium, with a very small number of leucocytes, and perhaps also a few crystals of 
triple phosphate and cholesterine. In other cases there are scarcely any attacks 
of colic, but merely a persistent discharge of the above-described membranes and 
bits of mucus. The true discharges of the bowels are almost always very sluggish 
and very hard. 



CHOLEKA MORBUS 



475 



There is still much uncertainty as to the true nature of this diseased condi- 
tion. Whether there is a genuine " enteritis " is doubtful, at least with regard 
to many cases. The noticeably frequent' association of the disease with hys- 
teria and neurasthenia seems to indicate nervous causes for the exaggerated pro- 
duction of mucus. The formation of the membranes probably takes place through 
the rolling up of the mucus in the depths of the longitudinal folds of the colon 
during its cramp-like contractions. 

The course of the disease is usually tedious, but complete recovery may occur ; 
there is no danger. The nutrition of the patient may remain perfectly normal, 
but in some cases it is greatly impaired. This depends chiefly upon the character 
of the other nervous symptoms present. 

The treatment is partly local, by means of irrigations with alkaline solutions, 
or diluted lime-water, and the injection of oil and similar measures; and partly, 
or rather chiefly, general, for the cure of the associated neurasthenia. The most 
common modes of treatment are by means of hydrotherapy, electricity, and mas- 
sage. In addition, we should combat the habitual constipation in the ordinary 
ways (vide infra). 



CHAPTER II 

CHOLERA MORBUS 

(Cholera JYostras. Cholera Infantum) 

By the name " cholera morbus " we mean an acute disease of the stomach and 
intestinal canal of a definite form, whose symptoms in severe cases greatly resem- 
ble those of genuine Asiatic cholera. It is in the highest degree probable, from 
the whole course of the disease, that cholera morbus also depends upon an acute 
infection of the body by a specific germ; but this germ has not yet been iden- 
tified. 

Cholera morbus comes on usually as an epidemic, and almost exclusively in 
the hot summer months — June to August. Hence it is often termed summer 
cholera. Children in the first two years of life are chiefly attacked, especially 
those who are artificially fed or who have recently been weaned. The disease 
also attacks older children and adults, but much more rarely. 

[Special opportunities are afforded in this country for the study of cholera 
infantum. The causative conditions are, briefly, unsuitable food, a high tempera- 
ture, and bad hygiene — conditions which are all combined and attain their maxi- 
mum intensity in large cities. That a high thermometric range alone is not suffi- 
cient is shown by the comparative immunity of all country districts. Those who 
live in the country, or who have never been busied among the city poor, have no 
idea of the atmosphere breathed by the children of the poorer classes, especially 
during the heated term, nor of the extreme difficulty — impossibility we can almost 
say — of getting really good milk. Even if the milk was good at the start and it has 
not been tampered with, the time which necessarily elapses after it is drawn from 
the cow and before it reaches the consumer permits marked fermentative changes 
during hot weather. And milk is and must remain the main article of diet for 
children under two years of age.] 

The symptoms of cholera morbus are those of a severe acute gastro-enteritis. 
The disease begins suddenly, or after some slight warning, with violent vomiting 
and severe diarrhoea. In some cases one of these symptoms predominates, and in 
others the other. The vomitus consists partly of the food taken, and partly of a 
slimy, watery substance. The stools at first retain their faacal character, but they 



476 



DISEASES OF THE DIGESTIVE OKGAXS 



soon become more colorless and more watery, so that they sometimes approach 
the well-known rice-water appearance of the stools in genuine cholera. Abdomi- 
nal pain is usually absent, but a feeling of pressure and constraint in the epigas- 
trium is often present. The diminished secretion of urine and the frequent mus- 
cular pains cause the whole type of the disease to resemble genuine cholera still 
more closely. There is sometimes a cutaneous eruption resembling roseola. 

The severe constitutional disturbance is especially characteristic. The pa- 
tient becomes extremely dull and has a wasted look, the voice is weak and hoarse, 
an unquenchable thirst sets in, the pulse is very small, the skin of the face and 
the extremities is cool and livid; in short, we have the pronounced picture of a 
general collapse. The body heat also falls, although at the first stage of the dis- 
ease there is often a rise of temperature. 

[The temperature is always high, even during the stage of collapse, when the 
skin and extremities are cool to the touch ; if the thermometer is introduced into 
the rectum — generally the best place, by the way, to take the temperature in 
young children — it will rise to 101° to 102°, and is more apt to reach 104° to 107°. 
This shows that inflammation plays a large part in the pathology of the disease.] 

The picture of a severe general disease is especially prominent in cholera infan- 
tum. In severe cases of this form of the disease the general restlessness, which at 
first exists, rapidly passes into somnolence. The child lies with sunken, half- 
closed eyes, the conjunctivse are slightly injected, the cornese are cloudy, the face 
is pale and cyanotic, the fontanelles are depressed, the skin is cool, and the pulse 
is small and frequent and it can scarcely be counted. Amid these symptoms, 
which are usually termed " hydrocephaloid " by specialists in children's diseases 
[Marshall Hall], death comes on in coma or with slight convulsions. There can 
scarcely remain room for doubt that these severe cases of gastro-enteritis are of 
infectious origin, and that the constitutional symptoms are the result of toxic 
matters generated in the intestine under the influence of the micro-organisms 
(vide supra, the chapter on acute gastritis). Another peculiar symptom which 
occurs in severe cholera infantum is the so-called sclerema adiposum. While the 
temperature keeps sinking the extremities become peculiarly stiff and rigid, and 
the skin grows pale and firm. This phenomenon is caused by the fat in the fat 
cells of the subcutaneous connective tissue stiffening as a result of the low 
[superficial] temperature. 

The mortality of children with cholera infantum is very marked, especially in 
large cities, and among the poorer classes of society. Severe cases usually end 
fatally in a few days, but, on the other hand, many cases recover, either because 
the course of the disease from the first is not so severe, or because cases appar- 
ently hopeless take a favorable turn. In adults it is extremely rare to see cholera 
morbus terminate unfavorably. Patients also recover quite rapidly from appar- 
ently severe conditions, although the stomach and intestines often remain rather 
sensitive for a long time. 

The anatomical appearances in children who die of cholera infantum usually 
contrast, from their insignificance, with the severe symptoms observed during life. 
The catarrhal affection of the gastric and intestinal mucous membranes is not 
at all prominent in the cadaver, and the solitary follicles and Peyer's patches 
show only a slight swelling. A careful microscopic examination of the intestinal 
mucous membrane shows, however, quite severe inflammation. The other lesions 
which are most frequently seen are lobular atelectases in the lungs, venous hyper- 
semia and cedema of the pia mater, and slight lesions of the kidneys. 

The diagnosis of cholera morbus presents no difficulty if the characteristic 
symptoms of the disease are present. The distinction between it and genuine 
Asiatic cholera used to be occasionally quite difficult, and it was rendered possible 
only by considering the ^etiological factors, and the evident connection between 



IXTESTIXAL CATAEEH OF CHILDEEX 



477 



the individual case and other cases of undoubted cholera^ By Koch's discovery of 
the comma-bacillus in Asiatic cholera the distinction between the two diseases 
has now become absolutely certain. In all suspicious cases, therefore, we must 
examine the dejections for comma-bacilli, and upon the result of this examina- 
tion depends the determination of the proper means of prophylaxis. 

The treatment of cholera morbus in adults must be first to take special care to 
limit the diet. The food should be only gruels, or at most broth, soft-boiled eggs, 
and milk. It is a good plan to give the milk iced, and in small amounts. The 
distressing thirst is best relieved by cracked ice. Wine (iced champagne) is to be 
given if the general weakness becomes marked. 

Among drugs, opium is the most effective remedy, and, whether in powder, as 
the extract, or in liquid form, as laudanum, it is the first thing to use to relieve 
the diarrhoea and vomiting. All other remedies which are recommended in chol- 
era morbus in adults, such as nitrate of silver, are quite subordinate to opium. 
We may combine small doses of calomel with the opium. If there is a severe col- 
lapse which threatens life, it is advisable to make a subcutaneous injection of 
water, containing 0.6 per cent, of salt, or 5 per cent, of grape sugar. 

We are more cautious in prescribing opiates for children, although here small 
doses of opium, one or two drops of laudanum according to the age of the child, 
may often be indispensable. In fresh cases calomel has obtained a great reputa- 
tion, a sixth of a grain (gramme 0.01) two or three times a day. Ice-cold cow's 
milk, given in teaspoonfuls, serves best as food, if the child can not be fed natu- 
rally by breast-milk. 

Many specialists recommend that no food at all should be given for a few days, 
but merely a sufficient amount of cold water or chamomile tea. If nothing will 
stay on the stomach, we may try a subcutaneous injection of 0.6 per cent, saline 
solution. If there are symptoms of severe collapse, we should immediately em- 
ploy hot baths at 100° F. (30° E.), with the addition of 10 to 15 ounces of mus- 
tard (300-500 grammes) and hot packs, as well as such stimulants as camphor 
or alcohol subcutaneously. To guard against desiccation of the sclera and cor- 
nea, the eyes should be covered with compresses moistened with solutions of ace- 
tate of lead, corrosive sublimate, etc. 



CHAP TEE III 

INTESTINAL CATARRH OF CHILDREN 

(Chronic Dyspepsia of Children. Pedatrophy) 

The great frequency and the practical importance of the " dyspeptic condi- 
tions " in children in the first years of life, which conditions are associated with 
severe disturbances of nutrition, justify a short description of them, but we must 
refer to the special manuals on children's diseases for a detailed account. 

That diseases of the digestive^organs play so large a part in children's troubles 
is owing, on the one hand, to the great sensitiveness which the digestive apparatus 
in children shows to the irritants which are brought in contact with it, and, on 
the other, to the too common foolishness and carelessness which the child's parents 
and nurses show in its feeding. Of course it is not always ignorance and neglect, 
but often, unfortunately, poverty and want which cause children to suffer, and 
explain the terrible mortality in the first years of life. 

The simple fact that by far the larger number of children who suffer from 
dyspeptic and atrophic conditions are fed artificially, leads us to the belief that 



478 



DISEASES OE THE DIGESTIVE OKGANS 



the cause of most of the intestinal diseases in children is to be found in faulty and 
injudicious feeding*. The food, which is not suited to the child's digestive powers, 
is only imperfectly absorbed; it undergoes many processes of decomposition, 
whose products irritate the intestinal mucous membrane and give rise to increased 
peristaltic action. Thus the imperfect digestion, or " dyspepsia," excites a ca- 
tarrh of the gastric and intestinal mucous membrane, by which again, in a vicious 
circle, the digestive power is still further reduced. Hence the boundary between 
" dyspepsia " and catarrh can be drawn only artificially. It is certain that infec- 
tious influences also play an important part in the intestinal diseases of children. 
One proof of this is that indigestion is much more frequent during the hot 
weather than during the winter months, but although numerous bacteriological 
investigations have been made, observers have not yet been successful in deter- 
mining special pathogenic organisms for the several varieties of intestinal catarrh. 

The anatomical changes of the intestinal mucous membrane in children who 
die of " chronic intestinal catarrh " are, as a rule, only slightly marked, and 
contrast, in their apparent insignificance, with the severe intestinal symptoms 
observed during life. Probably here also the toxic influences of the matters 
abnormally generated in the intestine, play a more important part than do the 
anatomical changes. We must remember, however, that most catarrhal condi- 
tions are hard to recognize in the cadaver because of the disappearance of the 
hyperEemia. The changes present are quite important, but they require micro- 
scopic examination for their detection. Sometimes the swelling of the follicles is 
especially marked — follicular catarrh. Follicular ulcers are also seen. In other 
cases the atrophy of the mucous membrane, which is often seen after chronic 
catarrhs, is the chief lesion. Chronic thickening and swelling of the mucous 
membrane is of rarer occurrence. In most of the severe cases the large intestine, 
and also the lower portion of the ileum, are the chief seat of the changes. We 
often find a swelling of the mesenteric lymph-glands, and also a fatty liver. In 
the lungs extensive atelectases or nodules of catarrhal pneumonia often develop 
as a result of the imperfect respiration. 

The symptoms of chronic intestinal catarrh are, in the first place, those due 
directly to the intestinal trouble, and, secondly, the quite rapid disturbance of the 
child's general nutrition. 

The condition of the stools is the most important intestinal symptom. The 
normal dejection in children until they are weaned is of the color of the yolk of 
an egg, of a rather pasty consistency, and of a faintly sour smell. In intestinal 
catarrh the stools are more frequent, six or seven, and even more, a day. They are 
thinner, more watery, contain large flakes and lumps of undigested bits of case- 
ine and other remains of food, and smell badly. They very often have a green 
color,* or acquire it on standing. We may find admixtures of mucus, sometimes 
in the form of the so-called " sago grains," especially in catarrh of the large 
intestine. With the microscope we find in severe cases, besides particles of food, 
leucocytes and epithelial cells, threads and clumps of mucus, and innumerable 
bacteria of all shapes. There are also crystals of triple phosphate, when the stools 
have an alkaline reaction, and needle-shaped crystals of the fatty acids, as well as 
plates of cholesterine, when the discharges are acid. 

There is no definite distinction in regard to the dejections in catarrh of the 
large and of the small intestines. On the whole, the rule holds that, in catarrh 
of the small intestines chiefly, the stools are larger, they are passed with more 
wind or gas, and show a more uniform consistency; while in catarrh of the large 
intestine they are smaller but more frequent, ten or twenty a day, are passed 
noiselessly, are associated with tenesmus, and show a different consistency in 



* The statement that this green color is due to a special variety of bacillus lacks confirmation. 



INTESTINAL CATAEEH OF CHILDEEN 



479 



their various parts, partly normal, partly thin, partly slimy, etc. Examination 
of the abdomen has some importance, for, as a rule, in catarrh of the small intes- 
tines the abdomen is much swollen, while in catarrh of the large intestine it 
is often deeply sunken. The liver is often enlarged and distinctly palpable, and 
sometimes the spleen also. 

We often find disturbances in the stomach, vomiting, eructations, etc., as well 
as trouble in the intestines. There may be thrush in the mouth, or the develop- 
ment of aphthous ulcers. 

Among other complications, we see diseases of the respiratory tract, includ- 
ing bronchitis, atelectasis, and catarrhal pneumonia; also albuminuria, eczema, 
furunculosis, and nervous disturbances. 

In almost all long-continued cases, however, the general disturbance of nutri- 
tion, the atrophy (athrepsia) of the child, takes the first place in the picture of 
the disease. The muscles become shriveled and flabby, and the whole body finally 
becomes so much emaciated that the pale, dry skin hangs in broad folds and wrin- 
kles about the bones, whose prominences are everywhere visible. The face is 
sharp, and has an aged expression (" Voltaire-face ") from the many little folds 
of the skin. The eyes are dull, lusterless, and wide open; the voice is merely a 
low, hoarse whimper. The abdomen is deeply sunken, or in some cases it is 
swollen by meteorism, in peculiar contrast to the emaciation elsewhere; and its 
surface is traversed by bluish veins. 

From this sad picture, unfortunately so frequently seen in practice among 
children, we can usually recognize the condition of things at the first glance, for 
by far the larger part of the cases called " pedatrophy " are due to chronic digest- 
ive disturbances. Very often it is combined with rachitic changes in the bones, 
of whose occurrence we shall speak further in the description of rachitis. Tuber- 
cular changes, too, are often found in the cadaver, especially in the lungs and the 
bronchial and mesenteric lymph-glands. In such cases, of course, the tuberculosis 
is usually to be regarded as the main disease, upon which the intestinal affection, 
which may be simple or even tubercular, has developed secondarily. During life 
tuberculosis in little atrophic children may very easily be overlooked. 

If we would give a full account of the treatment of the, atrophic conditions in 
children due to digestive disturbances, we must include in our consideration the 
entire hygiene and care of children in health and disease, for all children's physi- 
cians are united in the opinion that, as the cause of most intestinal diseases in 
children is to be found in improper feeding, so recovery from existing digestive 
disturbances can take place primarily only by a corresponding proper and judi- 
cious feeding. In what follows we can refer only to the most important principles 
and general points which are here to be considered. 

The only proper and natural food for a child in its first year is breast-milk. 
All dyspeptic conditions are much rarer in children who are nursed than in bot- 
tle-fed children, and, when they do occur in children at the breast, they often 
are only of brief duration. They are then to be referred usually to certain dis- 
turbances in the mother, such as disease, improper food, or severe mental excite- 
ment. The return of menstruation or a new pregnancy has sometimes an unfa- 
vorable influence on the character of the milk. Finally, we may mention that 
in spite of the best of milk, if the breast is given irregularly and too frequently, it 
may cause anomalies of digestion in nursing children. 

Most of these slight disturbances are easily quieted. Sometimes the fault 
lies in the unsuitable diet of the wet nurse. If this is too rich in fat or in albu- 
men, the breast-milk may not be well borne. Exceptionally it happens that, with- 
out any discoverable reason, the milk of a wet-nurse " does not agree " with the 
child. Then we must change the nurse. The atrophic conditions which develop 
and progress in children, in spite of plenty of normal food, are usually due, not to 



480 



DISEASES OE THE DIGESTIVE ORGANS 



simple digestive disturbances, but to deep-seated, general, constitutional diseases 
like tuberculosis, or syphilis. 

The great majority of cases of chronic intestinal catarrh and chronic atrophy 
are found, as we have said, in bottle-fed children. The first question which every 
physician should ask a mother who brings him such a child for treatment, must 
therefore refer to the sort of feeding which the child has. If the mother, for any 
reason, can not nurse it herself, and if the bottle-fed child has digestive disturb- 
ances, we must invariably consider, in the first place, the possibility of procuring a 
wet-nurse. Eeeding by the milk of a wet-nurse is a remedy which, at least in 
many cases, by saving the child's life, repays the many annoyances and quite 
large expense which a wet-nurse causes. We must tell the parents this, and repre- 
sent to them, without reserve, the great dangers which threaten the life of every 
bottle-fed baby. Complete, and sometimes even quite rapid, recovery may be ob- 
tained through a wet-nurse, even in cases of severe chronic intestinal catarrh, 
when atrophy and weakness are already very far advanced. 

Often, however, it is impossible to hire a wet-nurse, especially in the poorer 
classes of society. We must continue bottle-feeding, and these are the cases 
among which chronic intestinal catarrh demands the greatest number of victims ; 
yet even here the physician can always do much good by instructing- the parents. 

The best substitute for mother's milk is cow's milk. This must be as fresh as 
possible, and is given boiled. A great and most beneficial advance in the arti- 
ficial nourishment of infants was made by the introduction of Soxhlet's apparatus 
for boiling milk. This accomplishes an almost complete sterilization of the milk 
and the vessels which contain it. One part of the milk must be diluted, accord- 
ing to its quality, with two or three parts of boiled water in the first months, in 
children from four to six months old with equal parts of water, and in older 
children with about half as much water. At the age of about nine to twelve 
months, the child may have undiluted milk. In general we give the milk warmed 
to about 85° (28° C), but children with gastro-intestinal catarrh often bear 
cold milk, given in small amounts, better than warm. There are special addi- 
tions made to the milk, with the intent of rendering the cow's milk a better sub- 
stitute for mother's milk. Of these, the first to be mentioned is milk sugar. In 
feeble children experience shows that it is often very advantageous to dilute the 
milk with oatmeal water or rice water. Sometimes, also, the addition of veal 
broth is most satisfactory. 

Cow's milk, properly diluted, is better for children with chronic intestinal 
catarrh, in many cases, than any other food. In severe acute digestive disturb- 
ances, however, it is sometimes advisable to omit the milk entirely for a few days, 
and give instead of it only a little chamomile tea or some mucilaginous drink 
such as oatmeal gruel made with water and strained, or decoction of salep. In 
chronic dyspepsia we must first try good cow's milk. If the milk is not well borne, 
if the diarrhoea increases, and if the child becomes still more emaciated, we may 
try to get milk from another and better source ; but it often happens either that 
we can not procure good milk, or that the child can not bear even the best cow's 
milk. We are then obliged to have recourse to one of the many " artificial foods " 
and " substitutes for mothers' milk " in the market. We can not here go into par- 
ticulars concerning these. Each of these preparations has occasional good results 
to show, but none of them has an uncontested pre-eminence over the rest. We 
will mention the preparations most in use at present, of whose value in individual 
cases we have convinced ourselves: Swiss condensed milk and the infants' foods 
of Nestle, Kufeke, LofTlund, and Theinhardt, as well as many others. Gartner's 
cream-milk (Fettmilch) is sometimes advantageous. It is artificially prepared 
and contains little caseine but much fat. 

If we keep fast to the principle that every intestinal catarrh in children is to 



IXTESTIXAL CATARRH OF CHILDREN 



481 



be treated in the first place by a judicious regulation of the diet, in many cases we 
shall not have to use any drugs. These may be of service only when we have also 
carried out the dietetic measures which are specially necessary. 

Calomel has obtained the greatest reputation in the treatment of intestinal 
catarrh in children. It deserves to be tried, particularly in rather early cases, in 
doses of T V to | of a grain (gramme 0.005-0.01) in powder. If the diarrhoea lasts 
a long time, we may very well use opiates, although with great caution. The com- 
bination of calomel and opium often does good service. 

Calomel gr. g (grin. 0.01); 

Extracti opii gr. & ( " 0.002) ; 

Pulv. acacia? gr. ss ( " 0.03). 

M. et ft. pulv. 

Sig. : One such powder, three or four times a clay. 

With little children we may put two to four drops of laudanum in three 
ounces (grammes 100) of liquid, such as gum mixture, salep decoction, muriatic- 
acid mixture, etc., and give a dessertspoonful of this every two or three hours. 

Many attempts have been made to check the abnormal processes of decomposi- 
tion in the intestine by prescribing remedies which possess antiseptic and anti- 
zymotic properties. Creasote has been warmly recommended by many, four to 
six drops in two ounces (grammes 50) of water with half an ounce (gram m es 15) 
of syrup, a teaspoonful every two hours. Other drugs used for the same purpose 
are naphthaline, one-half- to one-per-cent. solution of dilute muriatic acid in 
water, and one-per-cent. solution of chloral in water. A prescription for naph- 
thaline is as follows : 



5 Xaphthaline 0.5 to 1.0; 

Mucilag. acacia?, 

Aqua? destillat aa 40.0; 

01. mentha? piperita? gt. j. 



M. Sig. : Shake. Teaspoonful every two hours. 

If the stools have a green color, it is said that lactic acid is especially beneficial. 
A teaspoonful of a two-per-cent. solution may be given fifteen minutes after every 
meal. 

A number of other remedies, " astringents," are given to act directly on the 
diseased mucous membrane. Those most to be recommended in chronic diarrhoea 
are subnitrate of bismuth, one or two grains (gramme 0.05-0.1) four to six times 
a day, which may be combined with opium, nitrate of silver (1 to 2.000 solution), 
alum (1 to 200 solution), guarana, five to fifteen grains (gramme 0.3-1.0), three 
times a day, and many others. Of late, tannalbine has been much recommended 
for diarrhoea in children; smaller children should receive four grains (gramme 
0.25) several times a day, and larger children twice as much, in milk or water. 

If a large amount of mucus in the stools points to a catarrh of the large intes- 
tine, we may sometimes employ irrigation of the colon with excellent results. We 
inject the fluid, one-per-cent. solution of tannin or alum, or solution of acetate of 
lead (1 to 3 to 1,000), once or twice a day. The amount of fluid to be introduced 
at once, by a Hegar's funnel, with a gum-elastic catheter, may reach one or two 
pints (half a litre to a litre). 

In many cases of chronic diarrhoea it is said that the continued use of the 
water of the Carlsbad ^liihlbrunnen proves wonderfully beneficial even for little 
children. If there are at the same time marked gastric symptoms, such as fre- 
quent vomiting, we may advantageously employ lavage. This is performed by 
means of a soft-rubber catheter, about six millimetres in diameter, connected 
31 



482 



DISEASES OF THE DIGESTIVE ORGANS 



with a rubber tube attached to a small glass funnel. For liquid we take a weak 
solution of hydrochloric acid, 1 or 2 parts per mille, or a 0.5-per-cent. solution of 
boracic acid. 

[In view of the great importance of this malady, it seems desirable to remark 
on one or two points. 

In the first place, prophylactic measures are deducible directly from the aeti- 
ology. No child should be kept in a large city in summer, if it can be provided 
for at the sea-shore or in the country. The vast number who must perforce re- 
main are to be kept under the best general hygienic conditions possible. Mothers 
should be encouraged to take their children to the relatively pure air of the public 
parks as much as they can. The relation between diet and the diarrhoea of chil- 
dren should be dwelt upon whenever there is opportunity. 

The establishment of boards of health has done much, and will do more, to 
check the ravages of summer diarrhoea. 

Great advances have been made in the artificial digestion of cow's milk within 
a few years. By the aid of the preparations of Fairchild Bros. & Foster the 
caseine is digested in part, and the remaining portions coagulate in light flocculi ; 
at the same time no appreciable taste is imparted to the milk, provided that a 
moderate amount of care is exercised. The importance of preventing the forma- 
tion of large, firm curds has long been recognized, and an older means of attain- 
ing this end was mechanically to separate the curd by adding to the milk a barley 
or other similar water-gruel. Mellin's, Horlick's, and Ridge's foods also deserve 
mention in this connection.] 



CHAPTER IV 

TYPHLITIS AND PERITYPHLITIS 

{Appendicitis. Typhlitis Stercoralis. Inflammation of the Coecum) 

^Etiology and Pathological Anatomy. — Inflammation of the caecum and its 
vicinity has a special place among the diseases of single portions of the intes- 
tines. The reason why circumscribed inflammation so often develops here is to 
be found in the peculiar anatomical arrangement of the caecum and its appendix, 
the vermiform process. It is evident that the conformation of the parts makes 
it particularly easy for inflammatory germs to settle in this place. 

Formerly it was believed that the inflammation might often be limited to the 
caecum itself. It was asserted that impacted faecal matter occasioned mechanical 
irritation of the intestinal wall, and thus facilitated the attack of chemical and 
infectious agents. In this way arose the doctrine of " typhlitis stercoralis," but 
no such simple typhlitis has ever been demonstrated post-mortem, and although it 
can not be absolutely denied that under certain circumstances there may occur a 
genuine typhlitis, as a result of the accumulation of faeces, / yet its frequency has 
certainly been much overestimated (Sahli). It is years since the author has 
made a diagnosis of " typhlitis stercoralis." 

By far the greatest number of cases of acute inflammation in the ileo-caecal 
region are perityphlitis; that is, inflammation of the peritoneum and the con- 
nective tissue surrounding the caecum. From the point of view of pathological 
anatomy, we might term the inflammation of the retro-caecal tissue paratyph- 
litis, inasmuch as it is extra-peritoneal, in distinction from the true intra-peri- 
toneal perityphlitis; but clinically we can not maintain this distinction, or at 
most, imperfectly. The starting point for perityphlitis is the vermiform appen- 
dix. To this there are rare exceptions in which the inflammation arises from 



TYPHLITIS AND PEBITYPHLITIS 



483 



perforation of the caecum itself. The appendix, although of so little physiolog- 
ical importance and a merely rudimentary portion of the intestine, plays an im- 
portant part in pathology. Small faecal masses from the caecum often enter the 
vermiform appendix, and, under some circumstances, they may remain there. The 
fluid in them is absorbed, they are very often incrusted with lime-salts, and thus 
the little so-called " faecal calculi " are formed. In many cases the return of 
faecal masses into the caecum is probably hindered by the valve at the orifice of the 
vermiform appendix, Gerlach's valve. Foreign bodies, such as little seeds of 
fruit, often enter the vermiform appendix and perhaps give rise to the formation 
of a faecal calculus; but one must be cautious in assuming that any small hard 
mass is a foreign body, for these calculi often have such a rounded shape that 
they were formerly considered, very erroneously, to be retained cherry-stones. 

In many cases faecal calculi may remain in the vermiform appendix for a long 
time without producing any further injurious results, but as a rule they cause a 
mechanical irritation of the mucous membrane which leads to inflammation, and 
often, in some circumscribed spots, to a pressure necrosis, and later to ulceration 
of the vermiform appendix. If the ulcer does not cicatrize — it always may — the 
ulceration gradually deepens. The pressure necrosis of the wall allows ingress 
to the ordinary pathogenic agents of inflammation and suppuration, among which 
the colon bacillus probably plays the chief role. The inflammation, once started, 
rapidly spreads to the surrounding tissues. In rare cases a diffuse general peri- 
tonitis is immediately developed. In by far the greatest number of cases there 
are timely adhesions around the appendix, so that the inflammation is limited 
and encapsulated. 

It is improbable that faecal calculi occasion the development of all cases of 
perityphlitis, but they certainly do of the majority. It may be that the inflam- 
matory germs sometimes reach and attack the appendix unaided. One circum- 
stance that would favor such an occurrence is the abundance of adenoid tissue 
in the appendix, which has suggested a comparison with the follicles of the ton- 
sils. Sonnenburg has insisted that in many cases the inflammation may be en- 
tirely limited to the vermiform appendix. This is possible, but in our opinion it 
is out of the question to make at the bedside an absolute diagnosis of " appen- 
dicitis simplex."' 

With regard to the nature of the inflammation in perityphlitis, there can be 
no doubt that it is almost always purulent, but this does not mean that there is 
always a marked destruction of tissue with the formation of an extensive abscess. 
Such results are found only in the severe and long-continued cases. In the ordi- 
nary milder cases there are usually merely an infiltration of the tissue with pus 
cells, and an inflammatory oedema of the tissue, or perhaps also a limited fibrinous 
exudation. There is an inflammatory tumor which consists essentially of the 
thickened intestinal walls and the coils of intestine glued together, and perhaps 
sometimes also of impacted faecal matter; and inside of this there is an actual 
abscess, small and localized, and lying usually in the immediate neighborhood of 
the appendix. 

Perityphlitic inflammation can very well be compared with the exudate of 
parametritis, for in this also the cellular infiltration predominates over the forma- 
tion of pus. In rare cases there may be an encapsulated exudation of a more sero- 
purulent character. 

The further pathological changes in perityphlitis will be best considered in 
connection with the clinical symptoms. 

Symptoms and Clinical Course. — We have already said that there is great 
doubt whether simple " typhlitis stercoralis " ever occurs, and therefore we shall 
refrain from giving a description of its symptoms, which we should have to invent, 
and turn at once to those clinical phenomena which we observe in acute inflam- 



484 



DISEASES OF THE DIGESTIVE OEGAXS 



mation of the ileo-csecal region, and which are now almost universally termed 
"perityphlitis" [appendicitis]. This disease has great clinical importance, for 
it is very frequent both in children and adults, and involves great danger to life, 
especially if there is not prompt surgical interference. 

The symptoms of perityphlitis have usually a rather acute development. The 
patient has felt perfectly well, and, as a rule, has not even suffered from consti- 
pation, when he has a rather sudden pain in the ileo-csecal region. There may be 
no occasion for this, or there may be some such cause as stooping, lifting, or a 
long walk. ISTot infrequently there is slight vomiting, and the patient feels 
languid and feverish. The bowels may be constipated, but sometimes they con- 
tinue regular. Many patients are obliged to go to bed at once, but others keep 
about for some days till they are forced to give up because of the aggravation of 
their symptoms, particularly the pain. It is a point of some practical importance 
that the pain is by no means invariably referred to the region of the CEeeum at 
first, particularly as the position of the appendix is very variable. Xot infre- 
quently the pain is localized more in the middle of the abdomen or toward the 
left, or upward. It is not until subsequent days of the attack that the pain grad- 
ually settles in the true ileo-csecal region. 

Upon objective examination we usually find distinct local changes in the ileo- 
cecal region, even in the first days of the disease. Our manipulations should be 
extremely cautious. It may be possible by careful inspection alone to recognize 
a limited swelling. In that case it is very important to determine whether ten- 
derness is present. This may be very considerable, or comparatively slight. The 
typical painful spot (McBurney's point) is said to be an inch to an inch and a half 
(three or four centimetres) inward from the anterior superior spinous process, 
on the line joining this process with the navel. This localization does not pos- 
sess great importance, because the painful spot varies in different cases. Some- 
times the greatest pain is felt posteriorly, in the lumbar region, suggesting a 
retro-CEecal paratyphlitic abscess (vide supra). Lastly, there is decisive impor- 
tance in the discovery of abnormal resistance, or of a more or less sharply-defined 
tumor due to the inflammatory exudation (vide supra). This tumor can usually 
be made out. For this purpose we recommend particularly the employment of the 
palm of the hand in gentle pushing movements, beginning on the left side and 
gradually proceeding toward the ileo-csecal region. This is the best way of 
determining the size of the inflammatory mass. In milder cases it is also per- 
missible to make deeper palpation, if we are cautious. The examination per 
anum may be very important : we have seen a number of cases in which no exu- 
dation could be demonstrated by external palpation, while a large inflammatory 
tumor could be distinctly felt through the rectum. The results of palpation are 
confirmed by percussion, which gives either a muffled tympanitic resonance, or 
marked dullness over the seat of the disease. In general, however, the results of 
percussion should not be interpreted too strictly, for they are ambiguous, because 
of the variations in the degree of intestinal distention. 

There are other symptoms to be considered besides the local ones. Of great 
importance are the aspect and general condition of the patient. If the patient 
has no suggestion of the " abdominal facies " (vide infra, chapter on peritonitis), 
it is very probable that the inflammation remains circumscribed. It is also im- 
portant to study the chart of the temperature and pulse. Elevation of the bod- 
ily temperature invariably suggests aggravation of the local process. Marked 
acceleration of the pulse almost invariably indicates active suppuration, and the 
advent of sepsis. In most cases the fever at first varies from 101° to 103° (38.5 °- 
39.5° C), and if the patient keeps quiet it falls in the next few days. The pulse 
varies from 80 to 100. !Not infrequently there is a decided remission in all the 
symptoms after the first two or three days. In the most favorable cases, con- 



TYPHLITIS AXD PEEITYPHLITIS 



4-5 



valescence may ensue upon this change, but very often the fever rises again, and 
in such cases there is great need of caution. The bowels are almost always con- 
stipated from the start. Vomiting occurs only temporarily, if at all. Frequent 
eructations and a return of vomiting later on in the attack are unfavorable symp- 
toms. In many cases there is temporary difficulty in micturition, so that a cath- 
eter must be employed. There is apt to be a distinct increase in the amount of 
indie an in the urine early in the attack. 

A question of the greatest clinical importance is whether the perityphlitis will 
lead to the formation of a large abscess or not. We have already said that in a 
pathological sense almost all cases of perityphlitis are suppurative, but the forma- 
tion of a large collection of pus is of practical importance. This is recognized 
by an increase in the fever, or by the mere persistence of the fever. If the fever 
lasts more than a week or a week and a half, suppuration is highly probable. It 
there is a temperature of 104° to 105° (40°— 40.5°) we may suspect suppuration, 
even at an early period, particularly if the rate of the pulse corresponds to the 
height of the fever. Rigors are not frequent at all, but, if they do occur, they in- 
dicate abscess formation. The local signs are not very valuable in the diagnosis 
of an abscess. Early in the attack it is scarcely ever possible to detect fluctua- 
tion, for the abscess is deeply situated and surrounded by infiltrated tissue. Tor 
an absolute decision it is usually necessary to resort to exploratory puncture. 
This should be done with a long, slender needle, carefully disinfected, and it need 
cause no apprehension; but still it should never be employed unless there is an 
important reason for it. 

The further course of perityphlitis is favorable in the overwhelming majority 
of cases. After a few days, or a week or so, if the treatment is appropriate, the 
symptoms abate and the fever disappears ; it may fall gradually or defervescence 
may be quite rapid, almost like a crisis. The inflammatory tumor shrinks, the 
pain abates, the bowels become regular, and the patient gradually regains com- 
plete health. Often there are manifold variations in the disease, which lengthen 
its duration. "With regard to the pathological changes in these cases that re- 
cover, of course we have no accurate knowledge. Sometimes it is probable that 
there never is a well-marked abscess formation, but only an inflammatory infiltra- 
tion of the tissue, which subsides again. It is probable that, in many cases, there 
is a small abscess which discharges spontaneously into the intestine, usually into 
the caecum, but exceptionally into other portions of the intestine. One thing 
which seems to us to suggest such a spontaneous discharge of an abscess is the 
not infrequent occurrence of a crisis, with rapid fall of temperature and simul- 
taneous cessation of all the other symptoms. Still, we scarcely ever detect pus in 
the stools, for the pus-corpuscles are changed during their passage from the colon 
to the rectum. Perhaps in some cases small localized abscesses are reabsorbed. 

If there is a larger abscess, and it does not discharge into the intestine or 
receive surgical attention, the pus seeks other paths. The worst occurrence is 
perforation into the general abdominal cavity, with consequent diffuse perito- 
nitis and speedy death. Or the abscess may continue to grow, and finally break 
through the abdominal wall; or it may extend downward into the iliac fossa or 
the groins, or perforate into the rectum, bladder, or other parts. It has also 
happened that the suppuration has involved the ileo-ctecal vein, with consequent 
pylephlebitis and the formation of abscesses in the liver. In most of these chronic 
cases the symptoms are those of a tedious septico-pya?mia such as is nowadays, 
thanks to the progress of surgery, very rarely seen. As the inflammation origi- 
nates from perforation of the intestine, the pus is apt to be extremely offensive, 
whenever there is any extensive abscess formation. 

The greatest caution is demanded even in cases in which the course of the dis- 
ease seems at first favorable. The improvement of the second or third day after 



486 



DISEASES OE THE DIGESTIVE OKGANS 



the sudden onset of the illness is often deceptive, as we have already mentioned, 
hut later on there may be manifold vicissitudes in its course, so that it is neces- 
sary to watch the patient constantly and closely. Often there will be a fresh 
elevation of temperature and the formation of an abscess late in the attack. If 
the bowels are obstinately constipated the symptoms of obstruction may appear, 
such as tympanites, frequent eructations, or even faecal vomiting. Complications 
in other organs are exceptional. 

Diagnosis. — In general, there is no difficulty in the diagnosis of perityphlitis, 
but it is difficult and to a certain degree impossible to determine accurately about 
the anatomical changes, the exact location and size of the inflammatory tumor, 
or the formation of an abscess. Here a careful examination, including palpa- 
tion per anum, is indispensable. In so far as this relates to the extremely impor- 
tant question of surgical interference, we shall revert to the matter when consid- 
ering treatment. 

In those rare cases of perityphlitis which have a chronic course, the disease 
may be confounded with new growths, particularly carcinoma originating in the 
caecum or the appendix. Mistakes in diagnosis have also been occasioned by 
tumors of the right kidney and the right ovary, and by psoas abscess due to Pott's 
disease. In this connection it may be mentioned that in rare cases the lumen of 
the appendix may become occluded. The portion of the appendix thus cut off is 
then gradually distended by the secretion of its mucous membrane, giving rise to 
so-called dropsy of the vermiform appendix. This may occasion a tumor which 
can be felt in the ileo-caacal region. 

Prognosis. — If we take all the cases of acute inflammation of the ileo-caecal 
region, we shall find that some 80 or 90 per cent, get well without operation, but 
still it should be emphatically stated that perityphlitis is a dangerous disease, 
and every year brings no small number of individuals, both children and adults, to 
sudden death. The main danger lies in the rapid onset of general peritonitis, or 
of severe sepsis. Even after the patient has survived the attack he may be trou- 
bled in various ways. Eor instance, the resultant adhesions and chronic exu- 
dates may impede the action of the bowels for a long while. The frequency of 
recurrent attacks is also to be considered. Many persons have repeated attacks 
of perityphlitis to the number of four or six, or even more during their lives. 
This is probably the result of peculiar anatomical conditions. 

Treatment. — Formerly, when the opinion was still held that many of the cases 
of acute inflammation of the ileo-caacal region were to be regarded as simple 
typhlitis stercoralis due to constipation, the first question in treatment was 
whether to give laxatives or opium. If there was typhlitis, laxatives ought to be 
given; if perityphlitis, opium. The aim of diagnosis, therefore, was to distin- 
guish between these two conditions. To-day the conception of simple typhlitis 
has been almost completely abandoned, or, at any rate, it has become very limited, 
and consequently the question of treatment has become simpler, for now laxa- 
tives are scarcely ever given at the onset of the disease. Perhaps we have gone 
too far in this direction, for most of the older physicians will certainly, like 
the author, recall many cases of what was supposed to be typhlitis stercoralis, in 
which rapid recovery followed the immediate use of castor-oil. Still, it can not 
be disputed that the premature employment of laxatives may do harm, while the 
administration of opium in a proper dose probably never leads to unfavorable con- 
sequences. Eor this reason we now make it a rule in any case of inflammation 
in the ileo-csecal region, with acute onset, to begin with opium; but it is impor- 
tant, above all, that upon the first appearance of pain the patient should remain 
perfectly quiet in bed, and should have for nourishment merely milk or soup, but 
no solids. An ice-bag should be applied at first over the seat of the disease, and 
this may be replaced later, or at once, in case cold is not well borne, by wet com- 



TYPHLITIS AND PERITYPHLITIS 



487 



presses or poultices. Opium is administered in the form of laudanum, giving fif- 
teen to twenty drops several times a day, or one half grain to a grain of the ex- 
tract (gramme 0.3-0.5). The amount of opium to be administered is determined 
by the pain. In severe cases one must not hesitate to use large doses, but, on the 
other hand, the dangerousness of the remedy, particularly in children, should 
never be forgotten. The local application of eight to ten leeches has become en- 
tirely out of fashion and may be dispensed with, but, nevertheless, it is unde- 
niable that leeches sometimes give the patient decided relief. With this treat- 
ment of rest, diet, opium, and ice, the pains are usually soon relieved. There is 
no necessity at first to be anxious about opening the bowels. Usually there is no 
harm if the patient goes without a movement for five to eight days, providing that 
his condition is satisfactory as regards his general health, pulse, and temperature. 
It is indeed not unusual to have a natural operation of the bowels while rather 
large doses of opium are being administered, but if the abdomen becomes more 
and more distended and there is rather long-continued constipation, we need not 
hesitate to make a cautious use of injections. For this we usually choose cool 
soapsuds, and let it run through an ordinary fountain syringe into the colon, 
while the patient is lying on his back. If necessary, the injections must be re- 
peated, and of their beneficial effect we have often been convinced. 

We have already insisted that every patient with perityphlitis should be most 
carefully watched, however favorable the course of the disease seems to be. The 
physician must ask himself every minute whether further symptomatic treat- 
ment is permissible, or whether it may not be necessary to have the abscess opened 
by surgical interference; for, although we are by no means of the opinion that 
every case of perityphlitis without exception demands surgical treatment, yet 
there is no doubt that prompt surgical interference can save many lives. The 
question when operation is required is consequently prominent at present in all 
discussions of this disease. Our answer can only be, in general, that immediate 
operation is invariably indicated as soon as we infer that perityphlitic suppura- 
tion is present. We dare not wait for its absorption or its spontaneous discharge 
into the intestine, because of the possibility of its breaking through into the peri- 
toneal cavity, or arousing a constitutional sepsis, or some chronic suppurating 
process. The most important signs of the imminence of these dangers may be 
again summed up as follows : persistence or fresh exacerbation of the fever, after 
the first three to five days ; increase in the frequency of the pulse beyond 100 to 
120, and diminution in the tension of the pulse (both pulse signs are important, 
because they almost invariably suggest a large abscess) ; increase in the local 
phenomena; and, finally, above all, unfavorable appearance of the patient, a be- 
ginning " abdominal f acies." If these symptoms appear there must be no hesi- 
tation about the operation. If we are still in doubt, we may first make an ex- 
ploratory puncture. If even a drop of pus is obtained, operation is absolutely 
demanded. 

It is impossible to give more detailed rules, of general application, with re- 
gard to the question of operating. The individual circumstances of each partic- 
ular case and the personal experience of the physician must always be controlling- 
factors. ISTo physician can avoid unfortunate occurrences in perityphlitis, and 
the most experienced practitioner will never escape a certain feeling of uneasiness 
in any case of the disease; still, it would certainly be better to operate too early 
than too late. It is true that when the general condition of the patient is favor- 
able, waiting is advisable, but, as Sahli has well said, it must always be an 
" armed peace." For particulars as to laparotomy and further treatment, as well 
as concerning the question of the necessity of removing the appendix, the reader 
is referred to text-books on surgery. 



488 



DISEASES OF THE DIGESTIVE ORGANS 



CHAPTER V 
PERFORATING ULCER OE THE DUODENUM 

There is a form of ulcer of the duodenum, especially of its upper, horizontal 
portion, which is precisely analogous to the round gastric ulcer in regard to aeti- 
ology, pathological anatomy, and, very largely, symptomatology. The ulcer is 
probably also due in most cases to the action of the acid gastric juice on the duo- 
denal mucous membrane, under conditions which have been detailed more fully 
in the aetiology of gastric ulcer. We must mention here the noteworthy fact that, 
after extensive burns of the external skin, ulceration of the duodenum, rarely of 
the stomach also, has been repeatedly observed. This is probably due to the 
thrombosis of a duodenal vessel, occasioned by the setting free of flbrine ferment. 

Ulcer of the duodenum is much rarer than the round gastric ulcer, and, in dis- 
tinction from the latter, it has been found decidedly oftener in men than in 
women. 

Many cases of ulcer of the duodenum run their course entirely without symp- 
toms, or they cause no symptoms until sudden haemorrhage appears (from erosion 
of the pancreatico-duodenalis, gastro-duodenalis, etc.) with haematemesis and 
bloody stools (quite often bloody stools alone without haematemesis), or until 
there are suddenly signs of peritonitis from perforation. In many cases a type 
of disease exists for a long time whose symptoms, as we have said, are so like the 
clinical symptoms of gastric ulcer that we can very rarely distinguish the two 
forms with certainty during life. We notice especially continuous or neuralgic 
pain, which, in ulcer of the duodenum, has its chief seat in the right hypochon- 
clrium. Severe gastric symptoms, especially vomiting, are not as common as in 
gastric ulcer. The general health and general nutrition may remain quite undis- 
turbed for a long time. 

Ulcer of the duodenum ends by cicatrization and recovery, or by cicatrization 
and the formation of stenosis, with secondary dilatation of the upper portion of 
the duodenum and of the stomach. In regard to the different adhesions and per- 
forations of the ulcer into neighboring organs, we may refer to what has been 
said of gastric ulcer. 

The treatment must be governed by the same principles which were laid down 
in the treatment of gastric ulcer, especially as the diagnosis is usually doubtful. 



CHAPTER VI 
TUBERCULOSIS OF THE INTESTINES 

Tuberculosis of the intestines is in most cases a secondary disease, and is one 
symptom of a more extensive general tuberculosis. It develops most frequently 
in the course of chronic pulmonary tuberculosis, and depends here, as we have 
seen (compare page 249), upon an infection of the intestines by the tubercular 
sputum that has been swallowed. 

Intestinal tuberculosis, however, may also be a primary disease, and the source 
of further extension of tuberculosis over the body. " Tuberculosis of the abdomi- 
nal organs," which usually comes from the intestines, has a clinical significance, 
especially in children. It is not improbable that in such cases the first infection 



TUBERCULOSIS OF THE INTESTINES 



489 



of the intestine comes from without, and that the tubercular poison is taken into 
the body with the food. Here we must suspect especially the milk from cows 
with pearly distemper — that is, with tubercular disease. 

The anatomical changes in intestinal tuberculosis are precisely analogous to 
the tubercular changes in other mucous membranes. The tubercular new growth 
has its origin usually in the lymph-apparatus of the intestine, in the solitary folli- 
cles, and in Peyer's patches. The first miliary tubercles form beneath the epi- 
thelium, and soon fuse with one another into a diffuse infiltration. In its further 
course the infiltration on one side extends deeper into the surrounding tissue, so 
that it attacks the submucous and muscular coats and even extends to the serous 
coat, and on the other side, by the destruction of the new growth which begins at 
the surface and constantly spreads, tubercular ulcers are formed. We can often 
make out with the naked eye single miliary tubercles or groups of them at the 
base or in the infiltrated edges of the ulcer. This is especially plain in deep- 
seated ulcers on the corresponding portion of the serous coat. The form of the 
larger tubercular ulcers is often irregular. In many cases the long diameter of 
the ulcer is parallel to the circumference of the intestine, so that the girdle-like 
ulcers, which are especially characteristic of tuberculosis, are formed. 

Tubercular ulcers are situated both in the large and in the small intestines. 
They are usually most marked in the vicinity of the ileo-caecal valve. Tubercular 
ulcers in the stomach are extremely rare. Besides the intestinal tuberculosis 
there is very often tuberculosis of the mesenteric lymph-glands, and also fre- 
quently tuberculosis of the peritoneum. 

The symptoms of intestinal tuberculosis are usually quite subordinate to the 
symptoms caused by other co-existing tubercular affections. There may often be 
quite extensive tubercular ulcers without any marked symptoms, but, as a rule, 
the onset of diarrhoea turns the attention to the intestinal complication (see the 
chapter on pulmonary tuberculosis). 

Tubercle bacilli have been repeatedly demonstrated in the fsecal discharges, 
but it is not very easy to find them, and, moreover, their diagnostic significance 
is impaired by the fact that they may be referable to sputum which has been 
SY\ T allowed. 

Primary tuberculosis of the abdominal organs sometimes presents quite a char- 
acteristic type of disease, especially in children. This was termed by the older 
physicians tabes mesenterica. The chief feature of this type of disease consists in 
a progressive general emaciation and anaemia, which are usually associated with a 
persistent hectic fever, which obstinately resists all the remedies employed. The 
abdomen is usually swollen by meteorism, but it is sometimes flat and sunken. In 
some cases, but less frequently than was formerly believed, we can feel the swollen 
mesenteric lymph-glands through the abdominal wall during life. The involve- 
ment of the mesenteric lymph-glands obstructs the lymph-channels which serve 
for the absorption of fat, a circumstance which undoubtedly contributes, along 
with others, to the excessive emaciation frequently seen. The liver may be en- 
larged and its lower border can often be felt. The bowels are irregular, and there 
is usually a moderate diarrhoea, persisting in spite of all remedies. The invari- 
ably fatal termination is due to an increase of the general marasmus, or to a final 
acute tubercular affection, such as miliary tuberculosis or tubercular meningitis. 
The autopsy shows tuberculosis of the intestines, peritoneum, lymph-glands, liver, 
etc., to a greater or less extent. The lungs may be quite free from tuberculosis. 
We will return to this affection in the description of tuberculosis of the peri- 
toneum. 

The treatment of intestinal tuberculosis can be only symptomatic. Besides the 
general dietetic treatment which seeks to keep up the patient's strength as far as 
possible, medical interference is demanded by the abdominal pain and diarrhoea. 



490 



DISEASES OF THE DIGESTIVE OBGANS 



The chief remedy is opium, either alone or combined with tannin, tannigen, ace- 
tate of lead, or subnitrate of bismuth. Sometimes a decoction of logwood is 
beneficial. Talc also has lately been recommended ; about six or seven ounces (200 
grammes) are given daily, suspended in milk. We have seen some good results 
from it. The most serviceable local applications are poultices or cold compresses. 

In other respects the treatment coincides with the general treatment of tuber- 
culosis (vide supra). 



CHAPTEE VII 
SYPHILIS OF THE RECTUM 

In not very rare cases we see in the rectum, especially in its lower portions, 
extensive syphilitic ulcerations^ which produce a severe and practically important 
type of disease. The more intimate relation between syphilis of the rectum and 
xhe general syphilitic process is not perfectly clear. According to quite a wide- 
spread opinion, the infection of the rectum comes from the secretion trickling 
down from the ulcers of the genitals. The facts seem to support this view, since 
syphilis of the rectum is seen much more frequently in women than in men. 
Some authors have even asserted that all the so-called " syphilitic " ulcers in the 
rectum have no connection at all with genuine syphilis, but are chancroids. It is 
in fact striking, even if it by no means proves such a hypothesis, that, at the 
autopsy of persons who have died of " syphilis of the rectum," we rarely find defi- 
nite syphilitic changes in other internal organs — a fact which we also can confirm. 

The most characteristic mark of syphilitic ulcers in the rectum is their tend- 
ency to form cicatrices and stenoses. This result of the ulcer is also important 
in its clinical relations, since the chief symptoms of the disease usually begin with 
the development of the stenosis. The seat of the stenosis is usually so low down 
that we can conveniently reach it with the finger, on a digital examination of the 
rectum during the patient's life. The rectum narrows like a funnel upward, and 
we can feel the quite sharp edge of the ring-like cicatrix with the point of the 
finger. This funnel-shaped stenosis of the rectum is so characteristic of syphilis 
of that organ that, in almost all cases, we can make the diagnosis with perfect 
certainty from this alone. 

The rectum and the descending colon are usually dilated above the stenosis, 
and here extensive, irregular ulcerations, with undermined edges, are usually 
found in the mucous membrane. These are partly of a specific nature, and partly 
diphtheritic ulcers caused by the pressure of the accumulated f aecal masses. 

The symptoms of syphilis of the rectum usually develop quite gradually. At 
first the bowels are irregular, and there are disturbances of defalcation which stub- 
bornly resist the ordinary remedies employed. There are sometimes, in the first 
stage of the disease, frequent and severe haemorrhages with' the dejections, as we 
have seen, and for a long time these may falsely be considered to be " bleeding 
from haemorrhoids." The symptoms become more marked as cicatrization of the 
ulcer increases and as stenosis of the rectum develops. There is usually a decided 
catarrh of the rectum, so that the thin stools contain a large admixture of mucus 
and pus. The patient's condition is extremely distressing, from the pains with the 
frequent but always scanty dejections, and from the severe tenesmus. Nodular 
thickenings and prolapse of the mucous membrane, and sometimes true haemor- 
rhoids, form about the anus. The patient's strength constantly diminishes from 
the pain and the continual diarrhoea. He finally becomes emaciated, looks very 
pale and wretched, and has fever toward night. Death ensues from increasing 



CANCER OF THE INTESTINES 



491 



general weakness, or rarely from a terminal peritonitis chie to perforation, after 
the whole disease has lasted one and a half to two and a half years. 

This unfavorable termination unfortunately seems to be the rule in all the 
cases described; hence the prognosis is to be regarded as very serious in all cases 
of syphilis of the rectum. Improvement worthy of mention, or even perhaps 
recovery, is possible only when the disease is recognized at the outset and properly 
treated. 

At the outset of the disease the treatment, of course, must consist chiefly of an 
energetic general attack upon the syphilis by mercurial inunction and iodide of 
potassium; but, when once the characteristic funnel-shaped stenosis of the rectum 
has formed, we can not expect much from anti-syphilitic medication, since this 
can no longer exert any influence on the cicatrices and their results, Improve- 
ment is now to be obtained only by mechanical dilatation of the stenosis by 
bougies, or, if this is not enough, by a surgical operation. A suitable local treat- 
ment by irrigation is also of benefit to the catarrh and to the ulcers that still exist 
in the rectum. Internally, we may continue to use iodide of potassium. 



CHAPTER- VIII 
CANCER OF THE INTESTINES 

The development of cancer is far more rare in the intestine than in the 
stomach. Carcinoma is seen with any frequency only at the lower end of the 
intestine, in the rectum. Next in frequency is carcinoma of the colon, particu- 
larly the caecum, the sigmoid flexure, and the hepatic and splenic flexures. Car- 
cinoma is very much less common in the small intestine, in which its favorite seat 
is the duodenum, particularly the neighborhood of the common duct. 

Most cancers of the intestine appear in the form of ring-like swellings that 
take in the whole circumference of the intestine. More rarely we find a more 
diffuse papillary proliferation, extending over a larger surface of the intestine. 
There is often quite an extensive destruction of the new growth on the surface 
of the cancer, from which deep ulcerations arise. Often metastases are found in 
the lymph-glands, liver, and other organs. Above a cancerous obstruction the 
intestine is usually dilated, with thickening of its muscular coat, and inflamma- 
tion or ulceration of its mucous membrane due to the impacted faecal matter. 
In its histological structure, cancer of the intestine is to be regarded as invariably 
a cylindrical-celled carcinoma, which sometimes shows a plainly glandular struc- 
ture — adeno-carcinoma — and sometimes that of the other forms of cancer — scir- 
rhus, medullary, or colloid. 

Cancer of the intestines, like all cancers, occurs chiefly, if not invariably, in 
advanced life. 

The clinical symptoms of cancer of the intestines are only in a part of the 
cases so pronounced that we can make a positive diagnosis of the disease. The 
symptoms vary with the location of the growth. 

Cancer of the rectum begins usually with distress at stool (tenesmus) and pain 
in the rectum, which at first comes only with def aecation, but later becomes almost 
continuous. The pain often shoots into the neighboring parts — the sacrum, the 
thighs, the genitals, etc. The local symptoms gradually increase, the stools often 
contain some mucus and blood, and diarrhoea alternates with obstinate constipa- 
tion. The patient also becomes emaciated, and constantly grows weaker and 
more miserable. Finally, we often find a complete paralysis of the sphincter ani^ 



492 



DISEASES OF THE DIGESTIVE OKGAXS 



so that a mucous, .bloody fluid constantly oozes from the half -open anus. An 
absolute diagnosis can usually be made with ease by digital examination of the 
rectum. This examination should never be omitted in any suspicious case, for 
otherwise it is only too easy to make a mistake. Many a fatal case might perhaps 
have been saved by a timely diagnosis. External piles are particularly common 
in cancer of the rectum, and their presence should by no means prevent the physi- 
cian from an internal examination. If there is cancer of the rectum, the finger 
upon being introduced detects an irregular, firm growth, and we can usually make 
out with approximate accuracy its extent and its invasion of neighboring organs, 
such as the vagina and bladder. Examination with the rectal speculum some- 
times makes the diagnosis more accurate. In some cases the destruction of the 
new growth may cause perforation into the organs mentioned, and we can easily 
understand the results of this, such as cystitis, purulent discharges from the 
vagina, etc. We may also have peritonitis from perforation. Secondary cancer 
appears with especial frequency in the liver, also in the peritoneum and elsewhere. 

Carcinoma of the colon causes, as a rule, only very indefinite symptoms, which 
for a long time are hard to interpret. These symptoms consist chiefly of distress 
at stool, obstinate constipation, dull pains in the abdomen, and the signs of slowly 
increasing general weakness and emaciation. If the stenosis of the intestine 
increases there are usually attacks of colic, with the gradual or perhaps rapid 
development of all the symptoms of obstruction of the bowels (vide infra, Chapter 
XI). In many cases the shape of the fasces is peculiar. They are ribbon-shaped, 
or consist of queer flattened nodules which have a certain resemblance to sheep's 
dung (scybala). ~Not infrequently we find in the dejections an admixture of 
mucus, pus, and, what is still more important, blood ; if blood is persistently pres- 
ent in the movements (to be determined by the guaiac-turpentine test, vide supra, 
page 422), or if there are bloody or muco-purulent masses in the discharges, 
cancer is suggested. Exceptionally there may be found in the stools small de- 
tached portions of the new growth. The examination of the abdomen is often 
negative, but sometimes it is possible to feel the new growth through the abdom- 
inal walls as a distinct tumor. One characteristic of the tumor occasioned by 
intestinal carcinoma is that it may be very movable, and change its position 
because of its own weight or of the collections of faecal matter. As a rule, the 
growth does not move with respiration, except possibly in carcinoma of the trans- 
verse colon. It is easy to confound intestinal carcinoma with carcinoma of the 
stomach, the mesentery, or the mesenteric lymph-glands. It is very important to 
know that in case of intestinal carcinoma the tumor which is felt may be not the 
new growth at all, but the hardened fsecal masses collected above it. Such frecal 
accumulations may cause all sorts of errors as to the situation and dimensions of 
the new growth. In such cases a correct conclusion may not be obtained until 
after continued observation and the use of laxatives and enemata. It is also 
true that ordinary f ascal masses may be mistaken for cancer of the intestine when 
there is no intestinal disease of any sort. In exceptional cases there may be 
perforation of cancer of the colon into the stomach, with the formation of a 
gastro-colic fistula; or perforation of cancer of the sigmoid flexure into the 
bladder or into the peritoneum, with a secondary peritonitis, which may be local- 
ized or diffuse. Carcinoma of the csecum is often indistinguishable for a long 
while from tumors due to chronic typhlitis, or perityphlitis. Cancer is suggested 
by the age of the patient, the tedious course, and the progressive aggravation of 
the illness, and sometimes also by swelling of the inguinal lymph-glands. In the 
surgical wards in Leipsic we observed a case of cancer originating in the vermi- 
form appendix, which penetrated through the skin. 

Cancer of the small intestine is very rare. It is distinguished by the very 
great movability of the tumor, if one is found. The symptoms are those of grad- 



H^EHOEBHOIDS 



493 



ually increasing stenosis (vide infra). Cancer of the duodenum is similar in 
many respects to cancer of the stomach, particularly of the pylorus. It leads to 
stenosis of the duodenum, and consequently to dilatation of that portion of the 
duodenum which is above the new growth, and of the stomach, and so occasions 
the well-known symptoms of gastrectasia (vide supra, page 438). Cancer which 
is seated in the neighborhood of the common duct usually causes excessive and 
persistent jaundice. 

The course of all cases of intestinal cancer is absolutely unfavorable. The 
disease may last for a considerable time, about two or three years. On the other 
hand, the duration of the special symptoms may be brief — that is, a few months 
or weeks; undoubtedly because the condition existed long before it caused symp- 
toms. The final result in intestinal carcinoma takes the form either of increas- 
ing general weakness, or of perforation with fatal suppurative peritonitis. Death 
may also be occasioned by extensive and foul suppuration in the surrounding con- 
nective tissue, or by phlebitis and pyaemia. Most cases run their course as a 
more or less rapid obstruction of the intestine, which may become almost com- 
plete. Sometimes, however, ulceration of the cancer occurs, and there is a tem- 
porary abatement of the symptoms of stenosis. 

The only possibility of successful treatment in intestinal carcinoma is by 
surgical methods. The results of operation are very favorable in cases of cancer 
of the rectum if the disease is not situated too high, and has not extended too far. 
Cancer of the other parts of the intestine has a much less promising outlook. 
If surgical interference is impracticable, treatment must be merely symptomatic, 
with a view of alleviating suffering. 

"We will append a few remarks about sarcoma of the intestine. This is a very 
rare disease, which originates from the submucous layer or else, in the form of 
lympho-sarcoma, from the lymph-follicles of the intestine, particularly of the 
small intestine. Both varieties exhibit a tendency to extend cylindrically over 
considerable areas along an intestinal coil. They usually do not lead to stenosis, 
but they may even cause dilatation of the affected portion of the intestine. The 
tumors which are formed may attain to very considerable size. The most promi- 
nent symptoms are general weakness and anaemia, associated with slight fever. 
These constitutional symptoms are more prominent than the local ones. The 
course is usually rapid and ends, after six to twelve months, in death. 



CHAPTER IX 
HEMORRHOIDS 

By the name " haemorrhoids " we mean diffuse or varicose dilatations of the 
hemorrhoidal veins, especially of the venous plexuses at the lower end of the 
rectum. Haemorrhoids are single large varices, which usually rise from the sub- 
mucous layer, and push the mucous membrane out before them. If they are situ- 
ated outside of the sphincter ani we speak of external haemorrhoids, in distinction 
from internal haemorrhoids, which lie above the sphincter. The size of the nod- 
ules varies with the fullness of the dilated veins ; but haemorrhoids, as a rule, do 
not consist exclusively of dilated vessels, for we often find, at the same time, 
considerable thickening of the surrounding connective tissue, so that the whole 
mucous membrane has a swollen appearance, with a polypoid proliferation in 
parts. The haemorrhoids usually present themselves as bluish tumors, from the 



494 



DISEASES OE THE DIGESTIVE OKGANS 



size of a pea to that of a walnut, which surround the anus like a garland. Most 
of them have a broad base, while others are apparently pedunculated. 

The chief cause of haemorrhoids is frequently-repeated stasis in the veins 
affected. The position of the hemorrhoidal veins is such that their contents are 
constantly pressing downward by the action of gravity, and the development of 
varices is further promoted by their complete lack of valves. Special local con- 
ditions often contribute also to render the escape of blood difficult; thus haemor- 
rhoids are particularly frequent during pregnancy, also in persons with habitual 
constipation, and consequently in individuals who follow sedentary pursuits. 
Haemorrhoids are sometimes found as a result of portal congestion (in hepatic 
cirrhosis and similar conditions), and finally in general circulatory disturbances 
due either to pulmonary or cardiac disease ; but these cases are not so frequent as 
was formerly supposed. Quite often, however, we can discover no sufficient cause 
for the development of the disease, and we are then forced to the hypothesis of a 
local disease of the affected venous plexus, which is probably often connected with 
an individual, and apparently sometimes hereditary, predisposition. We most 
frequently see haemorrhoids in men in middle life. 

Haemorrhoids sometimes cause only slight symptoms, or none at all, but in 
other cases they are a tedious, burdensome, and even distressing evil. The chief 
symptom is pain, which is felt as a constant burning at the anus, but which in- 
creases to great severity at each dejection. There is much pain when the haemor- 
rhoids and the surrounding tissue gradually get into an inflamed condition. In 
the skin about the anus, erythema, excoriations, and sometimes small but very 
painful fissures are formed. The mucous membrane at the lower end of the 
rectum is often found in a catarrhal state, which gives rise to the presence of pus 
and mucus in the dejections — " mucous haemorrhoids." The worst symptoms are 
caused when by pressing and straining at stool an internal pile is forced outward, 
and constricted by the sphincter. If the constriction is not speedily relieved the 
extruded varix becomes much swollen and inflamed. This change is favored by 
a cramp-like contraction of the sphincter. Under such circumstances there may 
result a purulent phlebitis associated with very great pain, high fever, and severe 
constitutional disturbance. Sometimes we find a thrombus, thrombo-phlebitis, 
or suppurative periproctitis, even if there is no previous constriction. 

Haemorrhoidal bleeding is a frequent and familiar symptom, which rises from 
a rupture of the dilated veins, and usually comes on at stool. The haemorrhage is 
seldom very large, so that the loss of blood is in itself very rarely dangerous. 
Still, the rectal haemorrhage may be repeated so often as to cause severe and per- 
sistent anaemia. The swelling of the varices after the haemorrhages have ceased 
explains why the haemorrhoidal symptoms are apt to be less marked as long as 
there are haemorrhages than when there are none. Hence the old term of the 
" golden vein " for haemorrhoidal bleeding. 

Besides the local symptoms mentioned, in the anus, there are sometimes other 
symptoms which are due to an implication of the neighboring venous plexuses, 
the vesical, prostatic, and sacral plexuses. There is often pain in the sacral 
region, difficulty in micturition, and in women vaginal catarrh, anomalies of men- 
struation, etc. Since the symptoms of some co-existing morbid conditions, such 
as abnormal corpulency, or chronic gastro-intestinal catarrh, may be added to the 
general picture, we can comprehend why medical superstition has found in haem- 
orrhoids an excuse for the strangest ideas, like that of " transposed haemor- 
rhoids " ! The scientific physician should be careful not to refer such manifold 
symptoms to haemorrhoids without due consideration, for otherwise important dis- 
eases may be readily overlooked. 

Treatment. — The treatment of chronic piles consists mainly in caring for a 
regular and easy evacuation of the bowels. This is the best means to diminish 



HABITUAL CONSTIPATION" 



495 



the local discomfort (see the next chapter). The diet to be prescribed should be 
determined by the constitution of the patient. It is usually advisable to limit 
the ingestion of milk and to recommend in its scead a larger proportion of vege- 
tables, in a broad sense, including fruit, such vegetables as grow below the surface 
of the ground, simple puddings, and rice. It is usually advantageous to pre- 
scribe a sufficient amount of physical exercise, also warm or cool sitz-baths, and 
cool sponging with rubbing. Moreover, laxatives are to be considered, particu- 
larly waters containing Epsom salts, also the regular use of injections of cold 
water or oil; compound licorice powder, or other laxative powders or pills; and 
perhaps a course of the waters at Carlsbad, Marienbad, Kissingen, or Tarasp. A 
laxative used with special frequency in the treatment of piles is sulphur. This 
is the chief constituent of most " pile powders," e. g. : 

aa §ss. (grm. 15) ; 
aa 3ijss. (grm. 10). M. 

The local treatment consists chiefly in protecting the piles from irritation. 
The parts are best cleaned after every movement of the bowels with cotton or soft 
linen, and the region of the anus is to be touched with oil, vaseline, or borated 
vaseline. If there are slight inflammatory symptoms we apply compresses wet 
with a solution of acetate of lead, or ice-water, or inject olive-oil into the rectum, 
or try suppositories containing morphine or cocaine. If the inflammation is 
more severe a few leeches are often beneficial. Constricted piles we should en- 
deavor as soon as possible cautiously to replace with the finger. The pain attend- 
ing this operation is often so severe that chloroform narcosis, or at least the local 
application of cocaine, is required. If there is suppurative phlebitis an incision 
is necessary. In some cases a radical operation for the piles may be performed at 
the same time. 

The bleeding from piles is, as we have said, seldom severe enough to demand 
special treatment, such as the use of ice, chloride of iron, or packing the rectum. 
If the haemorrhage is repeated and serious, or if the inflammation causes persist- 
ent and extreme discomfort, we should urgently recommend operative removal of 
the piles. Particulars as to the methods employed for this purpose, such as the 
use of the thermo-cautery or the knife, will be found in the text-books on 
surgery. 

[Persistent and intelligent treatment will often bring about very great relief, 
or even complete cure, in chronic cases. There are many local applications, each 
of which has its warm advocates — so many that it is not possible here to go into 
details. Suffice it to say that an astringent with or without an anodyne may be 
used as an enema, in suppository or in ointment. The fluid extract of hamamelis, 
glycerine, and some other remedies given by the mouth, are reported to have 
afforded good results.] 



CHAPTER X 
HABITUAL CONSTIPATION 

Persistent tendency to constipation is a frequent symptom in many different 
acute and chronic cases. We often see persistent sluggishness of the bowels in all 



IJ Sulphuris loti, 
Potassii bitartratis, 
Sacchari albi, 
Elseosacchari citri,* 



* Powdered stigar, 3 j; volatile oil, gtt. ij. M. 



496 



DISEASES OE THE DIGESTIVE OKGAXS 



sorts of conditions of weakness, in general anaemia, in diseases of the stomach, 
intestines, liver, lungs, heart, and nervous system, and it is caused by a great 
variety of circumstances. Often the weakness of the peristalsis of the intestine, 
and particularly of the colon, is merely one manifestation of a general debility; 
in other cases the activity of the intestine is subnormal because of the insuffi- 
cient and unstimulating diet, or because of the lack of physical exercise. In -a 
third class of cases there is disease of the intestinal wall itself, such as catarrhal 
conditions, circulatory disturbance, atrophy of the muscular coat, or constriction 
of the lumen of the intestine. And finally, a fourth cause is disturbance of the 
innervation of the intestine, because of disease of the brain or spinal cord. 

The above are examples of symptomatic constipation, but in this chapter we 
shall not discuss these, but rather cases of habitual constipation occurring as an 
apparently independent disease. This may appear alone or associated with other 
disturbances likewise purely functional. The causes of this frequent and impor- 
tant condition are by no means invariable, and we are still far from a clear under- 
standing of the nature of all the disturbances that belong in this category. Some- 
times habitual costiveness seems to be associated with a congenital functional 
weakness of the muscular coat, or perhaps of the nervous apparatus of the intes- 
tines. At any rate, it is often possible to trace the symptoms back to the earliest 
childhood. In other cases it is apparently an improper mode of life which exer- 
cises a disturbing effect upon the intestinal activity; lack of bodily exercise often 
leads to disorders of the bowels, and, still more, irregularity in eating and an im- 
proper choice of food. Sometimes external mechanical influences promote con- 
stipation. In women unsuitable apparel, tight bands around the waist, tightly- 
laced corsets, and the like, certainly produce in many cases a permanent malposi- 
tion of the intestinal organs (" enteroptosis," compare above the chapter on gas- 
troptosis, page 460), and particularly of the large intestine. It is not improbable 
that these conditions are in part the cause of the chronic constipation which is 
so frequent in women and girls. In women frequent pregnancies may also exert 
a causative influence by inducing laxness of the abdominal walls and a tendency 
to enteroptosis. 

Habitual constipation is associated still more frequently with general neuras- 
thenia than with any of the conditions thus far enumerated (compare the chapter 
on neurasthenia, page 1193). The nature of this association is probably not the 
same in every case. Often neurasthenia and constipation seem to be co-ordinate 
symptoms; sometimes the existing constipation has an unfavorable effect upon 
the psychical condition of the patient, rendering him feeble, fretful, out of sorts, 
and nervous. As a rule, however, neurasthenia is the primary disease, and then 
the irregularity of the bowels appears as a result of abnormal nervous influences, 
or of secondary conditions (vide infra). Often the two states act in a vicious 
circle, each sustaining and aggravating the other. The most essential factor is 
often the hypochondriacal tendency of the patient. He ascribes an excessive 
importance to irregularity of the bowels, and regards every slight disturbance as 
of extreme gravity. Even when the movements are sufficient he can not free 
himself from a disordered apprehension that they are not really adequate. Such 
patients come at last to devote almost all their thoughts to their illness and make 
the most painstaking observations and investigations of their dejections, having 
energy for nothing else and no joy in life. They seek aid from all sorts of physi- 
cians and quacks, and yet they have no actual confidence in any one and do not 
follow the practitioner's directions with the requisite persistence. In many of 
these cases the constipation is only apparent, or imaginary. The patient fears to 
eat any hearty food and takes little nourishment, and consequently the excreta 
are scanty. In other instances, however, the abnormal psychical conditions have 
a direct inhibitory influence upon the intestinal activity. The intestine gets out 



HABITUAL CONSTIPATION 



497 



of the habit of regular action. Moreover, the unwise use of internal laxatives 
may entail actual disease of the intestine. 

Consequently, if the physician wishes to form a reliable opinion with regard 
to the intestinal function in a case of chronic constipation from actual observa- 
tion, the first requisite is that he should himself see the dejections of the patient 
for some time, while the diet is normal and all laxatives are omitted. This is 
much easier in a hospital or sanitarium than in ordinary private practice. When 
a patient is under observation in this way it should be noticed whether the abdo- 
men becomes much distended, and whether hardened faecal matter can be felt in 
the colon or the sigmoid flexure. Furthermore, the dejections should be examined 
as to their amount and character. They may seem nubby, hard, or as if they 
were "burned," or of abnormally small diameter, or flattened, or covered with 
mucus. If we find that the evacuations are distinctly abnormal we infer that 
there is actual disturbance of the intestinal functions; while, on the other hand, 
our examinations often show that the complaints are exaggerated or imaginary. 

The treatment of habitual constipation is a difiicult and often a thankless 
task, and it demands patience and professional tact. It goes without saying that 
we must first of all look for the causal factors. If we succeed in improving the 
underlying disease — as, for instance, the chronic gastro-intestinal catarrh, the 
chronic affections of the heart or lungs, the anaemic conditions, or certain nervous 
troubles — a regulation of the bowels often follows of itself. In ordinary habitual 
constipation we must first attend to the patient's diet. Since most of these 
patients also suffer from symptoms of nervous dyspepsia, they are usually very 
careful in their diet, and take only a little, easily digestible, and chiefly liquid 
food. It is no wonder that no good dejections follow such food. Improvement 
can be obtained, in such cases, only by eating plenty of food which can mechan- 
ically stimulate the intestine. Hence we must try to bring the patient back to 
ordinary "household fare" — to take, besides plenty of meat, a sufficient amount 
of bread, vegetables, etc. It is a very good thing to recommend especially certain 
kinds of bread, such as Graham-bread or rye-bread, and also larger amounts of 
butter, besides fruit, prunes, grapes, apples, pears, dates, and figs either raw or 
boiled, almonds, nuts, and honey. It is often efficacious to have the patient drink 
a glass of cold water in the morning before breakfast. Of true laxatives we should 
be very sparing, for the patient readily becomes accustomed to them, and the dose 
has to be constantly increased. Among the milder laxatives the various waters 
which contain Epsom salts, such as Friedrichshall, usually one or two wineglass- 
fuls, are prescribed. For more continued use we may also recommend tamarinds, 
rhubarb, aloes, jalap, cascara sagrada, and extract of frangula. It is not possible 
in this connection to give a minute description of all these remedies. They are 
prescribed in the most varied combinations in the shape of pills and powders. It 
is often necessary to make repeated changes in the medicine and its dose before 
the most effectual prescription is hit upon, for there are many individual pecul- 
iarities in this regard. There are patients with simple habitual constipation who 
for years take, every evening, some powdered rhubarb, or one or two laxative pills, 
with a good result and feel perfectly well. In most cases, however, the efficiency 
of the internal laxatives gradually fails, the patient is obliged to take more and 
more powerful remedies, or increasing doses, in order to get any effect. In such 
instances it is always best to abandon internal laxatives altogether, and in their 
stead to employ external physical agencies, or to stimulate the rectum by means 
of injections, irrigations, and the like. 

The regular use of injections, if carried out in a proper manner, may be con- 
tinued for a long time without harm. The practice may indeed be carried to an 
injurious excess, and occasion at last a catarrh of the rectal mucous membrane, 
because of the constant local irritation, or, at any rate, a needless dependence 
32 



498 



DISEASES OE THE DIGESTIVE ORGANS 



upon local stimulation. The simplest way of making an injection is by means of 
the fountain syringe. There are also various shapes of injection syringes used by 
many. Eor a fluid we choose simple warm water, or, what is often more efficient, 
cold water. We can strongly recommend the employment of soapsuds (a tea- 
spoonful of powdered soap to a pint or two of water). Lately, again, injections 
of oil have been in great vogue. The patient is placed on his left side, and by the 
means of a fountain syringe, eight to sixteen ounces (250 to 500 grammes) of 
fresh poppy oil [or fresh cotton-seed oil] (olive-oil is much dearer) is slowly intro- 
duced into the rectum. Small injections of glycerine, one to two drachms 
(grammes 5-10) are also effectual. Still more convenient and often satisfactory 
is the employment of glycerine suppositories, which are dissolved in the rectum 
by the heat of the body. 

The external physical remedies employed in habitual constipation are mas- 
sage, electricity, and hydrotherapy. Regular massage is often attended with 
good results. The patient is stroked with the flat of the hands with moderate 
or even with considerable pressure, beginning at the csecal region, and proceeding 
along the colon to the sigmoid flexure. There may also be cautious kneading 
of the abdomen. A ball may be used for massage. This is very convenient, and 
can be carried out by the patient himself. An iron ball, weighing about five 
pounds and sewed up in flannel, is rolled for several minutes in a spiral course 
over the abdomen, its general direction being that of the hands of a watch. The 
electrical treatment consists of faradization of the abdominal walls, or galvaniza- 
tion of the intestine, one electrode being placed upon the back. In the way of 
hydrotherapy, cold rubbing and sponging are employed, and are often associated 
with massage. In addition to these methods medical gymnastics may be simul- 
taneously practiced, with a view to regular bodily exercise, and the invigoration 
of the abdominal muscles. 

In the treatment of habitual constipation associated with hypochondriasis, the 
first rule is to treat the patient's mental condition. We should not make merry 
over his trouble, nor should we rudely let him feel that we do not consider his 
complaints so important as he himself imagines. The patient does not deserve 
to be scoffed at, since his subjective symptoms are to him of the most urgent 
nature; but it is extremely important to divert his thoughts from his trouble. 
As in many other reflex processes, so in defsecation, the voluntary attention 
abnormally directed to it has an inhibitory action. Hence we admonish the 
patient to think of his trouble as little as possible and to begin his regular activ- 
ities again, and we try to convince him of the groundlessness of his fears. The 
cathartics, which most patients have already taken freely without the desired 
action, are usually of no advantage at all. On the contrary, it is almost always 
necessary to forbid the patient to use cathartics at all. 

We should not only employ a suitable dietary (vide supra), but we should seek 
to stimulate the intestinal peristalsis by such external means as massage and 
electricity (vide supra). It is true that a considerable part of the success of these 
methods is due to their psychical effect upon the patient, l?ut there is no doubt, 
also, of their direct invigorating influence upon the muscular coat of the intes- 
tine. We must not omit a proper general treatment: cold sponging, baths, a 
country residence, and sufficient physical exercise. Finally, it is often very useful 
to cause the patient to go to the closet at a fixed hour daily, even if there be no 
special desire for a stool, and to try to have a movement of the bowels. Thus a 
sort of training and education of the bowels is achieved, even when the patient 
at first believes it impossible. 

By these means only do we succeed in giving the patient renewed courage, and 
sometimes finally in attaining recovery even in severe and persistent cases. 
In all cases of habitual constipation we should, however, not only endeavor to hit 



STRICTURE AKD OBSTRUCTION OF THE LNTESTIXES 499 



upon the proper means for making the bowels act, but if it is in any wise possible 
we should also strive to arrange the patient's life so sensibly and suitably that he 
will have regular and satisfactory evacuations without any special means. To ac- 
complish this, it is often requisite that we should persuade the patient to give up 
all laxatives, no matter how constipated he may be. Such a course is naturally 
much more practicable in an institution than in a private house. The author has 
himself repeatedly treated patients with habitual constipation simply by regimen 
— i. e., by proper diet, cold sponging, and sufficient exercise or gymnastics, with- 
out any other remedies. In such patients the stool would often be delayed for 
five, eight, or ten days, and yet, what is remarkable, without any special incon- 
venience. Then at last the bowels would move spontaneously, or with the aid of 
a small injection of cold water, and would gradually assume complete normal 
regularity. 



CHAPTER XI 
STRICTURE AND OBSTRUCTION OF THE INTESTINES 

etiology and Pathological Anatomy. — Different pathological processes may 
lead to stricture or complete obstruction of the intestinal tube in different parts. 
Since in this affection the purely mechanical effect of the intestinal stenosis is the 
chief cause of the clinical symptoms, the type of the disease is very similar in all 
the cases of this class, in spite of the manifold anatomical causes. Hence, after 
enumerating the individual affections which may lead to stricture of the intes- 
tines, we shall describe their symptoms in common. 

The anatomical causes of stricture or obstruction of the intestines are as fol- 
lows: 

1. Congenital closure of the intestines is found at the anus, atresia ani, and 
much less frequently in the colon or small intestines. The form first mentioned 
is the only one of clinical interest, since it may be relieved, at least in some cases, 
by operation. All the other forms of congenital closure of the intestines are 
incompatible with a long duration of life. 

2. Tumors and Cicatricial Strictures. — Cancer of the intestine is the only 
tumor that has any clinical significance. We have already described its most 
important anatomical relations and the possibility of intestinal stenosis as a re- 
sult of it. 

We see cicatricial strictures most frequently in the large intestine after recov- 
ery from dysenteric ulcers. The syphilitic stenosis of the rectum, which we have 
already described, is also of practical importance. Syphilitic ulcerations with 
cicatricial stenosis also occur in higher portions of the colon, perhaps even excep- 
tionally in the small intestine. Typhoid ulcers scarcely ever lead to cicatricial 
stenosis. Strictures consequent upon tuberculous ulcers of the intestine are 
somewhat more frequent than typhoid strictures, but still they are very rare. 
Cases have been observed in which there were several tuberculous strictures of 
the intestine, while no sign of tuberculosis could be found elsewhere in the body. 
Stenosis of the duodenum after the healing of a duodenal ulcer {vide supra) re- 
sembles, in its clinical symptoms, stenosis of the pylorus, and not stenosis of the 
intestines. 

3. Intestinal Obstruction. — The most frequent form of intestinal obstruction 
comes from the impaction of faeces. From the different conditions which cause 



500 



DISEASES OE THE DIGESTIVE OKGANS 



enfeeblement of the peristaltic movements, an accumulation of faeces (copro- 
stasis) may arise, especially in the colon. This accumulation gradually but con- 
stantly increases until it leads to well-marked symptoms of intestinal obstruction, 
and in cases of obstruction from other anatomical causes, faecal impaction not 
infrequently aggravates the condition. 

We see obstruction of the intestines from other causes much less frequently 
than from impaction of faeces. In some cases impacted gall-stones have been 
found, especially in the lower part of the ileum and in the neighborhood of the 
ileo-caecal valve, almost completely stopping up the lumen of the intestine. Gen- 
uine intestinal calculi (composed of phosphates) may exceptionally lead to ob- 
struction. Likewise, occasionally conglomerations have been found, composed of 
indigestible portions of food, vegetable fibers, the seeds of fruit, potato skins, 
grape skins, and also clumps of round-worms. We must also mention here the 
very rare cases in which a large foreign body has been swallowed and wedged itself 
into some part of the intestine. Such a thing has been seen, especially in chil- 
dren and among the insane. 

4. Intestinal Constriction. — Although the mechanism of intestinal constric- 
tion in external hernias lies in the domain of surgery, we must mention here the 
chief causes of the so-called internal intestinal constriction, internal incarcera- 
tion, or strangulation. In the abdominal cavity itself pouches and diverticula 
are found, as either normal or abnormal formations, in which single loops of in- 
testine may be caught and constricted. The duodeno-jejunal hernia — the so-called 
Treitz's retro-peritoneal hernia — is worthy of special mention, and comes from the 
entrance of a loop of intestine into the duodeno-jejunal fossa. This hernia may 
become very large. It is sometimes found by accident in the cadaver, not having 
caused any symptoms during life, but in rare cases it may be the cause of acute 
internal constriction. We must also mention the hernia of the omental bursa — 
where a loop of intestine passes through the foramen of Winslow — the intersig- 
moid hernia, the subcaecal hernia, etc. Diaphragmatic hernia is of greater prac- 
tical significance because it is somewhat commoner. By this name we designate 
both genuine protrusions into the diaphragm, and also the passage of abdominal 
viscera through congenital or acquired (traumatic) defects in the diaphragm. 
These herniae may exist without symptoms, or at least without causing any signs 
of severe disease, but in some cases they cause obstruction by constricting or 
twisting a dislocated loop of intestine. 

Those cases in which abnormal slits and holes in the omentum or mesentery 
give rise to internal constriction are to be added to the list of the internal herniae. 
Einally, abnormal cords, membranes, and false ligaments in the abdominal cav- 
ity are a comparatively frequent cause of internal constriction. Such cords 
and bands are sometimes left as the results of a former peritonitis, and may cause 
constriction or kinks of single loops of intestine. Small diverticula of the colon 
sometimes form adhesions due to localized peritonitis, as we have ourselves seen, 
and thus occasion dangerous intestinal stenosis. One such false ligament, which 
must be specially mentioned, is found as a prolongation of Meckel's diverticulum. 
By this we mean that diverticulum which must be regarded as the remains of the 
omphalo-mesenteric duct, still persisting, which has its seat, corresponding to the 
duct, from half a metre to a metre above the ileo-caecal valve. A firm cord some- 
times arises from the free end of this diverticulum, the obliterated omphalo- 
mesenteric vein, which adheres to some part of the internal abdominal wall and 
may cause constriction of the intestine. Adhesion of the free end of the vermi- 
form appendix has been the cause of internal constriction in some cases. 

5. Twists (volvulus) and Knots of the Intestine. — Twists about the mesenteric 
axis, and complete constriction of a portion of intestine from this cause, are seen 
most frequently in the sigmoid flexure, especially if the mesentery of the flexure 



STRICTURE AXD OBSTRUCTION OE THE IXTESTIXES 501 



is unusually narrow congenitally. The spontaneous correction of this abnormal 
condition is hindered by the weight of the loops of intestine filled with gas and 
masses of fasces, and by other portions of intestine lying on the place of twisting. 
Sometimes other portions of intestine wind themselves several times about the 
pedicle of the twisted loop so as to form a regular knot. Such twistings 
have been seen especially between the sigmoid flexure and a portion of the ileum. 
External injury sometimes gives rise to the formation of a knot. In some cases 
abnormally great peristalsis, severe diarrhoea, precedes the appearance of obstruc- 
tion. We have observed a fatal case of volvulus in the highest part of the small 
intestine, consequent upon violent vomiting, excited by a remedy administered by 
a quack, for tapeworm. A most important factor in the development of the 
symptoms of twist is the mechanical strangulation of the blood-vessels of the in- 
testine. This causes a great disturbance of the circulation, leading to paralysis, 
tympanitic distention, and final gangrene of the intestinal coils which are in- 
volved. 

6. Invagination of the Intestine (Intussusception) . — If a portion of intestine 
is pushed into the lumen of the portion that lies next below, we term the process 
invagination. The cause of this is usually assumed to be a diminution or a com- 
plete absence of peristalsis in a circumscribed portion of intestine. If now there 
are energetic movements in the portion immediately above, they push this into the 
paralyzed portion. According to Nothnagel, the beginning of the invagination 
is a spastic contraction of a limited portion of the intestine, in the shape of a ring. 
This furnishes a fixed point, and the contractions of the longitudinal muscles of 
the intestine below the constricted area are said to draw the lower portion of the 
intestine upward over this ring. 

In the post-mortem examinations of children we frequently find intussuscep- 
tion of the ileum, which has occurred shortly before death and so is of no clinical 
importance. Sometimes intussusception has occasioned the most severe symp- 
toms of intestinal obstruction. It occurs particularly in children up to the tenth 
year, and it may be of sudden onset without any apparent cause. Intussusception 
of this sort, which often involves a considerable extent of the intestine, may have 
its seat at almost any part of the bowels. The intussusception most frequently 
involves the caecum and the lowest part of the ileum, pushing thence into the 
colon (invaginatio ileoccecalis) ; intussusception of this sort may be so extensive 
in children that the invaginated ileum reaches into the rectum, or even projects 
from the anus. There are cases in which the ileum alone is involved, and less 
frequently the colon alone. The invaginated portion of intestine usually suffers 
compression of its blood-vessels, particularly the veins. This is followed by in- 
flammation of the constricted portion, and the inflammation often extends to the 
peritoneum. Not infrequently there is gangrene of the inner portion of the intes- 
tine, as a result of strangulation of the afferent vessels. The necrotic portions 
may slough off, and be discharged at stool. Such an occurrence has, in a few re- 
corded cases, led to spontaneous recovery from the intussusception, and from the 
obstruction which it had caused. 

We must mention intestinal polypi as a special cause of intussusception, as 
they gradually pull that portion of the intestine in which they are situated into 
the neighboring portion next below by their weight. This has been repeatedly 
observed. 

7. Compression of the Intestine from without, by tumors of the uterus, ovarian 
cysts, pelvic abscesses, omental tumors, etc., has been met with in rare cases as a 
cause of intestinal stenosis. The symptoms of stricture in such cases develop 
either very gradually or sometimes rather suddenly. 

We must now mention certain pathological changes which may follow every 
obstruction, from whatever causes it may arise. 



502 



DISEASES OE THE DIGESTIVE OBGANS 



The further changes in the intestine deserve the chief attention. Above the 
constricted point it is usually greatly swollen from gas and the accumulation of 
fasces. But it should be noted that the abundant fluid found above the narrow 
part of the intestine is by no means due exclusively to the ingesta, but probably is 
largely the result of transudation, and the secretion of intestinal juices. The 
intestinal contents are very apt to undergo putrid decomposition. This gives rise 
to a large amount of gas which may not be reabsorbed, so that above the obstruc- 
tion there is apt to be a very marked tympanites. This may distend almost the 
entire intestine above the constriction, or the distention may be limited to the 
constricted coils in which circulation has been impaired, and in which conse- 
quently there is a greater tendency to decomposition and the formation of gas. 
The intestinal coils thus distended, being irritated by their decomposing contents, 
usually soon become inflamed; their walls become permeable for bacteria, and 
thus all forms of intestinal obstruction lead to enteritis, and usually promptly to 
peritonitis. A severe diphtheritic process often develops in the intestine, with 
ulceration above the stenosis. In the inflamed, softened intestinal wall, thin 
from its abnormal distention, a little tear easily occurs in some spot, or more 
rarely a genuine perforation following an ulcer. Some of the putrefying contents 
of the intestine thus enter the abdominal cavity, and an intense purulent or ichor- 
ous peritonitis is unavoidable. This is why acute peritonitis is so frequent a le- 
sion in persons who die of intestinal obstruction. If the intestinal stenosis has 
lasted a long time, we usually find in the upper portion of the intestine, besides 
the signs of inflammation, a manifest hypertrophy of the muscular coat, the re- 
sult of the abnormally active peristalsis by which the muscle has tried to over- 
come the obstacle. The intestine below the constriction, in contrast to the part 
just described, appears narrow, contracted, and empty. 

The changes in the other organs correspond to the general inanition. The 
frequent development of inhalation-pneumonia is easily explained, if severe vom- 
iting has preceded (vide infra). 

Clinical History. — In regard to the clinical symptoms we must distinguish the 
cases with a rapid, complete obstruction of the intestine from those in which the 
condition develops gradually, and where there is, therefore, at least for a time, 
merely a constriction of the intestine. 

1. Intestinal Constriction. — The first symptom of the partial intestinal con- 
strictions, which arise from cicatricial strictures and new growths, from partial 
blocking up of the lumen, from intussusceptions, etc., is usually a disturbance in 
defaeeation. The bowels are costive, they move only at long intervals, and their 
motion is often associated with pain and tenesmus. In the description of cancer 
of the intestines we have already mentioned that the faeces passed sometimes 
have a peculiar, flat, compressed, or scybalous form. Blood and mucus are often 
mixed with the dejections and are due to the character of the primary disease. 
In some cases there is no constipation, and there may be even constant diar- 
rhoea. We can easily understand from the physiological conditions that in ste- 
nosis of the small intestines, whose contents have an apprbximately fluid con- 
sistency, disturbances of defsecation are less apt to take place than in stenosis 
of the large intestine, where the faecal masses have already assumed a more firm 
consistency. 

Physical examination of the abdomen often gives important and valuable 
information. The abdomen is usually swollen by meteorism (vide supra). The 
intensity of the meteorism varies very much in different cases and at different times 
in the same patient. Meteorism is sometimes absent, especially in stenosis at the 
beginning of the intestine. There may then be gastrectasis. The marked peristal- 
tic movements, plainly visible through the abdominal walls, are very character- 
istic of most intestinal contractions. The contour of single loops of intestine is 



STRICTURE AND OBSTRUCTION OF THE INTESTINES 503 



often marked, at times quite sharply, and then we can semetimes feel the thick- 
ened intestinal walls through the lax abdominal wall. As a rule, these vigorous 
contractions are associated with severe colic. W e may often decide upon the seat 
of the stenosis from the location and course of the visible peristaltic movements. 
In general, it is true that peristalsis is much more noticeable when the stenosis 
is in the small intestine than when it is in the colon. We must finally state 
that we have been repeatedly struck by the great extent and strength with 
which we could feel the pulsation of the aorta through the swollen loops of in- 
testine. If we put our ear to the anterior abdominal wall we can often hear 
many gurgling and splashing noises, which sometimes have a distinct metallic 
quality. Eructations are frequent, and in some cases there is occasional 
vomiting. 

The duration of all these symptoms varies with the nature of the primary 
lesion. Of course the greatest importance attaches to the condition of the mus- 
cular layer of the intestine above the constricted spot. Eor a time the muscle 
may overcome the obstruction because of its gradual hypertrophy, but at last the 
muscular coat becomes insufficient, and consequently the symptoms become more 
severe. This explains why the symptoms of intestinal stenosis change gradually 
or suddenly into those of complete intestinal obstruction. With this change we 
have grave symptoms. Sometimes, in cases of chronic stenosis of the intestine, 
some temporary causes may occasion repeated attacks of intestinal obstruction, 
which, however, are relieved and give place again to the milder symptoms of mere 
stenosis. 

The duration of all these symptoms differs with the form of the primary dis- 
ease. Either gradually or sometimes quite suddenly the symptoms of intestinal 
constriction pass into those of obstruction. Then the same type of disease devel- 
ops as is seen in all acute internal strangulations. 

2. Intestinal Obstruction. — The symptoms of intestinal obstruction (ileus) 
form one of the severest and most frightful conditions known to pathology. The 
patient undergoes a rapid change for the worse. The signs of collapse quickly 
develop; the face sinks in and assumes a wasted and sharp expression, the ex- 
tremities become cool and livid, the pulse is frequent and can scarcely be felt, 
the voice is weak and lifeless. Respiration is impeded by the upward dislocation 
of the diaphragm. The temperature usually falls, but it occasionally rises. As a 
rule, there is profuse perspiration. The abdomen is much swollen from meteor- 
ism, and is usually very tender on pressure from beginning peritonitis. The 
passage of faeces and the escape of flatus cease entirely. We often see the peristal- 
tic motions of the intestines above the obstruction through the abdominal walls, 
but in some cases the muscular coat is so paretic that it is no longer capable of 
marked peristalsis. 

The most characteristic symptom of intestinal obstruction is the vomiting of 
feculent-smelling masses, the so-called stercoraceous vomiting. There is often 
frequent eructation at the beginning of the attack. The vomitus at first is of the 
usual character, but it soon acquires a manifestly putrid, faecal odor, and becomes 
finally precisely like the stools in diarrhoea. The old opinion is false that in 
this vomiting real faecal masses were forced backward from the large intestine 
into the stomach by an antiperistaltic action of the intestine. Stercoraceous 
vomiting occurs, not only when the obstruction is in the large intestine, but also 
(and oftener) in obstruction of the small intestines. In this case we have to do 
with a putrid decomposition of the contents of the intestine stagnating above the 
obstruction (vide supra). Part of this putrid mass reaches the stomach because 
of accumulation and regurgitation, since the pylorus gradually yields to the in- 
creasing swelling of the small intestines. It is very likely that retrograde " anti- 
peristaltic " movements of the intestinal muscles contribute to the passage upward 



504 



DISEASES OF THE DIGESTIVE OKGANS 



of the intestinal contents. The vomiting itself is probably caused in large part 
by the irritation of the peritoneum, and perhaps by the stimulation of the abnor- 
mal matter which has entered the stomach. If death does not occur in a short 
time, the clinical picture exhibits distinct indications of secondary peritonitis; 
the temperature rises a little, the skin grows dry and hot, and the abdomen is 
very tender upon pressure. 

We must mention, finally, the important changes in the urine which occur in 
the various forms of constriction. In the contents of the intestine, stagnating 
above the stenosis, large amounts of indol and phenol are formed from the decay 
of the albuminous substances, along with other products of decomposition; they 
are in part absorbed and excreted with the urine. Hence, in stenosis of the small 
intestines we often find that the urine contains an increased amount of indican * 
(Jaffe) and phenol (Brieger), but in stenosis of the large intestine the amount of 
indican in the urine is not increased, because the albuminous substances capable 
of decomposition are no longer present in the contents of the large intestine to 
cause it. 

The course of intestinal obstruction differs according to the anatomical causes 
which exist in different cases. In many cases of acute internal strangulation the 
severe type of general disease above described develops in a very short time, and 
may lead to death in a day or two. In such cases death is caused by the poisonous 
action of the absorbed gases, generated by decomposition, or it may be due to 
reflex paralysis of the cardiac nerves. Usually, however, the course is somewhat 
longer, and occupies about a week. In intestinal obstruction which develops 
gradually from intestinal constriction, the disease may go on longer and show 
many variations in its intensity. In mere intestinal constriction we can make 
fewer definite statements as to the duration and course of the affection, since 
the symptoms of the disease depend entirely upon the form of the primary 
disorder. 

In a great majority of cases intestinal obstruction terminates unfavorably. 
Death results either from increasing collapse or from secondary peritonitis (vide 
supra), or in rare cases from further complications, such as pyaemic conditions or 
pneumonia. Recovery (independent of operation) may occur even after the 
severest symptoms, but it is very rare. The obstructions from impaction are most 
hopeful for recovery. Impacted gall-stones, feecal accumulations, etc., may be 
evacuated, after which the severe symptoms disappear. The possibility of recov- 
ery in intussusception, by throwing off the gangrenous internal portion of intes- 
tine, has been mentioned above. We can not wholly deny that internal strangu- 
lations are capable of restoration, although the prognosis must almost always re- 
main doubtful on account of the uncertainty of the diagnosis in any indi- 
vidual case. 

In the partial intestinal constrictions, too, the nature of the trouble causes an 
unfavorable termination in most cases, either from the primary disease itself or 
from the complete obstruction that finally follows, but the possibility of recovery 
can not be wholly excluded in certain conditions, such as ihxpaction or external 
compression. 

Varieties of Intestinal Obstruction. — Diagnosis. — To go into details as to the 
clinical symptoms of all the separate forms of intestinal constriction and obstruc- 
tion would lead merely to repetitions. In most of the acute and many chronic 
cases the diagnosis can generally be made only as to the presence of a mechanical 



* The indican test is performed in the following way : We mix equal volumes of urine and officinal 
hydrochloric acid (P. G.), and then add, drop by drop, a concentrated solution of chloride of lime 
shaking it after each drop. If now chloroform is added, upon shaking again, the chloroform will take 
on a striking blue color, if the urine contains any considerable amount of indican. 



STKICTUKE AND OBSTRUCTION" OF THE INTESTINES 505 



obstacle in the intestine, but the nature of the obstruction can at best be merely 
surmised. Yet in many cases we may reach a more exact diagnosis by careful 
questioning and examination. Above all, we should accurately examine all the 
known localities for external rupture, including the inguinal canal, the thighs, 
and the navel, and we should never omit to make rectal and vaginal examinations. 
Often valuable conclusions can be reached by inflation of the colon by means of a 
rectal tube attached to an ordinary Davidson's syringe, for in this way stenosis of 
the colon is sometimes rendered distinctly palpable. It is also very important to 
make a careful examination of the abdomen as early as possible, employing sight, 
touch, and percussion. We can often recognize the place of obstruction because 
of the localized protuberance, and the tenderness of certain intestinal coils. It 
is of the greatest importance to detect intestinal peristalsis, if present. With 
regard to distinguishing between stenosis of the colon and of the small intestine, 
stenosis of the small intestine is indicated by a special prominence of the central 
portion of the abdomen, by the visible and active peristaltic motion of many coils 
of intestine, by the occurrence of faecal vomiting, and by the presence of a strong 
reaction of indican in the urine ; while stenosis of the large intestine is char- 
acterized by a distention which corresponds more with the course of the colon, 
without much visible peristalsis, and a slow development of severe constitutional 
symptoms. We shall recur later to the differential diagnosis between intestinal 
obstruction and diffuse peritonitis, when considering the latter. 

Of the special varieties of intestinal obstruction, we will call attention to two 
as of practical importance. Intussusception appears, as we have indicated, 
mainly in children. Its symptoms usually begin rather suddenly with violent 
abdominal pain. There soon appear, also, liquid dejections of bloody mucus or 
almost clear blood, originating from the constricted portion of the intestine. 
Often there is great tenesmus and protrusion of the anus. We have already men- 
tioned that sometimes the invaginated portion of intestine may be felt in the 
return. The further course corresponds with the ordinary symptoms of intes- 
tinal obstruction, except that it should be said that faecal vomiting does not 
occur in the ordinary ileo-csecal intussusception, until comparatively late in the 
attack. The other form of intestinal obstruction which we wish to mention here 
is due to the accumulation of large amounts of faecal matter in the rectum. We 
sometimes find monstrous accumulations of faeces in the rectum, especially in old 
women who have previously suffered from habitual constipation, or in whom 
constipation is due to some other affection. Severe symptoms usually come on 
quite suddenly, after long-continued mild prodromal symptoms, and these severe 
symptoms are much like the picture of internal strangulation — severe, sometimes 
colicky, abdominal pain, great tenderness of the abdomen, which is usually 
swollen, marked general collapse, loss of strength, a small pulse, an outbreak of 
cold sweat, vomiting, etc. If we try to give an enema in such cases, very little 
fluid runs into the rectum. On introducing the finger, it usually strikes solidly 
on old, hard, faecal masses above the sphincter, and there is often nothing left but 
to undertake the dirty task of removing at least a part of the scybala with our 
own hands. We may then succeed, by repeated enemata and by giving cathartics 
internally, in removing sometimes quite an incredible amount of accumulated 
faeces, and in obtaining thus a rapid recovery from the condition. 

[The diagnosis of the nature of an intestinal obstruction is so difficult in many 
cases, and yet so important with reference to treatment, that the editor ventures 
to introduce tables of differential diagnosis of the more common forms of the 
condition. These tables are based upon the masterly prize-essay of Treves, of 
London. 



506 DISEASES OF THE DIGESTIVE ORGANS 



ACUTE INTESTINAL OBSTRUCTION 

Chief Common Symptoms.— Sudden pain, intermittent or constant, with exacerbations : tends to become 
constant with time. Vomiting, early, severe, becoming feculent. Constipation, more or less abso- 
lute. Abdominal distention. Shock. 



Age and Sex. . 
History 

Onset , 

Pain 

Local Ten- 
derness . . 

Vomiting 

Constipation . 

Prostration . 

Tenesmus 

Abdominal 

Wall 

Tumor 

Meteorism 



Strangulation by Bands or 
through Apertures (25 
per cent, of all cases of 
acute obstruction). 



Young adults ; rare after 40. 

Previous peritonitis in 68 per 
cent.; previous attacks of 
obstruction in 12 per cent. 

Sudden in 70 per cent. 

Early, severe, continuous, 
with exacerbations. 

Absent at first, appears later. 

Early, marked ; in 60 per cent. 

becomes feculent ; affords 

no relief. 
Continuous and absolute ; no 

blood. 

Marked. 
Absent. 

Flaccid unless peritonitis. 
Very rare. 

Slight, appears about third 
day. 



Volvulus of Colon. 



Males as 4 : 1 ; 40 to 60. 
Previous constipation. 



Sudden. 

Early, less severe, intermit- 
tent at first, becoming con- 
stant with exacerbations. 

Early over distended coil, 
and constant. 

Less early, severe and con- 
stant ; often affords relief. 

Early and absolute ; no 
blood. 

Rather less marked ; may be 

dyspnoea. 
In 15 per cent. 

Rigid from earuy peritonitis. 
Absent. 

Early, rapid, increases, and 
is extreme. 



Acute Intussusception. 



More than 50 per cent, under 

10 years. 
Usually negative. 



Sudden in 75 per cent. 
Early and severe : increasing 

and later subsiding; at first 

paroxysmal. 
Common about a tumor. 

Still less early and severe ; in 
25 per cent, becomes fecu- 
lent. 

Seldom absolute ; diarrhoea 
not uncommon ; blood in 80 
per cent. 

Marked. 

In 55 per cent., and often 
early. 

Flaccid unless peritonitis. 

In 50 per cent.; invagination 
sometimes felt in rectum. 

Rare, unless marked consti- 
pation. 



N. B.— No trustworthy conclusions can be drawn from the seat of the pain as to the seat of the ob- 
struction unless local peritonitis comes on. The pain is usually referred in all forms to the region of the 
navel. In complete obstruction the pain is constant, though with exacerbations ; intermittent pain shows 
that the obstruction is partial. Coils of intestine are not visible through the abdominal wall in acute cases. 



CHRONIC INTESTINAL OBSTRUCTION 



Stricture of the Small 
Gut. 



Adults. 



Cancer, trauma, tuberculo- 
sis ; disordered, imperfect, 
irregular action of bowels 
from time to time, with 
intervals of comparative 
ease. 

Gradual. 

Intermittent. 

Late, scanty, feculent only to- 
ward end of acute attack ; 
may be provoked by food. 

May alternate with diar- 
rhoea ; blood points to can- 
cer. 

Absent. 

Not marked, unless acute at- 
tack. 

Only iu cancer, and then in 
30 per cent. 



Marked in proportion to 
emaciation. 



Stricture of the Large 
Gut. 



Adults. 



Cancer, trauma, tuberculo- 
sis, dysentery ; disordered, 
imperfect, irregular action 
of bowels from time to 
time, with intervals of 
comparative ease. 

Gradual. 

Intermittent. 

Less prominent, rarely fecu- 
lent or provoked by food. 

Form of faeces may be al- 
tered ; blood points to can- 
cer. 

Often present. 
Often marked. 

Only in cancer, and then in 
40 per cent. ; may be felt 
in rectum. 



Marked in proportion to 
emaciation. 



FiECAL Accumulation. 



Adults ; more common in fe- 
males, the hysterical, the 
insane, hypochondriacs. 

Previous constipation. 



Gradual. 
Less prominent. 
Late, scanty, rarely feculent, 
often absent. 

Gradually increasing : may 
be spurious diarrhoea ; no 
blood. 

Absent. 

Late : generally increases with 
1 obstruction. 
Common and distinctive ; 

most easily felt in caecum ; 

little or no tenderness ; 

sometimes movable, and 

can be changed in shape. 
Rarely seen. 



N. B.— In any form of chronic obstruction, the symptoms of acute occlusion may suddenly supervene.] 

Treatment. — As soon as the dangerous signs of intestinal obstruction are rec- 
ognized by the physician, his first duty is to make as careful an examination (vide 
supra) as possible, so as to determine whether the obstruction may not be within 
the reach of direct treatment. If there is an incarcerated external hernia, it 



STRICTURE AXD OBSTRUCTION OF THE IXTESTIXES 507 



demands such operative treatment as is taught by surgery. If there is an impac- 
tion of gall-stones, or intestinal calculi, or foreign bodies, we may in some cases 
furnish appropriate assistance by the cautious use of laxatives. The treatment 
of faecal impaction is of special importance. We have described the most fre- 
quent form of this in detail above. As has already been said, it is usually neces- 
sary to remove at least a part of the faeces vrith the fingers, or some instrument 
like a dressing-forceps or a spoon. In the second place, we may use large enemata 
of pure water, or preferably soap-suds, which must often be repeated four or five 
times a day, until they have a satisfactory result. These are best given by a fun- 
nel and an oesophageal tube (" intestinal tube ") introduced as high as possible 
into the intestine. Cathartics administered internally serve as aids, especially 
castor-oil and rhubarb. 

In stenosis of the rectum from cicatrices and new growths we can also some- 
times employ local surgical treatment. The treatment of faecal accumulations 
usually plays an important part here. Finally, the cases of ileo-caecal invagina- 
tion, in which the lower end of the invaginated ileum reaches the rectum, may 
receive local treatment. We may try a partial replacement by a " sponge-sound " 
(an elastic oesophageal tube to the end of which a sponge is fastened). Blowing 
in air by the bellows was also recommended for this purpose by the old physicians. 
As a rule, however, we use here large enemata of warm water, which sometimes 
seem to exert a favorable mechanical action. Very often it is impossible to apply 
direct treatment to the cause of the obstruction, or even to determine with any 
approach to correctness, the anatomical cause and the seat of the obstruction. In 
these difficult cases the physician must resort at first to merely symptomatic treat- 
ment. It goes without saying that the patient should have complete physical rest. 
All food should, if possible, be entirely forbidden. The torturing thirst may be 
relieved by bits of ice or sips of cold bitter tea. Eormerly when there was obstruc- 
tion of the bowels it was the custom to make trial of laxatives, first employing 
milder remedies, then more vigorous drugs, and finally, as a " last resort," metallic 
mercury in single doses of from 5 to 10 ounces (150 to 300 grammes), which is 
sometimes claimed to act mechanically in " desperate cases " by its weight. Ex- 
cept among some champions of mercury, the present opinion among physicians 
tends far more to the belief that cathartics are usually of no service, but are often 
directly injurious by increasing the resistance. Hence we have at present gone 
over to the treatment of severe internal incarcerations with large doses of opium 
(20 drops of laudanum or 2 to 3 grains [gramme 0.1-0.2] of opium, several 
times a day). Opium acts favorably on the patient's pain, the vomiting is dimin- 
ished, and, by quieting the peristalsis, the danger of increasing the stenosis and 
tearing the intestine is also lessened. In fact, the opium treatment has many 
favorable results on record. Sometimes the first dejection appears during the 
administration of opium. Morphine subcutaneously injected has much less effect 
upon the intestine than opium; its employment is therefore limited to cases in 
which pain is so violent as to demand relief. 

Since, therefore, there are many objections to the internal use of cathar- 
tics, we may try large enemata in those cases in which the seat of the stenosis is 
not known to be in the large intestine. They must be given with caution, but 
persistently, and they must often be repeated; then they sometimes give good 
results, even in severe cases. Unpleasant effects have been reported by other 
observers, but we ourselves have never seen any. The introduction of air into 
the rectum, instead of water, has been recommended and has been useful, particu- 
larly when the obstruction was situated low down and was the result of a kink or 
some similar trouble. The employment of regular lavage (Kussmaul, Cahn, and 
others) is very beneficial in many cases of faecal vomiting; if this is a prominent 
symptom, the stomach should be washed out, in every case of intestinal obstruc- 



508 



DISEASES OF THE DIGESTIVE ORGANS 



tion. Large amounts of feculent liquid are frequently removed through the 
stomach-tube; and it is easy to see that freeing the stomach of its accumulations 
may favor a more vigorous peristalsis. Even when the nature of the intestinal 
obstruction precludes definitive recovery, lavage usually gives no inconsider- 
able relief. 

We need not enter into details as to the general treatment. It goes without 
saying that the patient's strength must be kept up as much as possible, and that 
in severe states of collapse all possible stimulants must be used, such as stro- 
phantus, camphor, and ether. Local applications to the abdomen are usually ill 
borne on account of the tenderness, but still we may try ice poultices or wet com- 
presses. Opium is the best remedy for pain and vomiting, as already stated, but 
it must often be replaced by subcutaneous injections of morphine. In cases of 
extreme gaseous distention the intestinal coils may be punctured with the needle 
of a subcutaneous syringe and the gas in part evacuated. This sometimes proves 
very beneficial. 

Finally, the surgical treatment of intestinal obstruction is most important. 
It is true that we should not, as a rule, proceed immediately to laparotomy at the 
beginning of the characteristic symptoms, but if we produce no effect by means 
of opium, injections, lavage, and similar measures, and if the general condition 
and the pulse grow decidedly worse, then in many cases laparotomy is the only 
means of possible salvation. Sometimes the existing obstruction may be thus 
detected and removed. (For particulars, see text-books on surgery.) 

[The safety with which laparotomy is now performed has stimulated the study 
of all affections on which the operation has any bearing. Internal strangula- 
tions and invaginations may be relieved, and the portion of intestine containing 
a non-cancerous stricture can be excised. An early operation offers much better 
chances, of course. In these days persons should not be allowed to die directly 
from intestinal occlusion without an attempt being made to restore the permea- 
bility of the canal by surgical means.] 



CHAPTER XII 

INTESTINAL PARASITES 

( Helmin tliiasis) 

1. Tape-worms 

Natural History of the Tape-worm. — Three of the tape-worms (cestodes) 
which are found in the intestines have a clinical significance: the tcenia solium, 
the tcenia medio canellata, and the bothriocephalus latus. 

1. The tcenia solium is, when fully developed, two or three metres long. Its 
head (Figs. 47 and 48) is about the size of that of a pin, and has four projecting 
cup-like suckers, and in front a beak with about twenty-six hooks. The top of the 
head is, as a rule, plainly pigmented. A small neck, about an inch long, is 
attached to the head, and then follow the single "joints" (proglottides) of the 
tape-worm, of which the youngest, lying near the head, are still very small and 
short. They gradually increase in length and breadth, and at about a metre from 
the head they have an approximately quadrilateral shape. The segments which 
lie farther down, and which have already reached puberty, have the form of pump- 
kin seeds, and are nine or ten millimetres long and six or seven wide. The matrix 
or uterus runs through the middle of each mature segment (see Fig. 49), and from 
it, on each side, go seven or eight side branches, which ramify like a tree. On 



INTESTINAL PAEASITES 



509 



one side, a little below the middle, lies the sexual orifice (Fig-. 49, a) . The male 
sexual organs consist of a number of little clear vesicles in the anterior portion of 
the segments. The thick-shelled eggs (Fig. 50, 3) develop in the uterus, and con- 
tain an embryo with six hooklets. 

The taenia solium inhabits the small intestines of man. Its head clings to the 
mucous membrane so tightly, usually at some point in the upper third of the small 




Fig. 47.— (.From Heller.) Fig. 48.— (From Hfller.) Head of cj'sticercus of 

Heau of taenia solium. the brain. 



intestine, that the neck is often torn off in trying to loosen the worm from the 
intestinal wall. The rest of the worm, which is in part in many coils, extends 
to the lower part of the ileum, but only exceptionally into the caecum. From the 
lower end long chains, or single mature segments, are often detached, mix with 
the contents of the intestine, and are passed with the faeces, together with some 
of the eggs from the uterus. 

The further development of the eggs of the taenia solium takes place in another 
" host," almost always in the hog. Hogs are infected by eating faeces, offal, 
etc., containing taenia eggs. The thick shell of the eggs 
is dissolved in the hog's stomach, and the free embryos 
pierce the walls of the stomach and intestines and travel 
with the blood-current, or through the tissues, into the 
different organs, especially into the muscles. Here they 
develop, in two or three months, into cysts something 
larger than a pea, from whose walls a newly developed 
taenia-head arises, a so-called scolex (nurse). These 
cysts are termed worm-cysts, measles, or cysticerci cellu- 
losae. They live from three to six years; then they die 
and become calcified. If a cysticercus gets into a man's 
stomach from his eating raw or imperfectly cooked ham 
or pork, a new and complete taenia sprouts from the 
scolex, which forms mature segments in three or four 
months. 

We usually find only one tape-worm in a man, but sev- 
eral specimens have been seen at the same time in the same intestine. The 
length of a tape-worm's life is not certainly known, but it has happened that 
some persons have lodged the same tape-worm for ten or fifteen years. 

Although the fully developed taenia solium is seen only in man, as we have 
said, the cysticercus cellulosae has been found, in rare cases, in dogs, rats, and mon- 
keys, etc., as well as in hogs. It is a particularly important fact that the cysti- 
cercus cellulosae itself may also occur, as such, in man. If tape-worms or mature 




Fig. 49. — (From Heller.) 
Taenia solium. Mature 
segment. 



510 



DISEASES OF THE DIGESTIVE OEGAXS 



segments get into a man's stomach in any way, probably by auto-infection by the 
finger, etc., the embryos travel into other organs. Cysticerci are often found in 




Fig. 50.— Comparative view of the eggs of some of the commoner intestinal parasites. 1. Egg of distoma 
hepaticum. 2. Distoma lanceolatum. 3. Taenia solium. 4. Taenia mediocanellata. 5. Bothriocephalus 
latus. 6. Oxyuris vermicularis. 7. Trichocephalus dispar. 8. Ascaris lumbrieoides. 

men, singly or in groups, especially in the skin, the brain, the eye, and the mus- 
cles. There is a special form of cysticercus of the brain, in which we find a whole 
chain of cysts, like a cluster of grapes, but sterile, the so-called cysticercus race- 
mosus. 

2. The taenia mediocanellata, or tamia saginata (from saginare, to fatten), is 
far more common than the taenia solium in many parts of Germany. It is longer 
than the taenia solium, being about three or four metres 
long, and its individual joints are, on the whole, broader 
and thicker. The head (Fig. 51) has also four prominent 
cup-like suckers, but it has no 
crown of booklets. The mature 
segments differ from the proglot- 
tides of taenia solium, in that the 
central uterus sends off many more 
(twenty to thirty) side branches, 
which divide dichotomously, and 
not like a tree. The sexual open- 
ing is also on the side (Fig. 52, a). 

The life-history of the taenia 
mediocanellata is, on the whole, 
like that of the taenia solium. The 
taenia mediocanellata, however, 
throws off single mature segments 
much more frequently than the 
taenia solium. These segments are 
found in the faeces, and here they often exhibit a crawling motion. A kindred fact 
is that it is always easy to find large numbers of tape-worm eggs in the faeces 
of individuals who harbor the taenia mediocanellata. This is usually difficult 
in the case of taenia solium. The cysticercus of taenia mediocanellata does not 
inhabit pork, but beef, so that the infection of man by this tape-worm comes 
from eating raw beef. In man the cysticercus of taenia mediocanellata, 





Fig. 51.— (From Heller.) 
Head of taenia medio- 
canellata. 



Fig. 52.— (From Heller.) 
Taenia mediocanellata. 
Mature segment. 



INTESTINAL PAEASITES 



511 



cellule 



has never yet been 





Figs. 53 and 54.— (From Heller.) 
Fig. 53.— Head of bothriocephalus latus. a. 

Lateral view, enlarged, b. Natural size. 
Fig. 54. — Bothriocephalus latus. Mature 

segment. 



which is somewhat smaller than the cysticercus 
observed. 

3. The "bothriocephalus latus occurs in Holland, Switzerland (Geneva), Pome- 
rania, East Prussia, Hamburg, and Russia (the German Baltic provinces). It has 
not yet been observed in middle Germany. It is the largest tape-worm; it may be 

six or eight metres long, and sometimes has over four thousand 
joints. The head of the bothriocephalus (Fig. 53) consists of a 
little club-shaped swelling, with two slit -like depressed suckers on 
the sides. A long, thread-like neck joins the head to the youngest 
segments. The full-grown segments (Eig. 54) are short, but are 
distinguished by their great breadth. The largest segments meas- 
ure in length about three or four millimetres, and in breadth ten 
or twelve, but the last joints are longer and 
are not so broad, so that they have an ap- 
proximately quadrilateral form. The uterus 
consists of a very tortuous canal in the cen- 
ter. The sexual orifice does not lie on one 
side, as in the taenia, but in the middle of 
the abdominal surface, nearer the anterior 
border of the segment than the posterior. 
The eggs (vide supra, Eig. 50, 5) are of an 
oval form, and have a hood-shaped lid at 
one end. They are to be found in almost every dejection of persons affected with 
a bothriocephalus. Single joints of the tape-worm are not passed with the stools, 
but portions of the worm, several feet long, come away from time to time, espe- 
cially in the spring and autumn. 

The eggs develop only in fresh water. The embryo (Fig. 55), which is formed 
in them in a few months, and is provided with six hooklets and with vibrating 
cilia, is swallowed by fishes (chiefly pike and eel-pouts according to Braun, salmon 
according to Kiichenmeister), and develops in 
their muscles and internal organs into cysticerci. 
The infection of man with bothriocephalus comes 
from eating such fish containing cysticerci. 

4. These three kinds of tape-worms that have 
been enumerated are the most important, but we 
will briefly mention the taenia nana and the taenia 
cucumerina (tcenia elliptica). The first of these, 
the taenia nana [dwarf], is the smallest tape-worm, 
being only 1.0 to 1.5 centimetre long. The long 
head is provided with four suckers and a circlet 
of hooks which can be extended far out. The 
anterior joints are very narrow and short, those 
farther back broadening not inconsiderably. The 
taenia nana is very frequent in Italy and also in 
Sicily. In Germany it has been seen only excep- 
tionally. Its cysticercus is said to inhabit snails. It is seen especially in chil- 
dren, and in them sometimes in very great numbers. Single joints are difficult 
to find in the dejecta, but the discovery of its eggs with the microscope is very 
easy. The expulsion of the worm by means of santonine and thymol (vide infra) 
is usually a simple matter. 

The taenia cucumerina is twenty to twenty-five centimetres long. Its poste- 
rior joints are six to eight millimetres long, but have a width of only one milli- 
metre. The head is provided with many hooklets ; the beak can be extended and 
retracted. The taenia cucumerina occurs especially in children. Its cysticercus 
is found in the dog. 




ig. 55.— Embryo of bothriocephalus 
latus, with its ciliated coat. 
(Leuckart.) 



512 



DISEASES OE THE DIGESTIVE ORGANS 



Symptoms and Diagnosis. — In many cases tape-worms are lodged in the intes- 
tines without causing any morbid symptoms. We can recognize their presence 
only by occasionally finding the joints in the dejections. 

In other cases, however, tape-worms cause a list of disturbances which are 
often exaggerated by anxious, hypochondriacal, and nervous persons, but which 
ought not to be too little regarded. The symptoms are referred chiefly to the 
intestinal canal. Sometimes there is quite severe abdominal pain, which may 
assume a colicky character. The patient also frequently complains of irregularity 
of the bowels, and of occasional diarrhoea, which alternates with constipation. 
Many general symptoms are also added to those mentioned — loss of appetite, or at 
times marked voracity, general languor, disinclination to work, mental disturb- 
ance, depression, etc. Often the general nutrition is considerably impaired. 

There are also certain symptoms to be mentioned which were formerly ex- 
plained as " reflex." Still, it is very possible that poisonous matter may be pro- 
duced by the tape-worms under certain circumstances, about which we do not yet 
have accurate knowledge, and that these poisons occasion some of the symptoms 
of tape-worm (vide infra). Among these we sometimes see marked salivation, 
tickling in the nose, dilatation of the pupils, palpitation, vomiting, headache (mi- 
graine), etc. In some cases even severe spasms and choreic conditions have been 
referred to the presence of tape-worms (particularly the taenia nana) in the intes- 
tinal canal, but it is hard to decide how far such a supposed connection can really 
be regarded as justified. 

Thus in most cases tape-worms cause comparatively little disturbance, but they 
may occasion severe illness. Of late years it has been observed that when the 
bothriocephalus latus, or exceptionally a taenia, is present in the intestines 
there will often be an extremely severe anaemia, quite like pernicious anaemia 
(q. v.). The patient becomes excessively pale and feeble, the blood shows marked 
oligocythemia and poikilocytosis ; there are anaemic cardiac murmurs and simi- 
lar symptoms. This condition also is probably referable to poisonous matter 
produced by the bothriocephalus latus, absorbed by the intestines, and fatal to 
the red blood-corpuscles. If the tape-worm is promptly expelled there is rapid 
and complete recovery. 

Although many of the symptoms mentioned may arouse suspicion as to the 
presence of a tape-worm, the diagnosis can be made only by finding the joints 
or eggs of the tape-worm in the dejections. In many cases the patient himself 
brings some of the segments found by him in the dejections to the physician, but 
in judging of them a certain caution is always necessary, since shreds of mucus, 
remains of food, etc., are quite frequently presented to the physician, under the 
idea that they are segments of tape-worm. But, on the other hand, it is also very 
important that the physician himself should not forget the possibility of a tape- 
worm and should himself direct attention in suspicious cases to the dejections of 
the patient. If there is a taenia mediocanellata or a bothriocephalus latus, it is 
usually easy to find the eggs in the faeces, but in the case of taenia solium this is 
more difficult. With taenia solium we usually have to search for segments of the 
tape-worm in the stools. Many patients with all sorts of indefinite, mild, gas- 
tric and intestinal symptoms, or such general symptoms as headache or languor, 
or even graver disturbances, such as apparent pernicious anaemia, are finally 
cured when the true cause of the disease is found to be a tape-worm. 

If we obtain a few joints of the tape-worm we should endeavor to determine 
from them the species. If we spread out the pieces of tape-worm between two 
microscopic slides, the thicker, fatter segments of the taenia mediocanellata, with 
its many-branched uterus, may usually be distinguished without difficulty from 
the more tender and more translucent segments of the taenia solium, with a 
smaller number of lateral branches to its sexual apparatus. The statement of 



IXTESTIXAL PAEASITES 



513 



many patients that single segments of tape-worm come from them at other times 
than when at stool, and that they find them on their underclothing, almost always 
points to the presence of a taenia mediocanellata in the intestine. The eggs of 
taenia solium and taenia saginata can be distinguished from one another with 
extreme difficulty in the faeces, while it is easy to diagnosticate the bothrioceph- 
alus latus by its eggs, as they are so characteristic (vide supra, Fig. 50). 

If we suspect a tape-worm, without having secured the certain evidence of seg- 
ments or eggs in the dejections, it is a good plan to give the patient a mild cathar- 
tic, such as castor-oil, or a dose of boiled pumpkin-seeds, since after this, if the 
intestine harbors a tape-worm, single portions of it often come away. 

Treatment. — The " tape-worm cures," which are recommended in so great a 
number that we can by no means mention all of them here, but only the most 
important and the most serviceable, aim at killing or benumbing the worm, and 
then at removing it from the intestine in toto by cathartics. 

We usually begin with a so-called " preparatory treatment." This is to cleanse 
the intestine, especially the large intestine, from old faecal masses, in order to pre- 
pare as free a passage as possible for the worm. For this purpose we give the 
patient a mild laxative, or, better still, a large enema of cold water. Many physi- 
cians recommend that there should first be given some active purge, such as calo- 
mel or castor-oil, but this is exhausting to the patient, and we believe it is not 
usually necessary. We also forbid for a day or two the use of vegetables, black 
bread, etc., and prescribe instead a limited diet of white bread, some meat, milk, 
and coffee. It is a wide-spread practice to take during the preparatory treatment 
certain articles of food to " make the worm ill." Among these a salad of finely 
chopped and very salt herring with onions and garlic is especially recommended. 
A similar action is also ascribed to strawberries, cranberries, and bilberries. Hence, 
on the day, and especially on the afternoon, before treatment, we have the patient 
take a large amount of the articles of food mentioned, such as herring salad. 

On the next morning, after everything has been prepared, after the bowels 
have moved the night before, etc., the patient takes no breakfast, or only some 
strong sweet cafe noir. Then he takes the special anthelmintic, and in one or 
two hours, if he feels a great pressure in the abdomen, he also takes a few spoon- 
fuls of castor-oil or rhubarb. 

The number of taenicides recommended is, as we have said, very great. At 
present the following are most in use : 

Many experienced physicians and we ourselves now employ almost exclusively 
the ethereal extract of male fern (oleoresina aspidii). It is true that the reliabil- 
ity of this drug as dispensed by different apothecaries varies, but in most cases, if 
we can obtain a good fresh preparation, the result is perfectly satisfactory. It 
should be said, however, that the drug is not entirely free from danger ; in excep- 
tional cases large doses have caused symptoms of poisoning, particularly amauro- 
sis, also jaundice; and even death has occurred. We should, therefore, hold 
firmly to the rule of never exceeding a dose of two and a half to three drachms 
(grammes 10-12). We have never seen unfortunate results from this amount. 
The best way of administering the drug is in the gelatine capsules which are for 
sale, of which each contains thirty grains (two grammes) of the extract. 

The bark of pomegranate-root (cortex radicis Punicce granati) is one of the 
most efficient remedies. We formerly prescribed it in combination with the 
ethereal extract of male fern, in the following prescription: 

ly Granati radicis corticis . oiv-v (g Tm - 120-150) ; 

Aquae O ij (grm, 1,000). 

Macerate for twenty-four hours, and boil until it is reduced to §v (grm. 150). 

Add: Oleoresinae filicis gr. Ixxv (grm. 5). 

33 



514 



DISEASES OF THE DIGESTIVE ORGANS 



The whole amount is to be taken in three or four doses as near together as pos- 
sible. In order to obviate the bad taste of the remedy and to increase the action 
by administering a larger amount at once, it has been recommended to introduce 
the whole amount of a still stronger decoction of pomegranate-root directly into 
the stomach by means of an oesophageal tube. As a rule, it is well to avoid this 
procedure. — The tannate of pelletierine, prepared from the pomegranate-root, is 
also to be recommended. It is almost tasteless, and in doses of eight to twenty- 
five grains (gramme 0.5-1.5) is said to be a very certain taanicide. 

Another remedy, which has often proved successful, is kousso-flowers. We 
give three or four powders, each containing seventy-five grains (grammes 5) of 
powdered kousso-flowers, in white wine, giving a glass of wine containing one pow- 
der about every half -hour. Rosenthal's " kousso tablets " are more agreeable to 
take and are very good, but they are more expensive. Twenty of these, of fifteen 
grains each (gramme 1), may be taken without danger within an hour with cafe 
noii' or lemonade. During the period of treatment the patient must lie as quiet 
as possible in order to avoid vomiting. Up to the present time we have not had 
sufficient experience of the koussine or kosseine, prepared from the alcoholic ex- 
tract of kousso-leaves, which is said to be very efficient in doses of thirty to forty- 
five grains (grammes 2-3). 

Of the other remedies we may mention kamala. We give the powder or 
tablets, in doses of 75-150 grains (grammes 5-10). This is a mild remedy and used 
chiefly for children. We may also give oil of turpentine, one or two ounces 
(grammes 40-60) in two doses in milk — an efficient but rather dangerous remedy 
in these doses; and finally chloroform. Lately, physicians have recommended 
pumpkin-seeds, which have long been known as a popular remedy. One advan- 
tage is that they do not have the bad taste of almost all the other remedies for 
tape-worm. About one hundred and twenty seeds, or for children half as many, 
are peeled, pounded up, and mixed with sugar, or else made into an emulsion, and 
administered. 

The treatment is to be regarded as absolutely successful only when we find the 
head of the tape-worm, as well as its joints, in the patient's dejections. We may 
best search for the head in the faeces by diluting the dejection repeatedly with 
water, and pouring off the water. The tape-worm then remains at the bottom of 
the vessel. As it may be that the head has been dislodged even if it has not been 
found, we should not repeat the treatment for tape-worm until, some months later, 
there are indubitable signs that the tape-worm still exists. 

Every tape-worm treatment is rather drastic, and hence it is well, after the 
treatment is over, to recommend the patient to be prudent in his diet, and to 
be careful about his digestive tract for some time. In persons who are very weak, 
or who have some other disease, we do not willingly undertake to remove a tape- 
worm without urgent reasons; but in people who are otherwise healthy it is 
always well to get rid of a tape-worm, even if it causes no severe symptoms. The 
chief reason for this is that taenia solium might occasion cysticerci in the brain. 
The best time for undertaking a treatment is when joirits or large pieces of the 
worm come away quite frequently of their own accord. We should never pre- 
scribe a treatment on the mere statements or suspicions of the patient. We must 
always convince ourselves with complete certainty of the presence of a tape-worm 
in the intestine. 

We must finally mention that the only efficient prophylaxis against acquiring 
a tape-worm lies in entirely avoiding the use of raw or half-cooked beef or pork. 
The more widely spread the taking of raw meat is, as in Abyssinia, the more com- 
mon are tape-worms in man. Certain callings, like those of the cook or the 
butcher, are also especially exposed to infection. 



INTESTINAL PAEASITES 



515 



pointed at 
thirty or 



2. Eo and -worms 

(Ascaris lurnbricoid*s) 

Natural History. — Ascarides are pale-reddish, cylindrical worms 
both ends, with the sexes in different individuals. The females are 
forty centimetres long, the males about twenty-five. 
At the cephalic end of the worm are found three lips 
furnished with fine teeth. The tail is straight in the 
females and curved in the males. In the female sex- 
ual organs (Fig. 56) sixty millions of eggs may de- 
velop, at a rough estimate. These eggs are often 
found in the fasces of persons who have round-worms 
in their intestines (see Fig. 50, 8). They have a great 
capacity of resisting external influences, and a worm- 
like embryo develops in them in about nine weeks. 
The further dissemination of round-worms takes 
place without any intermediate host in this manner: 
the eggs containing the embryo worms are, through 
some chance, swallowed and then grow in the intes- 
tines into sexually-mature worms. Experimental in- 
fection with the eggs of round-worms gives distinctly 
positive results (Lutz, Epstein). 

The round-worms inhabit chiefly the small intes- 
tine. In severe vomiting they often reach the stom- 
ach and are vomited up. In individual cases they 
have been found in the bile-ducts, in the air-passages, 
and, after perforation of the intestine, in the abdom- 
inal cavity. The number of round-worms existing 
at the same time in the intestine may be very con- 
siderable. We find them most commonly in chil- 
dren and in adults from the lower classes. Round- 
worms have been repeatedly observed to crawl out 
of the anus, the mouth, or the nose of children during 
sleep. 

The round-worm is also common in hogs and cat- 
tle as well as in man. 

Symptoms. — In general, round-worms are innocent 
parasites, which may exist in large numbers in the 
intestines without any bad results. In other cases 
they cause symptoms similar to those ascribed to 
taeniae — abdominal pain, languor, itching of the nose 
and skin, urticaria, burning in the eyes, salivation, 
etc. — symptoms which are all ambiguous, and whose 
definite connection with the presence of round-worms 
it is hard to make out. Occasionally they excite long- 
continued and persistent vomiting, or violent diar- 
rhoea, these symptoms persisting until the worms are 
expelled, when they promptly cease. Leichtenstern 
found that it was not very exceptional for children to 
be noticeably anaemic when harboring ascarides, and 
to improve remarkably when the worms were expelled. 

The cases recorded in literature are quite numerous in which severe nervous 
symptoms have been caused by round-worms and have disappeared after the re- 
moval of the parasites. However cautious we may be in accepting such state- 




Fig. 56.— (From Heller.) Asca- 
ris lumbricoides. Female. 143 
millimetres long. a. Vagina. 
b. Intestine, c. Boundary be- 
tween the uterus and oviducts. 
d. Longitudinal bands. e. 
Coil of oviducts and ovaries. 



516 



DISEASES OE THE DIGESTIVE ORGANS 



merits, nevertheless their credibility can not be wholly denied. We would men- 
tion especially convulsions, epileptiform seizures, choreic and cataleptic conditions, 
contractures, and temporary mental disturbances, which are claimed to be excited 
by ascarides. It is said that children with ascarides not infrequently exhibit 
mild nervous disturbances, such as headache, vertigo, mydriasis, and chills. All 
these symptoms, and also those above enumerated, are perhaps not so immediately 
dependent upon the presence of the worms in the intestinal canal, but are due 
rather to toxines developed under certain circumstances. 

In some cases the presence of ascarides may excite much more severe symp- 
toms by unfortunate accidents, as, for example, sudden suffocation from the 
entrance of a round-worm into the larynx. When a very large number of round- 
worms have been present in the intestine, severe symptoms of intestinal stenosis 
have been observed from their rolling together into a ball. If a round-worm 
crawls into the bile-ducts, it may give rise to jaundice, and even to the develop- 
ment of an abscess of the liver. In the abscesses of the anterior abdominal wall, 
usually termed " worm abscesses," the round-worms probably play a purely acci- 
dental part. We have to do in such cases with perityphlitic abscesses or with 
inflamed hernige, which have perforated externally, by which the round-worms 
which are accidentally found in the intestines pass out, without having any causal 
relation to the abscess. 

The diagnosis of round-worms is not usually difficult. Often a few worms 
appear of themselves, or as the result of a simple laxative. If not, search must be 
made in the dejections for the eggs of the ascarides. These are always easily 
found. It is advisable to obtain a particle of the contents of the rectum for the 
purpose of microscopic examination by introducing an elastic catheter. 

Treatment. — The oldest remedy for ascarides is worm-seed — santonica. 
This is best given in the form of an electuary — santonica, a drachm (grammes 5) ; 
jalap, fifteen grains (gramme 1) ; and syrup, an ounce (grammes 30), to be taken 
in three doses — in combination with a cathartic. Of late, worm-seed, on account 
of its bad taste, has been almost wholly replaced by santonine, which is derived 
from it. This is prescribed in one- or two-grain (gramme 0.05-0.10) powders, or 
still more frequently in the form of santonine troches ("worm-tablets"), which 
may be had of any apothecary. It is well to give santonine also in connection with 
a cathartic, such as calomel. We give the patient one or two doses of santonine 
in the morning for three days, and on the fourth we give a cathartic. Severe 
symptoms of poisoning — spasms — have been seen only occasionally from the care- 
less use of it. Milder symptoms, such as a yellowness of the urine and conjunc- 
tiva?, and xanthopsia, or seeing everything yellow, are somewhat more frequent. 

In exceptional cases santonine fails to expel the ascarides. We may then try 
male fern or thymol (grains 8-24, gramme 0.5-1.50) in two or three doses given 
in the course of the day. 

3. Oxyuris vermicular is 

{Seat-worms. Pin-worms) ( . 

Natural History. — The oxyures are little round worms, the females ten or 
twelve millimetres long, the males only three or four (see Eigs. 57 and 58). The 
eggs, when they reach the human stomach, develop very rapidly. The embryos, 
set free, collect in the small intestine and later mainly in the caecum. As soon 
as they become sexually mature they pair, and then wander gradually down 
into the rectum, where they collect in great numbers. When the eggs inside 
the female become ripe, the female leaves the rectum and lays its eggs outside, 
where they are soon destroyed (Leichtenstern). The eggs may easily, however, 
be conveyed by fingers or by articles of diet, or by similar means, to the stomach 
of the same host or of some other person, whereupon the development of the worm 



INTESTINAL PAKASITES 



517 



begins afresh. As will be readily understood, children, with their untidy habits, 
are much more exposed to infection with the oxyuris than adults. The fact that 
the female oxyuris never lays its eggs in the intestine explains why the eggs of the 
oxyuris are rarely if ever found in the stools. The female crawls out of the anus 
to deposit its eggs. Male as well as female worms 
are discharged with the stools. The entire cycle of 
development of the oxyuris occupies about fourteen 
days. The number of these worms which may be 
present at the same time in the intestine is very 
considerable, so that " the entire mucous mem- 
brane of the colon is covered with them like 
a fur." 

Symptoms and Treatment. — The oxyures found 
in the upper portions of the intestine and in the 
caecum cause no symptoms whatever, but in the 
lower part of the rectum their presence causes local 
symptoms, especially a very severe feeling of itching 
and burning in the anus, which makes the child con- 
stantly scratch and dig with his fingers. This 
itching of the anus is most severe at night in bed. 
In girls the oxyures frequently travel into the va- 
gina, by which an intense itching is also set up 
there, which sometimes leads to masturbation. In 
some cases in boys and men, oxyures have been 
found to be the cause of abnormal sexual irritation. 
Other clinical symptoms are rare, but sometimes 
there may be anaemia or nervous disturbances, and 
in rare cases marked intestinal catarrh, or inflamma- 
tion of the vulva. 

The diagnosis of oxyures is not difficult. Our 
attention is called to the itching of the anus, etc., 
and we look for worms. Single worms are easily 
found in the dejections, and often on the skin about 
the anus. 

Treatment is directed first to the expulsion of the 
thread-worms from the rectum, and the prevention 
of any fresh self-infection. For this purpose the 
chief means are large injections, which must be em- 
ployed persistently, once or twice a day, for weeks; 
for fluid we may choose simple warm water, or water 
containing vinegar, salt, or glycerine. Injections 
containing corrosive sublimate or carbolic acid are 
effective, but they should never be employed because 
of the danger of poisoning. It is difficult to remove 
completely the oxyuris from the upper part of the 
intestine, particularly from the caecum. For this 
purpose the most efficient remedy seems to be san- 
tonine, perhaps combined with calomel or castor- 
oil. The itching at the anus is alleviated by cold 
compresses or by the inunction of small amounts of unguentum hydrargyri. 

Extreme cleanliness is very important. The anus should be frequently washed, 
and also the fingers, particularly the finger nails, to prevent the spread of the 
parasites. 

[Enemas containing infusion of quassia, alum, eucalyptol, tannin, etc., are 




Fig. 58. 

Fig. 57. — Oxyuris v.ermicularis. 
Natural size. 1. Female. 2. 
Two males. 

Fig. 58.— (From Heller.) Oxyuris 
vermicularis, enlarged, a. Ma- 
ture female, not yet impreg- 
nated, b. Male. c. Female 
containing eggs. 



518 



DISEASES OF THE DIGESTIVE ORGANS 



7 i 



Fig. 59. 



much in use. A plain enema should be given first, to unload the rectum and clean 
the membrane as far as possible, so that the anthelmintic may reach the worms 
when introduced.] 

4. Anchylostoma duodenale 

(Dochtnius sen Strovgyius duodenalis) 

The anchylostoma duodenale is a worm first observed in upper Italy and in 
Egypt in large numbers, of which many inhabit the upper portion of the small 
intestine, especially the duodenum, but also the jejunum and ileum. The male 
is six to ten millimetres long, the female ten to eighteen. At the cephalic end 
(Figs. 59, 60) is found a bell-shaped mouth-capsule, which is 
provided with two small teeth on its dorsal edge, and four 
larger curved teeth on its ventral edge. With this sucking 
and biting apparatus the worm fixes itself firmly, like a wet 
cup, on the intestinal mucous membrane, and is nour- 
ished by the blood which it sucks out. The place in the in- 
testine to which an anchylostoma has fastened may be rec- 
ognized in the cadaver as a little ecchymosis. The worms 
sometimes bore completely into the inner part of the mucous 
coat. 

The eggs of the anchylostoma are discharged in great 
numbers with the faeces (vide infra). From these the larvae 
develop and thrive, particulaiy in the dirty water of mud 
puddles and ditches; and by means of water that is spat- 
tered, or more often by dirty hands, they reach the mouth 
and the intestinal canal of man again, and then rapidly 
develop to sexual maturity. 

If the intestine harbors many anchylostomata, the small 
but constant loss of blood caused by them is not without in- 
fluence on the organism. In addition there are probably spe- 
cific toxic influences which have an injurious effect upon the 
red blood-corpuscles. The symptoms of a severe anaemia 
gradually develop. Griesinger first made the discovery, in 
the year 1854, that the disease long known by the name of 
" Egyptian chlorosis " was caused by the anchylostoma 
duodenale. Since then confirmatory observations have been 
made in many parts of the tropics. 

The disease caused by the anchylostoma has become par- 
ticularly known in Europe because of the great frequency 
with which it occurred among the Italian laborers who were employed in building 
the Saint Gothard Tunnel. Since then many well-established cases have been 
found in other lands ; e. g., Hungary ; Germany, particularly in the brickmakers 
of the Rhine ; also repeatedly in miners and laborers in tunnels. 

The symptoms of the disease consist, as we have said, of a gradually increas- 
ing general anaemia, for which no special organic lesion can be made out objec- 
tively as a cause. The patient also suffers from very great general weakness and 
languor, dyspnoea, palpitation, headache, oedema, etc. The changes in the blood 
(oligocythemia, poikilocytosis) are precisely similar to those seen in pernicious 
anaemia. The disease may last for months, or even years, and it often ends 
fatally, if it be not recognized and treated in time. 

Leichtenstern has made numerous and accurate observations with regard to 
the brickmakers of Cologne. He states that no symptoms are observed for three 
or four weeks after infection with the embryos of the anchylostoma. Some five 
or six weeks after infection, when the parasites become sexually mature and breed, 




Fig. 60. 

Fig. 59. — Anchylostoma 
duodenale. " Natural 
size. a. Male. b. 
Female. 

Fig. 60.— (From Heller.) 
Anchylostoma du- 
odenale, enlarged. 
Head with bell-like 
mouth. 



INTESTINAL PAEASITES 



519 



there appear bloody diarrhoea, intestinal colic, and accompanying progressive 
anaemia. At this time there is probably more shifting about of the parasites in 
the intestine, while they later become more fixed. This explains why the dis- 
ease evinces a more acute and severe character at first, and then takes on the 

form of a chronic anosmia, with great 
diminution or cessation of the bloody 
stools. 

The diagnosis is easy if we only think 
of the possibility of anchylostoma. It is 
not very difficult to find an abundance of 
eggs in the fasces. They are of oval shape 
and characterized by the frequent pres- 
ence in them of two or more spherules due 
to subdivision (see Fig. 61). The worms 
themselves are not usually found in the 
stools unless anthelmintics have been ad- 
ministered. Charcot's crystals are often 
found in the dejections previous to the ap- 
pearance of the anchylostoma eggs (Leich- 
tenstern). 

If the disease is recognized, treatment is usually satisfactory. We prescribe 
the same anthelmintics as for the other intestinal parasites, particularly extract 
of male fern in suitable doses (2-3 drachms, 10-12 grammes), besides laxatives 
and injections. In this way it is often possible to banish the parasites entirely 
from the intestinal canal, and thus to induce, even in severe cases, a complete and 
often surprisingly rapid recovery. Besides extract of male fern, thymol has been 
found an effectual remedy. Of this, about two and a half to three and a half 
drachms (10-14 grammes) are given daily in doses of thirty grains (two grammes) 
each. For children the dose is proportionally less. Leichtenstern recommends 
that a few doses of calomel and one or two injections should be administered on 
the day preceding the specific treatment with male fern or thymol. 

The prophylaxis from infection with anchylostoma is an important matter in 
industrial hygiene. The points chiefly to be considered are to enjoin the greatest 
cleanliness upon the workmen, to arrange properly for the reception and removal 
of the excreta, and to provide good drinking water. 




d e 

Fig. 61.— Egg of anchylostoma duodenale. a 
to d, various stages of segmentation ; e, 
egg with embryo. (From Pekroncito and 

SCHULTHESS.) 



5. Trichocephalus dispar 

( Whip-worm) 

The trichocephalus dispar is a worm four or five centimetres long, whose ante- 
rior part is very thin, but whose posterior part is decidedly thick (Fig. 62). It 

resides chiefly in the caecum, but also in the 

colon, where it is often found in small num- 
bers, and sometimes in abundance. The yellow 
or reddish-brown eggs of the parasite are 
characteristic, and they may be easily found 
in the faeces upon microscopic examination, but 
the parasites themselves scarcely ever come 
away spontaneously with the dejections. As 
a rule, the trichocephalus has no clinical sig- 
nificance, but lately Mossbrugger has reported a few cases of severe trouble in 
children, due to this parasite. The infection was supposed to be due to eating 
earth. The symptoms consisted in great anaemia and in long-continued and vio- 
lent diarrhoea, with watery movements containing mucus and blood. The dejec- 



Fig. w.- 



fioin ±iEi,LER.j Tricliocepnaius 
dispar. 



520 DISEASES OF THE DIGESTIVE ORGANS 

tions also showed many eggs of the trichocephalus, and Charcot's crystals. Treat- 
ment was very difficult and tedious, for the ordinary anthelmintics seemed to 
have slight effect. The most promising remedies in such cases would probably be 
extract of male fern and thymol. 



SECTION VI 

Diseases of the Peritoneum 

CHAPTER I 

ACUTE PERITONITIS 

(Inflammation of the Boivete) 

iEtiology. — There are two ways by which inflammatory agents most fre- 
quently reach the peritoneum: one is from the gastro-intestinal tract, and the 
other — in women — is from the genitals. 

All the diverse forms of ulceration which attack the digestive canal may in- 
volve the serous layer. In such a, case an inflammation arises which is at first 
limited, but which may under certain circumstances become more extensive. 
This inflammation may be regarded as analogous to that of the pleura in pneu- 
monia ; but the anatomy of the stomach and intestine is such that very often an 
ulcer in their walls ends in a complete perforation. If this occurs, the inflamma- 
tory germs contained in the primae vise at once escape into the peritoneal cavity 
and there excite an inflammation; which, from the specific character of its cause, 
is invariably purulent, and very frequently is at the same time septic or ichorous. 
The possibility of a peritonitis due to perforation, as a result of the various ulcera- 
tive processes of the stomach and intestines, has been frequently referred to in the 
previous sections of this work. Thus, it may occur in simple ulcer and in ulcerat- 
ing cancer of the stomach ; in typhoid, tubercular, or dysenteric ulceration of the 
intestine ; in ulceration of the intestine above intestinal stenoses of many varie- 
ties; and in the small ulcers of the vermiform appendix due to the pressure of 
hard substances. 

The female organs of generation are the other frequent source of peritonitis. 
In labor and premature delivery the genital tract is often directly infected. The 
infection may also occur, although much less frequently, at other times; for ex- 
ample, during menstruation. The various forms of inflammation which are thus 
set up, including endometritis, metritis, and parametritis, may in several differ- 
ent ways reach the peritoneum and excite peritonitis. A septic inflammation of 
the endometrium may involve the peritoneum by direct extension up the Fallo- 
pian tubes. In other cases it is through the lymph-vessels that a purulent metritis 
or parametritis spreads to the peritoneum. The larger parametritic abscesses may 
break into the peritoneal cavity. It is to be particularly noticed, however, that in 
many cases of septic puerperal peritonitis the uterus and its appendages are in a 
perfectly normal condition, having served merely as a gateway to the inflamma- 
tory agents without suffering any harm themselves. 

Besides these two chief sources of peritonitis, numerous others are possible, 
although much less frequent. 

Sometimes peritonitis is due to an extension of inflammation from other 
abdominal viscera. Hepatic abscess, suppurating hydatid cysts of the liver, ulcer 



ACUTE PEKIT (OTITIS 



521 



of the biliary ducts, splenic abscess or infarction, purulent nephritis or pyelitis, 
abscess near the bladder or in the prostate, suppurating ovarian cysts, tubal preg- 
nancy, psoas abscess, and Pott's disease — all these may produce peritonitis, either 
by direct extension or by perforation. 

It is worthy of note that peritonitis may occur as a sequel of pleurisy. The 
pleural and peritoneal cavities are directly connected by the lymph-vessels of the 
diaphragm; and empyema as well as tubercular pleurisy (see next chapter) may 
spread to the peritoneum. 

Penetrating wounds of the abdomen are a fruitful source of acute peritonitis. 
Surgical operations upon abdominal organs come under the same head. A large 
number of laparotomies proved fatal before antisepsis was introduced, because the 
inflammatory germs thus admitted excited a diffuse septic peritonitis. Even tap- 
ping the abdomen for ascites may cause acute peritonitis if the trocar is not asep- 
tic. Abdominal injuries, in which the walls are not penetrated, very rarely, if 
ever, give rise to peritonitis. One way in which they have been said to produce 
it is by exciting internal haemorrhage. In the new-born, peritonitis exceptionally 
results from infection through the navel. 

Far less frequent are those cases of acute peritonitis which occur as a part of 
certain general diseases. In this class belong first the peritonitis associated with 
acute articular rheumatism (q.v.). This is usually benign. It must be re- 
garded as analogous to the " rheumatic " inflammation which occurs in other 
serous membranes, including the endocardium, pericardium, and pleura. It is 
possible that rheumatic peritonitis of this sort may exceptionally occur as an 
apparently primary disease. It is a well-established fact that peritonitis may 
also develop in the course of acute or chronic nephritis. This we have ourselves 
observed. It is of course comparable with the inflammation which not infre- 
quently attacks the pericardium and pleura in the course of nephritis. The exact 
cause of it has not yet been settled. Perhaps one factor is the retention in the 
blood of the solids which ought to be excreted with the urine. We must also 
mention that in very rare instances a specific gonorrhoeal peritonitis occurs, either 
in connection with a constitutional infection from gonorrhoea, perhaps associated 
with gonorrhoeal synovitis or endocarditis, or from the direct extension of gonor- 
rhoea! inflammation from other parts to the peritoneum. 

From all that has been said, it is evident that, from a purely aetiological stand- 
point, peritonitis is by no means a stereotyped and uniform disease. The actual 
pathogenic agents, exclusive of the rare cases of mere intoxication, are always 
bacteria, but bacteria of diverse kinds. In the cases of peritonitis due to per- 
foration, the bacterium coli seems to play an important part, and often also 
streptococci are influential. The cases of septic or puerperal peritonitis are 
mostly occasioned by streptococci; rarely the peritonitic exudation has been 
found to contain pneumococci, gonococci, proteus forms, and other germs. Not 
infrequently there seems to be a mixed infection from the start. Actinomycosis 
of the peritoneal cavity has been already briefly mentioned (see diseases of the 
pleura, page 303). 

Pathology. — Like the analogous inflammations of the pleura and pericardium, 
peritonitis is divided into different varieties according to the character of the 
inflammatory exudation. The nature of the exciting cause of most cases of peri- 
tonitis is such that by far the most frequent variety is the fibrino-purulent. If the 
process involves the entire peritoneum — that is, if there is a " diffuse general peri- 
tonitis " — we generally find upon opening the abdomen that the parietal layer of 
the peritoneum and the outer surface of the intestinal coils are distinctly red- 
dened, from marked vascular injection. There may even be small ecchymoses 
here and there. The serous membrane is clouded, a result partly of desquamation 
of its endothelium, and partly of the more or less abundant fibrinous exudation 



522 



DISEASES OE THE DIGESTIVE OEGAXS 



■which covers the peritoneum with a sheet of coagulated fibrine. Very often the 
coils of intestine have formed numerous adhesions with one another (compare 
pleuritic adhesions). In cases of brief duration these can still be easily broken 
up, but after a prolonged illness they are extremely firm. There is usually also 
some free, fluid, fibrino-purulent exudation in the abdominal cavity. Its amount 
varies greatly. Sometimes there is only a small quantity of opaque fluid in the 
dependent portions of the cavity ; sometimes there are many quarts, causing great 
distention of the abdomen. The exudation seldom inclines to a sero-purulent 
character. It is usually predominantly purulent. Very often the purulent 
exudation undergoes decomposition into the offensive sanious fluid of septic 
peritonitis. This is particularly apt to occur when the disease originates from an 
intestinal perforation or from puerperal poisoning. The perforation through the 
walls of the intestine is sometimes so large as to admit considerable amounts of 
intestinal gases and fasces into the peritoneal cavity. It is also possible that the 
putrefaction of peritoneal exudations may generate offensive gases. In rare in- 
stances the exudation is haemorrhagic ; but most cases of hemorrhagic peritonitis 
do not belong here, but come rather under the tubercular or cancerous forms (vide 
infra). 

In severe and protracted cases of peritonitis the intestine is involved to a cer- 
tain extent. There is a collateral inflammatory oedema of its w r alls, causing some- 
times a considerable increase in thickness, while at the same time they may be 
non-resistant and easily torn. The weakness of the muscular layer of the intes- 
tine may amount to complete paralysis, and thus permit excessive intestinal tym- 
panites, either diffuse or local. 

Milder forms of general peritonitis with sero-flbrinous, or chiefly serous, exuda- 
tion are relatively infrequent. Under this head would come certain apparently 
primary and usually chronic cases with favorable issue, and also the peritonitis 
which sometimes occurs as a sequel of an ascites which has existed for some time 
(see next chapter). Probably also in those rare cases of peritonitis arising in the 
course of acute rheumatism and ending in recovery, the exudation has been 
sero-flbrinous. 

We have spoken thus far of diffuse general peritonitis, but cases are not 
rarely seen of circumscribed or " encapsulated " peritonitis. Here, also, we have 
mild varieties with fibrinous exudations on the one hand, and on the other puru- 
lent inflammation. The milder inflammation is a result of the extension of the 
most varied forms of inflammation from neighboring organs. Thus, deep intesti- 
nal ulcers, for example, give rise to a mild circumscribed inflammation of the cor- 
responding portion of the serous layer. A similar condition results from super- 
ficial splenic infarctions ; from various hepatic diseases, when they reach the sur- 
face of the liver; and from numerous pathological conditions of the female 
genitals. In many of these cases the peritonitis takes a chronic course and leads 
to adhesions, and hence is called adhesive peritonitis. 

Circumscribed purulent peritonitis has precisely the same aetiology as the 
general form, with this single difference, that firm adhesions are quickly formed 
around the spot whence the inflammation proceeds, limiting it and preventing it 
from involving the entire peritoneum. It occurs most frequently as a purulent 
perityphlitis (q. v.) consequent upon perforation of the vermiform appendix; and 
also as pelvic peritonitis, which is a possible sequel of most of the forms of puer- 
peral inflammation to which the uterus and its appendages are liable. But we 
may also have encapsulated purulent peritonitis after the perforation of gastric 
and intestinal ulcers, or of suppurative processes in the biliary passages, and from 
similar causes. If the abscess is situated directly below the diaphragm it is 
termed subphrenic. 

Histologically considered, acute peritonitis is perfectly analogous to the in- 



ACUTE PERITONITIS 



523 



flammatory processes which, attack other serous membranes. The endothelium 
becomes degenerated, and, for the most part, is cast off. There is an exudation 
from the blood-vessels of a fibrinous fluid, which is partly coagulable, and with 
this exudation round cells escape in greater or less abundance. In the further 
progress of the disease there is an inflammatory new growth of vascular connect- 
ive tissue, which probably originates chiefly from the endothelium and the perma- 
nent tissue-cells, but, according to some, starts in part also from the wandering 
cells. The new formation of blood-vessels certainly seems to be due chiefly to 
budding from the capillaries of the serosa. Thus arise the adhesions of connective 
tissue and the false membranes found in chronic cases between the different coils 
of intestine. They lead in process of time to marked thickening and retraction 
of the omentum and mesentery (peritonitis deformans). Most cases of purulent 
peritonitis prove fatal in the early acute stage. If a case recovers, the exudation 
undergoes fatty degeneration, and its cellular constituents are thus disintegrated 
and then are absorbed. 

The results of circumscribed purulent peritonitis are detailed in connection 
with the clinical history. 

Clinical History. — 1. Acute General Peritonitis. — The following description 
applies chiefly to the severe purulent form, the one by far most frequently met 
with. It occurs in most instances after perforation, in puerperal cases, and after 
external injuries, such as surgical operations. In most of these cases the perito- 
nitis is a secondary disease, so that it must obviously be greatly modified in its 
general characteristics and behavior by the original trouble. In the first place, the 
onset is modified. Many cases of peritonitis due to perforation begin abruptly, 
the patient having been previously in perfect health. Thus, as already men- 
tioned, the first indication of a gastric or duodenal ulcer may be given by perfora- 
tion. Most cases of perforation of the vermiform appendix present equally sud- 
den and unexpected symptoms. 

There are many other cases in which the symptoms of peritonitis supervene 
upon those of some grave disease already existing. Eor example, typhoid fever, 
intestinal tuberculosis or intestinal stenosis, may, by causing perforation, excite 
a peritonitis. Here the symptoms of this secondary disease may be more or less 
completely veiled by the other grave local and constitutional disturbances. 

Again, an acute general peritonitis may, as we have already said, be the sequel 
to a local and circumscribed inflammation of the peritoneum. Thus, a purulent 
perityphlitis, or a purulent puerperal pelvic peritonitis, may finally become uni- 
versal. In such unfortunate cases the change in symptoms is often gradual, and 
is not clearly pronounced. 

We have now indicated certain variations from the general course of the dis- 
ease; but, with these exceptions, almost every case of acute general peritonitis, 
whatever its aetiology, presents clinical symptoms which are so characteristic and 
typical that a general description of the disease will be both easy and advanta- 
geous. 

The symptoms of acute peritonitis form two groups, the local and the constitu- 
tional. The latter are the result of the local disturbance acting upon the general 
condition of the patient. 

Of the local symptoms, pain deserves to be named first. It is usually the 
earliest symptom; and, as the disease progresses, it is generally the excruciating 
abdominal pain which attracts most attention. The localization of the pain in 
the beginning of the illness may be of diagnostic value in doubtful cases, if such 
as to indicate the possible starting-point of the inflammation, for example, the 
vermiform appendix or a gastric ulcer. Later the pain extends over the whole 
abdomen. As a rule, there are brief remissions followed by fresh exacerbations. 
The pain is aggravated by voluntary movements, by deep inspirations, and prob- 



524 



DISEASES OE THE DIGESTIVE OEGAXS 



ably by intestinal peristalsis. The abdominal tenderness is often extreme in 
peritonitis, and is very characteristic. The gentlest palpation is torture, and often 
the slightest pressure of the bed-clothes is almost unbearable. Erequently the 
greatest tenderness is in the umbilical region. 

Acute peritonitis seldom exists without pain. The exceptions to this rule are 
seen chiefly in patients who are extremely prostrated, and whose sensibility and 
intelligence are much impaired. Here the peritonitis itself may escape notice — 
as in severe typhoid or in the last stage of tuberculosis. 

Physical examination of the abdomen greatly aids the diagnosis in many 
ways. 

As a rule, the abdomen is distended. This is an early symptom, and gradually 
becomes more and more pronounced. It is due mainly to the intestinal tympa- 
nites, which we have already mentioned, which sometimes becomes very great 
if the muscular fibers of the intestine are paralyzed. In the later stages the 
liquid effusion into the peritoneal cavity of course contributes to the prominence 
of the abdomen, but even then the distention is seldom so uniform or so broad as 
in ascites. In peritonitis, coils of distended intestine can often be recognized by 
their characteristic contour through the abdominal wall. Palpation also often 
shows a very characteristic diversity in the sense of resistance in different por- 
tions of the abdomen, occasioned by variations in the amount of exudation, by 
adhesions, or by the dilatation of some of the intestinal coils, and similar causes. 

In general, if the abdominal wall is yielding and thin, the peritonitic disten- 
tion will be greater, so that it is most marked in puerperal cases, where the preced- 
ing pregnancy has rendered the walls lax. In a person with powerful muscles and 
tense abdominal walls the convexity of the abdomen is seldom great. In some 
cases there is no convexity whatever. The walls may be as hard as a board, and 
the abdomen flat or slightly concave. In such cases the diagnosis may be difficult. 
Sometimes, again, the original retraction of the abdominal walls is succeeded by 
more or less distention of the abdomen. 

Percussion over the distended intestinal coils yields a resonant and usually 
tympanitic sound. It is not till a considerable amount of liquid effusion has 
collected that there is dullness, most marked in the dependent portions of the 
abdomen. If there is much tympanites, however, quite a large effusion may exist 
without being detected on percussion. Percussion also gives results analogous to 
those of palpation, in that there is often a diversity in the quality of the reso- 
nance of different portions of the abdomen in peritonitis. 

Usually there is too much pain to permit a careful examination of the change 
of dullness consequent upon change of decubitus. In general, the numerous adhe- 
sions between the separate coils of intestine also not infrequently interfere with 
the free motion of the peritonitic exudations. 

Percussion not only gives information about the existence of a liquid, puru- 
lent effusion, but is also of value in determining the level of the diaphragm, as 
affected by abnormal abdominal distention. The upper limit of hepatic dullness is 
raised to the fifth or even the fourth rib. The heart is also pushed up. There is 
a tympanitic resonance above the margin of the ribs on the right side. The area 
of hepatic dullness is not only displaced upward, but is also evidently diminished. 
This is due in part to coils of distended intestine overlapping the anterior edge of 
the liver, and in part to the organ being tilted upward in such a way that its 
area of contact with the anterior wall of the body is less than normal. Various 
authors formerly laid great stress upon the total disappearance of hepatic dull- 
ness, regarding it as a sure sign that gas has escaped from the intestine into the 
abdominal cavity. The inference is not always correct. The liver may be dis- 
placed backward by coils of intestine, and hepatic dullness be thus abolished, 
although there is no air free in the peritoneal cavity. 



ACUTE PEKITOKETIS 



525 



If there is a considerable effusion, it is possible, as in ascites (q. v.), to get a 
sensation of fluctuation by gentle, quick palpation. 

As a rule, auscultation of the abdomen does not throw much light on a case 
of peritonitis. In the distended coils of intestine we not infrequently hear all 
sorts of gurgling and splashing sounds. Sometimes we hear a peritonitic friction- 
sound, due to the movements of respiration, causing two rough surfaces to rub 
against each other. In particular, perihepatic friction is heard not very infre- 
quently. 

If the results of physical examination leave us still in doubt as to the pres- 
ence of a peritonitic exudation, we may attain certainty by an exploratory 
puncture, and at the same time, if there be any exudation, determine its 
character. 

Almost always the stomach and intestinal canal are disturbed by any severe 
case of peritonitis. 

As to the stomach, vomiting is the most frequent and important symptom. 
Vomiting is often seen early in the disease, and recurs frequently as the illness 
progresses. It sometimes is spontaneous, and sometimes follows the ingestion of 
food. If spontaneous, the vomitus consists of watery mucus, usually of a green- 
ish tinge. We do not know absolutely the cause of the vomiting in peritonitis. 
Apparently it is in part a reflex action, excited by the inflammation of the serous 
membrane. Possibly the external pressure of the exudation also affects the stom- 
ach ; and it may be that absorbed toxines also excite vomiting. It must be added 
that vomiting may be absent in acute peritonitis. This is seen when the patient 
is comatose, and sometimes also when the peritonitis has developed upon perfora- 
tion of a gastric ulcer, because the contents of the stomach are thus emptied out 
through the hole in its walls. The vomiting is usually accompanied by frequent 
eructations. 

Of the intestinal symptoms, the reader has already become acquainted with 
the tympanites, and also with the fact that it is due mainly to a paresis of the 
muscular fibers of the intestine. This same muscular weakness furnishes an 
obvious reason for the persistent constipation usually observed in peritonitis ; but 
we may have diarrhoea instead, from increased peristalsis and secondary intes- 
tinal catarrh. 

The pushing up of the diaphragm has a noteworthy effect upon the thoracic 
organs. The lower lobes of the lungs are compressed, so that considerable dysp- 
noea results. The heart is likewise crowded upward, so that the apex-beat is usu- 
ally to be felt in the fourth intercostal space. 

Every case of acute peritonitis that is at all extensive has marked constitu- 
tional effects. These are in part the result of the wakefulness due to pain, and 
the restlessness and fever. But perhaps there are also definite reflex inhibitory 
influences, originating in the irritation of the peritoneal nerves and affecting 
chiefly the heart, just as Goltz in his well-known experiment killed a frog by 
blows upon the abdomen. The chie^ factor, however, is in all probability the tox- 
ines which are very readily absorbed from the peritonitic exudation by the peri- 
toneum, and thus enter the circulation. 

There is no other disease, except internal strangulated hernia — and the effect 
of that is perfectly analogous — which produces general collapse so quickly as 
does peritonitis. The countenance (" fades ahdominalis ") is rapidly altered, the 
cheeks fall in, and the eyes become hollow. The nose grows sharp and cool, the 
lips and tongue dry. The skin of the extremities is also cool and bluish, as a re- 
sult of impaired circulation. The patient is extremely feeble. The chief cause of 
all these symptoms is the excessive weakness of the heart. The peritonitis has 
hardly begun before we find the pulse small and soft. In many severe cases the 
pulse finally becomes almost imperceptible. At the same time the pulse-rate in- 



526 



DISEASES OF THE DIGESTIVE ORGANS 



creases, as is usual in collapse from any cause, so that 120 to 110 beats per minute 
is not an. exceptional rapidity. 

The temperature varies greatly in different cases. It may be high in the 
rectum, although the skin feels cool. Still, Very high fever is not usual; and 
there are often considerable remissions. We even frequently observe the subnor- 
mal temperature of collapse. The number of respirations per minute is usually 
30 to 40. This increased rate is due not only to the compression of the lower 
lobes of the lungs, but also to the pain caused by full inspirations and to the im- 
peded circulation. 

The intellect remains in most cases almost unimpaired to the end. There may 
exceptionally be mild delirium, or an approach to stupor, toward the close. 

The course of acute general peritonitis in the great majority of cases is unfa- 
vorable. With the appearance of the grave symptoms just depicted the prognosis 
becomes almost hopeless. The course of the disease is also comparatively rapid. 
Marked variations in the intensity of the symptoms are infrequent. The grave 
local and constitutional symptoms persist, and, as a rule, the patient dies at the 
end of a few (two to six) days. Still, it is not well to make general dogmatic 
statements as to the clinical history, for the aetiology of each individual case im- 
presses upon it individual characteristics. A peritonitis resulting from gastric 
or intestinal perforation is usually quickly fatal. The same is true of almost all 
cases of puerperal septic peritonitis. In a few cases, however, the inflammation 
is limited, by the encapsulation of the exudation. These may finally end in 
recovery through perforation of the abdominal walls or perforation into the in- 
testinal canal. Now and then an acute general peritonitis may assume a chronic 
form. The effusion is mostly reabsorbed, and the newly-formed adhesions and 
false membranes contract into firm bands of connective tissue. The liver, spleen, 
and other abdominal viscera acquire a tough coating of connective tissue. The 
omentum and mesentery are shortened and thickened. Indeed, the omentum 
may roll itself almost completely up. Although the clinical symptoms become less 
severe, weakness usually persists, with gradual exhaustion and death. Often the 
intestine is so bent or pinched as to give rise to grave symptoms from stenosis. 

Recovery from acute general peritonitis is very exceptional. If seen, it is usu- 
ally in mild cases, such as sometimes occur after menstruation, abortion, or labor. 
Peritonitis as a complication of acute articular rheumatism is a very rare event. 
Its termination is generally favorable. In all cases of this kind the inflammation 
is probably not purulent, but sero-fibrinous. 

2. Acute Circumscribed Peritonitis. — The local symptoms of this are essen- 
tially the same as we have just ascribed to the general form ; except that, a smaller 
extent of tissue being involved, they are correspondingly limited. The pain and 
tenderness are confined mainly to one region, but its boundaries are never sharply 
defined. On palpation of this region, we find an increased resistance which is 
sometimes almost like that produced by a tumor. If there is an encapsulated 
effusion, we may detect fluctuation, particularly if the abscess is going to point 
outward. On percussion over the affected spot, there is either, dullness or a muffled 
tympanitic resonance. 

The constitutional symptoms are likewise those of general peritonitis, only 
usually less severe. Keflex vomiting does occur, but is seldom so persistent as in 
the diffuse inflammation. The physical weakness and symptoms of collapse are 
decided, but do not usually become extreme. There is generally an irregular fever, 
which may now and then assume an intermittent, pyasmic character. Most 
cases run a chronic course. If the illness be very much prolonged, death may 
finally ensue from general debility. Recovery is possible if the pus can be let out. 
This may be accomplished either by the surgeon or by Nature. Spontaneous dis- 
charge of the abscess may take place through the abdominal walls, into the in- 



ACUTE PERITONITIS 



527 



testine, or even, in rare instances, through the p-leura into the lungs. But if the 
pus finds its way into the general peritoneal cavity, the peritonitis becomes diffuse 
and causes death. 

To describe in detail each separate variety of circumscribed peritonitis would 
occupy too much space, and would also lead to useless repetitions. We have 
already spoken at some length of one especially important form — namely, peri- 
typhlitis. Perimetritis and pelvic peritonitis are chiefly puerperal affections, and 
are fully discussed by writers on gynaecology. 

Abscesses which are very deeply situated — as, for instance, behind the stomach 
or in front of the spinal column, or perinephritic — may prove very difficult to diag- 
nosticate, being so far out of reach. Sub-diaphragmatic abscesses containing air 
deserve a brief mention (pyo-pneumothorax subphrenicus). They are sometimes 
observed as a result of perforation of the stomach or transverse colon. Lying 
between the liver and the diaphragTn, they crowd the latter upward and the liver 
downward, and are liable to be mistaken for pyo-pneumothorax. It is to be noted 
that in subphrenic, abscess the lower limit of the lungs moves up and down with 
respiration (see above, page 438). Sub-diaphragmatic abscesses containing no 
air a*lso occur, originating in the liver or spleen. Finally, there is a rare form of 
circumscribed purulent peritonitis to be noted, to which children seem especially 
exposed. It declares its presence by a painful fluctuating tumor above the left 
groin, which usually points into the rectum and ends in recovery. 

Diagnosis. — The diagnosis of peritonitis is in many cases an easy matter, when 
we have the characteristic symptoms of tenderness and tympanites, vomiting, and 
collapse. Often the starting-point of the inflammation is equally obvious, in 
cases of secondary peritonitis supervening upon some disease which we have 
already clearly recognized, such as typhoid fever, gastric ulcer, or puerperal dis- 
eases. But where the peritonitis is apparently primary, we must inquire care- 
fully into the previous history and the earliest symptoms of the attack, in order 
to form even a surmise as to aetiology. 

The diagnosis is sometimes greatly obscured by the fact that under certain cir- 
cumstances very similar symptoms may be excited by other disorders affecting 
the intestines. Thus, in typhoid fever there may be great tympanites and grave 
constitutional symptoms, with abdominal pain, so -that peritonitis may be diagnos- 
ticated, while the autopsy, if there be one, discloses no signs of it. Deep ulcers of 
the intestine, however produced, may give rise to such great abdominal tender- 
ness as likewise to simulate peritonitis. The differential diagnosis between peri- 
tonitis due to perforation and acute intestinal obstruction (q. v.) is often very 
difficult. In both, when there is severe constitutional infection, the symptoms 
are almost the same, and, furthermore, diffuse peritonitis may occasion such a 
paralysis of the intestine or such excessive tympanites as to prevent any motion 
of the bowels, and even to cause faecal vomiting. On the other hand, intestinal 
obstruction is not infrequently complicated by general peritonitis, so that the 
two conditions may both exist simultaneously. The following are the chief points 
of distinction between them, although even these are not infallible : 



Peritonitis 

1. Begins with fever and with abdominal 
pain, often localized. 

2. Abdomen very sensitive to pressure, 
hard, and tense. 

3. Pain tends to abate as the disease 
goes on. 

4. No visible peristalsis of the intestines. 

5. Seldom faecal vomiting, frequently hic- 
cough and simple vomiting. 

6. Exudation demonstrable in the perito- 
neal cavity. 



Intestinal Obstruction 

1. Begins without fever and without 
marked abdominal pain. 

2. Abdomen at first soft and not espe- 
cially tender upon pressure. 

3. Abdominal pain gradually and con- 
stantly increasing. 

4. Visible peristalsis; intestinal coils can 
be felt like rolls. 

5. Distinct faecal vomiting, hiccough rare. 

6. No free exudation in the peritoneal 
cavity. 



528 



DISEASES OF THE DIGESTIVE ORGANS 



Another diagnostic error, which we have already mentioned, is not infrequent 
— that is, the occurrence of peritonitis may be entirely overlooked. This is espe- 
cially likely to happen when the localized symptoms, such as pain and tympanites, 
are very slight. Sometimes the only things which call attention to the onset of 
peritonitis are the rapid change in the general condition of the patient, and in 
his pulse and temperature. 

It is not always easy to diagnosticate circumscribed peritonitis, even when the 
trouble is not deep-seated and therefore inaccessible. It is not infrequently mis- 
taken for a new growth. In doubtful cases, a careful use of the aspirating needle 
is the more necessary, because the presence of an encapsulated peritonitic exuda- 
tion in almost all cases demands operative interference. 

It is well to remember that a pregnant uterus and a distended and therefore 
painful bladder have each repeatedly been mistaken for peritonitis ! Hysterical 
meteorism (see the chapter on hysteria) may also be erroneously ascribed to peri- 
tonitis. 

Treatment. — Although severe cases are generally almost hopeless, yet we must 
try to meet the symptomatic indications, and must do all in our power to promote 
a limitation of the process, if it be possible. 

External counter-irritants or " revulsants " are seldom of much use. Painting 
with tincture of iodine and mercurial inunctions seem so utterly purposeless that 
they should be discarded. The local abstraction of blood can not be employed in 
an extensive peritonitis with constitutional prostration. It is only in a circum- 
scribed peritonitis which is very painful, and when the general condition of the 
patient remains comparatively favorable, that bleeding is to be considered. 
Under these circumstances, the application of eight to fifteen leeches sometimes 
causes decided abatement of the pain. The local application of ice to the abdomen 
is universally in vogue. It usually moderates the pain, and it may also have a 
beneficial influence in quieting peristalsis. Still, some patients can not bear ice, 
and sometimes hot cloths and poultices give great relief. 

Of all internal remedies, there is but one of great value, namely, opium. This 
in large doses (15 to 20 drops of laudanum or a grain — gramme 0.05 — of extract of 
opium every one or two hours) almost always proves beneficial. It moderates 
both the pain and the vomiting or eructations; and also, by diminishing the 
peristaltic movements of the intestine, opium contributes in another way to 
assuage the suffering and possibly to limit the spread of the inflammation. Ex- 
perience shows that almost all patients bear even very large doses of opium re- 
markably well in peritonitis. Perhaps this is because the drug is only slowly 
absorbed. To substitute injections of morphine for opium is wise only in cases 
where we wish to produce narcosis as rapidly as possible, or when the vomiting 
or pain does not prove amenable to the ordinary treatment. In such cases we 
may. also prescribe laudanum by enema. 

Sometimes particular symptoms demand special attention. Eor vomiting we 
may employ, besides opium, bits of ice, small quantities of sherbet, and perhaps 
chloroform or cocaine. If tympanites is excessive, we may try to remove some of 
the gas through a rectal tube passed as high up as possible. Many physicians also 
puncture the distended intestinal coils with a fine trocar. Collapse and cardiac 
failure require the exhibition of stimulants, such as champagne or other alcoholic 
liquors, or doses of ether or camphor given subcutaneously. It is generally very 
difficult to nourish the patient. As a rule, small quantities of ice-cold milk are the 
best of anything, as food. 

The surgical treatment of acute peritonitis is constantly growing in impor- 
tance. It is self-evident that in the case of a circumscribed abscess in the abdom- 
inal cavity the only way of giving prompt relief is by operative interference : but 
even in acute diffuse peritonitis the results obtained by laparotomy, while not 



CHRONIC AND TUBERCULAR PERITONITIS 



529 



brilliant, are encouraging, and further trials are the more imperative, because 
otherwise the prognosis of such cases is almost absolutely hopeless. The more 
promptly the inflammatory germs and septic matter are removed from the ab- 
dominal cavity, the greater is the possibility of permanent cure. The details 
of the surgical treatment of peritonitis must be sought elsewhere. 



CHAPTER II 
CHRONIC AND TUBERCULAR PERITONITIS 

etiology. — Chronic non-tubercular peritonitis is a rather rare disease. It is 
found most frequently in post-mortem examinations of patients who have had for 
a long time ascites due to venous stasis — for example, in chronic cardiac or 
hepatic cases. The chronic peritonitis, however, is not the direct result of the 
passive hypersemia in such cases, but is, as already hinted, due in most instances 
to the puncturing of the abdomen during life for the removal of the ascitic fluid. 
Exceptionally, a chronic peritonitis occurs as a sequel to some severe intestinal 
disorder, such as ulceration. Thus, chronic peritonitis is sometimes observed to 
follow typhoid fever. 

Chronic peritonitis may furthermore be the result of an acute peritonitis. 
The latter seldom terminates in this way, but still it may, when rather mild and 
not quickly fatal. The encapsulated exudations of peritonitis usually persist a 
long while, as was implied in the preceding chapter. 

There is still great uncertainty about the aetiology of those cases which start 
in a subacute or chronic manner, without special cause. Sometimes they seem to 
be due to an injury of the abdomen; in other cases there are special constitu- 
tional influences, such as alcoholism, which may occasion the disease. In chil- 
dren, and less often in adults, we sometimes see cases of " simple exudative peri- 
tonitis," with a serous exudation, which we are inclined to regard as analogous to 
the ordinary cases of pleurisy with effusion. It is possible that in such instances 
pathogenic organisms of various kinds occasion the inflammation; but in order 
of frequency there is scarcely a doubt that tuberculosis should be named first. 
Just as in pleurisy, many cases of what is apparently primary " simple " perito- 
nitis turn out eventually to be tuberculous. 

The tubercular is the most frequent form of chronic peritonitis. It is often 
merely a part of the tuberculosis of serous membranes in general (vide pages 289 
and 365), of which mention has been already repeatedly made. In these cases it is 
usually due to a conveyance of the process from the pleura through the diaphragm. 
Another way in which tubercular peritonitis may arise is by infection from neigh- 
boring tubercular organs. Tubercular intestinal ulcers are among the chief 
causes of this kind, the ulcer extending to the peritoneum ; or the peritonitis may 
be excited by tubercular retroperitoneal or mesenteric lymph-glands. In women 
tubercular peritonitis may be developed in consequence of tuberculosis of the 
genital organs. Tuberculosis of the uterus sometimes affects the Eallopian 
tubes by direct extension, and thence the virus enters the abdominal cavity and 
excites its specific inflammation. In conclusion, we have to mention that, in gen- 
eral miliary tuberculosis, the peritoneum also may be the seat of numerous tuber- 
cles, although these do not as a rule give rise to important symptoms. 

Pathology. — In severe cases of chronic peritonitis — and scarcely any others 
have come to autopsy — the peritoneum is usually found to be considerably thick- 
ened. The intestinal coils are joined to one another and to the neighboring 
34 



530 



DISEASES OF THE DIGESTIVE OKGANS 



organs by numerous and extensive adhesions. The false membranes are often 
delicate and easily separable, but in some cases it is a hard matter to disentangle 
the confused mass into which the intestines have been rolled. Sometimes the liver 
and spleen are covered by firm, tough capsules. The omentum and mesentery are 
much shrunken; hence the name peritonitis deformans. The omentum may in- 
deed be transformed into a single thick cord. As a rule, there is little liquid effu- 
sion, and perhaps none. In simple chronic peritonitis, such fluid as may be pres- 
ent is usually a cloddy serum, sero-pus being seldom seen. 

There are sometimes many clots of fibrine suspended in the fluid. If the abdo- 
men has been repeatedly punctured during the life of the patient, we often may 
recognize the separate punctures, on the inner surface of the peritoneum, from 
the hcemorrhages, adhesions, or similar changes which have occurred. In rare in- 
stances a peculiar form of chronic peritonitis has been observed as a sequel to 
punctures for ascites, called by Friedreich " chronic hemorrhagic peritonitis with 
hsematoma." In it almost the entire peritoneum is covered by a newly formed 
membrane permeated with large ecchymoses. 

We will also mention briefly a peculiar form of chronic peritonitis, which 
has not yet been sufficiently investigated. This leads to the formation of 
numerous small nodules in the peritoneum, which are usually at first regarded 
as tubercles, but upon microscopic examination are found to be nodules of con- 
nective tissue. 

Tubercular disease of the peritoneum may be divided into two forms : tuber- 
culosis of the peritoneum, which may be acute or chronic; and tubercular peri- 
tonitis, which is usually chronic. In tuberculosis the peritoneum is covered 
with numerous tubercular nodules, varying in size from a millet-seed up to a pea ; 
but there is not much coincident inflammatory change. In genuine tubercular 
peritonitis, on the other hand, the inflammatory changes above described are well 
marked, while sometimes it requires a microscopic examination to demonstrate the 
tubercular nature of the inflammation, by the detection of tubercles and cheesy 
degeneration in the newly formed tissue. Tubercular peritonitis is usually rather 
chronic, so that the adhesions are numerous and strong. The amount of liquid 
effusion varies, being sometimes considerable and sometimes scanty. Just as in 
tubercular pleurisy, it is not rare for the exudation to be bloody. In long-con- 
tinued peritoneal tuberculosis the omentum is found irregularly thickened, and 
the whole intestinal cavity filled with tumor-like masses (lymph-glands, etc.). 
Among the more important associated conditions we have tuberculosis of other 
organs, and also the comparatively frequent combination of tubercular perito- 
nitis with hepatic cirrhosis (q. v.). 

Clinical History— Diagnosis. — If an acute peritonitis becomes chronic, the 
violent symptoms gradually abate, while another group of symptoms takes their 
place. In other cases the chronic disease develops gradually and insidiously. 

The sensitiveness of the abdomen is never so extreme as in the acute inflamma- 
tion. Sometimes, to be sure, the patient complains of dull pains and a sense of 
abdominal oppression, but quite often the pain is either constantly or at times 
insignificant. On physical examination, we usually find moderate distention of 
the abdomen. Frequently this is not perfectly uniform, certain coils of intestine 
being especially prominent. Occasionally there is no abdominal distention what- 
ever, the belly is flat or concave, and the walls are tense and unyielding. The 
abdomen is more distended if there is a large amount of liquid exudation or if 
there is extensive tuberculous new growth. 

In many instances palpation furnishes very characteristic signs ; for sometimes 
the thickening of the omentum and the numerous fibrous inter-intestinal bands 
above described can be felt through the abdominal walls as peculiarly resistant 
masses or uneven prominences. Indeed, if the omentum is rolled up, it may 



CHRONIC AND TUBERCULAR PERITONITIS 



531 



closely simulate a new growth. The same is true of enlarged lymph-glands. Not 
infrequently, particularly in tubercular peritonitis, the liver is enlarged so that 
its lower edge can be felt. But in other cases of chronic peritonitis there are no 
changes discoverable by palpation; or they may be concealed by an effusion or 
by the tenseness of the abdominal walls. A large exudation can be demonstrated 
by the great distention, or by its causing fluctuation, or by the signs yielded on 
percussion. As a result of the adhesions of the intestines to one another, the fluid 
does not change its position very readily upon change of position of the patient. 
This circumstance is indeed one means of differentiating between peritonitic ex- 
udation and ordinary ascites. Not infrequently the resonance upon percussion is 
very greatly impaired, even when there is no large amount of fluid exudation. 
This is probably due to thickening of the peritoneum, fibrinous deposits, and sim- 
ilar changes. Peritonitic friction-sounds are sometimes audible, particularly in 
the hepatic region. It has been already stated that the distortions and flexions 
which the intestines may undergo in chronic peritonitis may result in obstruction. 
In the same way the duodenum or the ductus choledochus may be so occluded as 
to occasion persistent jaundice. 

The objective signs of both the simple and tubercular forms of chronic peri- 
tonitis have been embraced in one description, because the abdominal signs of the 
two are identical. To differentiate between them, other factors must be consid- 
ered. We regard the patient's constitution and general appearance, and inquire 
into his family history, or discover if there are other ^etiological factors, such as 
previous tubercular disease. A careful thoracic examination is extremely impor- 
tant. If we find the signs of coincident pulmonary tuberculosis, or of pleurisy, 
then it is almost indubitable that the peritonitis is tubercular. The course of 
the fever is very important. Persistent hectic fever must always arouse strong 
suspicions of tuberculosis. The character of the exudation obtained by aspira- 
tion may be significant, for the admixture of blood, as we have already said, 
occurs mainly in tubercular peritonitis; but we may also have serous exudation 
in tubercular peritonitis, just as in the ordinary tubercular pleurisy. Tubercle 
bacilli are not usually present in the exudation of tubercular peritonitis. 

To diagnosticate simple tuberculosis of the peritoneum, when not attended by 
marked inflammatory changes, is generally a difficult matter,, Often it is abso- 
lutely impossible. Frequently there is no abdominal pain or tenderness whatever. 
The abdomen is usually but moderately distended, as a result of the effusion 
present. If we find such a condition in a patient who is known to have some other 
tubercular affection, we are justified in suspecting that there is a simple tubercu- 
losis of the peritoneum. 

It is not unusual to observe the combination of hepatic cirrhosis with 
peritonitis, which we have already briefly mentioned. We have then splenic 
tumor and the other signs of portal congestion, in addition to the symptoms 
of chronic peritonitis, such as pain and fever. The amount of fluid in the abdo- 
men is usually considerable. As a rule, the patients are hard drinkers. The 
hepatic cirrhosis may be the primary disease, and if so, it joins with the con- 
stitutional results of alcoholic excess in promoting the liability to tuberculous 
infection. 

Particular notice should be given to the chronic peritonitis of children, already 
mentioned. The occurrence of ascites in children between the ages of two and 
ten years has been observed repeatedly, both by other authors and by ourselves. 
The ascites, which may be considerable, can not be traced to any cause, and after 
a few months completely disappears. The child during this time is usually rather 
pale and languid, but not much emaciated, nor does he suffer great local discom- 
fort. There may be no fever. Since the cases often recover, their pathological 
anatomy remains obscure. Probably they are a mild form of simple chronic 



532 



DISEASES OE THE DIGESTIVE OKGANS 



peritonitis. Still, of course, there may be other causes for the ascites, such as 
hereditary syphilitic disease of the liver. 

In children, tubercular peritonitis plays an important part in general tubercu- 
losis of the abdominal organs, a condition known as tabes mesent erica. In these 
cases the tuberculosis probably originates, as we have already said, in the intes- 
tine, so that usually we find the intestine, peritoneum, liver, and abdominal lymph- 
glands all simultaneously involved. The clinical symptoms are often due mainly 
to the peritonitis. The abdomen is distended and painful, and there is an effusion. 
Often there is also obstinate diarrhoea, as a result of tubercular intestinal ulcers, 
with persistent fever of an intermittent character, emaciation, and ansemia. The 
tubercular process may eventually involve the lungs, pleura, meninges, and other 
organs, or it may never extend beyond the abdomen. 

As to the course of chronic peritonitis we have little to say. The simple 
chronic peritonitis may terminate in recovery, although on account of other 
co-existing lesions this event is rare, except in the special form which children 
present. Many cases of tubercular peritonitis prove fatal in a few months or 
weeks. The fatal termination of peritoneal tuberculosis may be occasioned by a 
septic peritonitis, due to perforation. We have seen two cases of this sort in 
which the tubercular focus perforated the intestinal wall from its outer side. 
In many instances, however, chronic tubercular peritonitis has a favorable issue, 
or at least there is very great abatement of all symptoms. This is particularly 
apt to be the case in what is called primary tuberculosis of the serous mem- 
branes in general (vide supra). If, in this disease, there is no simultaneous 
tuberculosis of the lungs, intestines, or other organs, then the final reabsorption 
of the exudation is possible, just as in tubercular pleurisy. It must be confessed 
that often the recovery is not permanent, for the tubercles may appear later in 
some other part of the body. 

Treatment. — The means by which we can exercise a favorable influence upon 
the course of chronic peritonitis are scanty. Attention to nourishment, absolute 
rest in bed, and hygienic surroundings are very important; but, beyond this, 
treatment is mainly symptomatic. The chief local applications are poultices or 
fomentations, perseveringly employed. There is seldom such persistent and severe 
pain as to demand opiates, but they may be required for the diarrhoea which is 
apt to occur. On the other hand, enemata and mild laxatives may be indicated. 

Of special drugs, the preparations of iodine should be mentioned, including 
iodide of potassium and syrup of the iodide of iron, although the use of these is 
seldom attended with obvious improvement. The persistent daily inunction of 
fifteen to thirty grains (one or two grammes) of mercurial ointment or oleate of 
mercury into the abdomen seems often to be beneficial. If there is considerable 
exudation, diuretine, acetate of potash, and similar diuretic remedies are indi- 
cated. Whether curative results are to be expected from tuberculine, further 
experience must determine. 

Of late, the surgical treatment of peritoneal tuberculosis has had very favor- 
able results. It has been observed that in many cases of tuberculous peritonitis, 
laparotomy, with as complete an evacuation of the exudation as possible (better 
than can be accomplished by mere puncture of the abdomen), exercises a won- 
derfully beneficial influence upon the course of the disease, and even seems in 
many cases to occasion complete recovery. This fact is interesting, although not 
yet wholly explained. Eurther observations must be collected with regard to this 
procedure, but our own experience justifies us in strongly recommending it. Par- 
ticulars with regard to its employment (leaving the abdominal wound open and 
packing with iodoform gauze) are taught in works on surgery. 

[In the opinion of the editor, what surgery has done for us in this affection is 
rather to demonstrate the curability of many cases than to work their cure. Eor- 



ASCITES 



533 



merly, if the diagnosis of tubercular peritonitis was made and the patient recov- 
ered, the very fact of recovery was held to invalidate the diagnosis. But the 
surgeon's knife has laid bare the miliary tubercles to the eye, given an exit to the 
serous exudation, and recovery has ensued. But we see other cases get well after 
simple tapping, and we see still others which present just as good a clinical picture 
of the affection and recover without interference of any kind. Such recovery 
may be temporary, tuberculosis breaking out afresh in the peritoneum or else- 
where, or it may be permanent. If, in spite of rest and appropriate general treat- 
ment, considerable effusion persists, aspiration or siphonage should be practiced. 
Laparotomy should probably be reserved for those rather rare cases which seem 
to be rapidly getting worse, and those in which the fluid reaccumulates after one 
or more tappings. 

In expressing the belief that tubercular peritonitis recovers, the editor does not 
lose sight of the fact that multiple fibrous nodules occur disseminated over the 
peritoneum, indistinguishable by the unaided eye from tubercles.] 



CHAPTER III 

ASCITES 

(Hydrojoeritoneitm) 

The name ascites is given to a collection of transuded serum in the abdominal 
cavity, due to venous stasis. The peritoneal veins belong to the portal system, so 
that among the diseases which lead to ascites those which impede the portal cir- 
culation are chief. As we shall see in the next section, ascites is, therefore, of fre- 
quent occurrence in cirrhosis of the liver, syphilitic disease of the liver, compres- 
sion of the portal vein by tumors, thrombosis of the portal vein, and similar 
disorders. Ascites is also frequently present as one of the dropsical symptoms in 
general circulatory disturbances, such as cardiac disease or pulmonary emphy- 
sema, and in the course of various acute and chronic renal affections. 

The clinical significance of ascites is due partly to the local discomfort occa- 
sioned by the presence of any considerable amount of fluid within the abdominal 
cavity. Small quantities of serum are often unnoticed by the patient ; but, where 
many quarts (fifteen to twenty, or even more) of transudation exist, the abdomi- 
nal walls become greatly distended, and the patient has a very troublesome feeling 
of pressure, weight, and tension. What is of still greater importance is the crowd- 
ing upward of the diaphragm. Respiration is thereby not a little impeded. If 
the ascites is great, the lower lobes of the lungs are so compressed that a consider- 
able degree of atelectasis is produced. 

To demonstrate ascites by physical examination is possible only when a con- 
siderable accumulation exists. Then the belly is prominent, its walls are tense 
and shining, and, the base of the thorax being gradually distended by the pressure 
of the liquid, the lower part of the thorax seems much broader than the upper. 
Distended veins are usually visible through the skin of the abdomen, like blue 
lines, here and there. As soon as the abdominal tension has attained a certain 
degree, fluctuation can be perceived, by laying both hands upon the abdomen and 
imparting gentle but quick impulses to the fluid through the walls. Percussion 
gives a dull sound everywhere that the fluid is in contact with the abdominal 
walls. Gravity, of course, leads the liquid to occupy the dependent parts. In the 
dorsal decubitus, and when the transudation is of medium amount, the dullness is 
bounded in the central and upper parts of the abdomen from a region of tympa- 



534 



DISEASES OE THE DIGESTIVE OEGAXS 



nitic resonance by a line concave toward the head of the patient. The surface of 
the liquid being horizontal, of course the dullness reaches nearer to the thorax 
along the sides of the abdomen than in the central line. "VTe would add, that 
where the layer of ascitic fluid is thin we can obtain dullness only by light, super- 
ficial percussion. If the pleximeter or finger is pressed deeply in, the fluid is 
crowded to one side, and we get a tympanitic sound from the underlying coils of 
intestine. A factor of great diagnostic value is the change of dullness on change 
of position of the patient. If he lies upon one side, the fluid seeks the dependent 
portions of the cavity, and gives rise to extensive dullness there, while the oppo- 
site side now yields a tympanitic resonance. Or, if he changes to the other side, 
it in turn becomes dull, and the side previously dull becomes tympanitic. Similar 
differences are found between the results of percussion in a horizontal and in a 
sitting posture. It is only when the accumulation is very abundant that there is 
dullness over the entire abdomen. 

The signs mentioned enable us in most cases to make a diagnosis of ascites 
with ease and certainty. It is, indeed, not always easy to distinguish a transuda- 
tion of serum from the exudation of chronic peritonitis, for, of course, either sort 
of fluid would yield the same physical signs. Only, the change in the area of 
dullness consequent upon a change of position is less pronounced in case of an 
exudation, because the peritonitic adhesions impede the movements of the fluid; 
and we have, besides, all the other symptoms to guide us : there may be pain, 
fever, or thickening of the peritoneum discoverable on palpation, or signs of tuber- 
culosis; or, on the other hand, there may be some cardiac or hepatic disease, 
which would render ascites probable. If the fluid is drawn off, its character will 
sometimes aid us in diagnosis. Ascites yields pure serum, containing almost no 
morphological constituents. Its specific gravity is usually less than that of a 
peritonitic exudation, because it contains less albumen. TVe may say that the 
specific gravity of the fluid found in peritonitis is generally above 1018, and that 
of ascites about 1012, or even lower. Hemorrhagic ascites sometimes occurs in 
anasmic patients who are suffering from marked portal obstruction, as we have 
ourselves seen, for example, in hepatic syphilis. 

Chylous ascites due to an abundance of fat in the fluid may appear as a result 
of occlusion of the thoracic duct, but it should be pointed out that ascitic fluid 
has sometimes a chylous opacity, even when it contains no fat (emulsion of albu- 
minous substances ?). 

There may be equal difficulty in the exclusion of ovarian cysts, particularly 
since the cysts are sometimes so large as to fill the whole abdominal cavity. We 
must first map out accurately the dullness on percussion, and also see if it varies 
with changes of position. In cases of ovarian tumor, change of position does not 
make much difference. The resonance on percussion of the deepest and most 
dependent portions of the abdomen may be misleading, in this way, that even in 
ascites a narrow zone here may be tympanitic. This should be remembered. 
Thus, just above the symphysis, there is sometimes a tympanitic resonance in 
ascites which might readily be mistaken for a proof of the existence of an ovarian 
tumor. The explanation is that in the places indicated a coil of intestine with a 
short mesenteric attachment may remain in contact with the abdominal wall in 
spite of ascitic accumulations. Further aid in the differential diagnosis is to 
be obtained from the history of the case (place where the swelling began), from a 
consideration of possible causative diseases, and from a vaginal examination, in- 
cluding direct palpation of the ovaries. In ascites the uterus is freely movable, 
while in case of ovarian tumors it is often bound down by adhesions. Further 
particulars may be sought in books on gynaecology. 

The treatment of ascites, of course, depends largely upon the disease of which 
it is a symptom. As to the symptomatic treatment of ascites itself, we will con- 



CANCER OF THE PERITONEUM 



535 



fine ourselves to a few words about tapping. This operation is indicated when 
the local disturbances caused by the ascites are great; that is, if there is an 
unbearable sensation of pressure and tension, and, above all, if the crowding up of 
the diaphragm causes much dyspnoea. The instrument to be used is a common 
trocar of medium size. If strength permits, the puncture can be most conven- 
iently done with the patient sitting in a chair, or crosswise on the edge of the 
bed. We then choose for the best place for the puncture the linea alba, about 
halfway between the navel and the symphysis. Of course we should first see that 
the bladder has been emptied. If the patient is very ill, we are often obliged to 
make the puncture while he is in bed ; we then insert the instrument in the lower 
and left side of the abdomen, about halfway between the navel and the anterior 
superior spine. As a rule, the removal of ascitic fluid is easy and free from 
danger. The exudation should never be allowed to escape too rapidly. We may 
permit large amounts of liquid (five or ten quarts, or more) to flow slowly away at 
one tapping. We close the puncture with a piece of sticking plaster, or with iodo- 
form-collodion. Often the fluid trickles out through the opening, because the 
abdominal walls have lost their elasticity on account of the persistent distention. 
We may then employ a suture to close it. After tapping, the laxness of the walls 
is favorable to palpation of the abdominal organs. 

Inasmuch as tapping does not remove the cause, there is in most cases a very 
rapid reaccumulation of fluid. Thus the system is deprived of much albumen, 
and nutrition is impaired, so that not infrequently the operation is followed by 
decided loss of strength. Therefore, we should not tap in ascites, as a rule, unless 
the indications for the operation are urgent. 

[If, as is very frequently the case, the fluid continues to drain away through the 
puncture after the trocar is withdrawn, good rather than harm results, provided 
the danger of irritation of the skin and of bed-sores is kept in mind and guarded 
against, and an instrument of moderate size is used. 

Flint advocates early and repeated tappings if the fluid causes discomfort and 
does not yield to diuretics or cathartics. The pressure is removed in a measure 
from the abdominal and thoracic organs, and nutrition is thus promoted. The 
fluid is likely to return, but it does not always do so, or it may do so only slowly. 
He reports cases in which, after repeated removal, the fluid ceased to return and 
the patient remained apparently well. The result must depend, of course, chiefly 
on the underlying cause, which is sometimes very obscure. 

In cases of cirrhosis the same principles govern Flint's treatment.] 



CHAPTER IV 
CANCER OF THE PERITONEUM 

Carcinoma is the only new growth of any practical importance to which the 
peritoneum is liable. Primary endothelial cancer, analogous to the growth which 
attacks the pleura, is very rare. Cancerous growths here are usually secondary 
to cancer of the stomach, intestine, pancreas, liver, or some other organ. Often 
the secondary nodules are numerous, and almost as small as peas, presenting what 
is called miliary carcinosis of the peritoneum. They cover the omentum, mesen- 
tery, and parietal peritoneum. Separate nodules of larger size are less frequent. 
These may be found in the omentum, in Douglas's pouch, around the navel, or in 
other situations. Colloid cancer attains the most diffuse and extensive develop- 
ment of any variety. The retroperitoneal lymph-glands may also present at the 



536 



DISEASES OF THE DIGESTIVE ORGANS 



same time large cancerous growths. Often the development of cancer in the peri- 
toneum is attended with pronounced inflammatory disturbances — that is, we have 
a cancerous peritonitis. 

The symptoms of peritoneal cancer resemble in many points those of chronic 
tubercular peritonitis. Simple miliary carcinosis may be very insidious and give 
rise to no special symptoms, so that it often is unsuspected. In many cases a 
moderate amount of fluid collects in the abdomen, and this, if we are aware of the 
existence of a primary cancerous growth, may lead us to surmise a secondary peri- 
toneal carcinosis. The symptoms are much more pronounced if there is cancer- 
ous peritonitis. In that case there is usually very severe pain, marked abdominal 
distention, and constipation. We may sometimes feel the larger nodules in the 
omentum or upon the inner surface of the anterior wall of the abdomen, or even 
those in the lowest part of the abdomen, by palpation through the vagina. We 
have repeatedly observed the development of palpable nodules in the navel in car- 
cinosis of the peritoneum. If the exuded fluid be drawn off, it is sometimes 
merely serous, but it may be hemorrhagic. When the new growth has been dif- 
fuse, and particularly in case of colloid cancer, the exudation has repeatedly been 
found to present a milky opacity. Sometimes this fluid also has been tinged with 
blood. The opacity is due to fat, from fatty-degenerated and disintegrated can- 
cer cells. Occasionally the microscope reveals characteristic cancerous elements 
in the fluid. [Diagnosis based upon the microscope alone has repeatedly proved 
to be erroneous. — V.] 

The diagnosis can not be made with any positiveness unless, as a sequel to a 
primary cancerous growth already demonstrated, we observe the evident tokens 
of peritoneal disturbance, such as free fluid, pain, points of resistance on palpa- 
tion, and distention of the abdomen. Other factors are the patient's age, cancer- 
ous cachexia, and secondary glandular enlargements, particularly in the groins. 

Treatment must be confined to efforts at mitigation of the suffering. Warm 
applications, morphine, and supporting measures are chiefly employed. 



SECTION VIE 
Diseases of the Liver, Bile-ducts, and Portal Vein 

CHAPTER I i 

CATARRHAL JAUNDICE 

(Ictertis catarrhalis. Gastro-duodenal Catarrh with Jaundice) 

^Etiology and Pathological Anatomy. — Catarrhal jaundice is still the almost 
universal term applied to the most common form of jaundice. It develops in 
previously healthy individuals, usually in a rather acute manner, and sooner or 
later (as a rule, after some weeks) terminates in complete recovery. The names 
"catarrhal" or "gastro-duodenal" jaundice rest upon the supposition that the 
entire process is due to a catarrhal inflammation of the duodenal mucous mem- 
brane. This catarrh is said often to spread from the stomach to the duodenum, 
and in the duodenum to invade the region of the duodenal papilla and extend up 
the common duct. The common duct, it was claimed, became obstructed by the 
swollen mucous membrane or by the tough mucus which was secreted, and thus 
blocked up the bile secreted in the liver. This mechanical obstruction was re- 
garded as the cause of the jaundice. 



CATARRHAL JAUNDICE 



537 



Of late it has been objected to this old doctrine of catarrhal jaundice that the 
supposed catarrh of the duodenum and larger bile ducts has never yet been abso- 
lutely demonstrated. In a few cases of jaundice, in which at autopsy a plug of 
mucus has been found in the lower portion of the common duct or the duodenal 
papilla, it is said that the explanation of the mucous plug is simply that the mucus 
has collected because the bile has not been secreted, and has not flowed through the 
duct. The jaundice should not be regarded at all as due to the obstruction, but 
rather as a result of a disturbance of the function of the liver cells (paracholia) , 
such that the bile is not secreted into the minute bile-ducts, but directly into the 
capillaries and smallest lymph-channels. 

In our opinion, this latter theory seems to be somewhat artificial and certainly 
not absolutely established, although it seems to offer a simple explanation of 
many other forms of jaundice, particularly of that following certain poisons. 
There is only one respect in which we think that there is an urgent necessity for 
change in the old doctrine of catarrhal jaundice. We do not associate the essen- 
tial process with ordinary gastric and intestinal catarrh consequent upon such 
causes as errors in diet, but we regard the disease as in most cases an independent 
one due to a special cause. This cause is in all probability a definite infection, 
the particulars with regard to which are as yet entirely unknown ; but meanwhile 
we can scarcely imagine that its anatomical effect is anything other than the 
development of an inflammatory catarrh of the bile-ducts, with a probably vary- 
ing involvement of the stomach and duodenum. It is, of course, very possible 
that there may also be toxic influences at work, but at present their thorough 
study seems impracticable. 

The main reason for assuming that there is an infectious factor in the devel- 
opment of catarrhal jaundice is, that not at all infrequently the disease appears 
in epidemics and endemics. Rather extensive epidemics of jaundice have been 
repeatedly observed in barracks, prisons, and communities in a manner to be ex- 
plained only by the supposition of some local source of infection. In some in- 
stances the epidemics of jaundice have followed revaccination, obliging one to 
think of the transfer of the pathogenic organism by means of inoculation. In 
the frequent sporadic cases it is not usually possible to demonstrate any special 
cause for the disease, except that there is often a connection with some marked 
error in diet, with catching cold, or some mental excitement, such as anger. In 
most instances there is nothing of this sort to be discovered, and this again sug- 
gests an infectious origin for the disease. Catarrhal jaundice is observed chiefly 
in youthful individuals; sex has no marked influence. 

Symptoms and Clinical Course, — Very frequently, though not invariably, 
there are, for some days before the appearance of the jaundice, definite signs of 
gastro-intestinal disturbance, as well as certain constitutional symptoms. Obsti- 
nate vomiting, marked pain in the stomach, and similar symptoms are not infre- 
quent. Very often the trouble begins with loss of appetite, a bad taste in the 
mouth, nausea, a sense of pressure in the epigastrium, eructations, and constipa- 
tion, accompanied by languor. Soon after, the patient himself notices the yellow 
color of the skin, or his attention is called to it by those about him. 

We still hold provisionally to the view that the cause of catarrhal jaundice is 
mechanical ; and we desire, with a view to preventing repetition, to describe here 
with some minuteness those symptoms which occur in varying severity in all cases 
of obstructive jaundice. 

The bile is secreted in the liver under an extremely low pressure, and conse- 
quently a comparatively slight obstruction in the bile-ducts suffices to prevent the 
discharge of bile into the intestine. In ordinary catarrhal jaundice, and also 
in other varieties of jaundice, the obstruction to the flow of bile is seldom com- 
plete, and if so, only for a time. Still a considerable amount of bile collects, and 



538 



DISEASES OF THE DIGESTIVE OKGAXS 



distends even the intrahepatic ducts. As soon as this stasis has reached a cer- 
tain point, the stagnant bile is absorbed by the hepatic lymph-vessels. Thus the 
bile and all its constituents are poured into the blood by way of the thoracic duct 
and carried to all parts of the body. ~No more than a few days need elapse before 
the bile-pigments are absorbed into the tissues, and give rise to the evident yellow 
color of the skin and visible mucous membranes which we call jaundice. Usu- 
ally the yellowness of the conjunctiva is the first thing to attract attention. Later 
the entire skin becomes yellow, and the same color is plainly visible in the 
mucous membrane of the mouth and throat, especially after we have produced 
temporary anaemia by pressure, as in the lips. Of course, the internal organs, 
which we can not see, are likewise stained. Any abnormal collection of liquid 
will also have a marked yellow color. The cornea, the peripheral nerves, and 
the cartilages alone escape unstained. In other parts we may not only find 
this diffuse impregnation with the biliary pigments, but even solid granules of 
the latter. 

A jaundiced patient often presents other indications of the presence of biliary 
coloring matter than the color of his skin. There is often an itching of the skin, 
which may be very troublesome. It may be so bad at night as to disturb sleep. 
The scratching thus induced often causes numerous excoriations and fissures, 
which may even occasion quite large furuncles. Urticaria is also sometimes ob- 
served. A peculiar disease of the skin, which has been described in connection 
with jaundice, is called xanthelasma. It presents bright-yellow spots, usually 
somewhat elevated, which are found mainly on the eyelids, though also on other 
parts of the body. 

The remaining symptoms of hepatogenous jaundice may be divided into two 
groups. The first group comprises the symptoms excited by the presence of the 
biliary constituents, and particularly of the biliary acids, in the blood, while the 
second group is due to the lack of bile in the intestinal canal. 

We have seen that, when the biliary outlets are occluded or narrowed, the con- 
stituents of the bile are absorbed by the lymphatics. We have already learned in 
part what becomes of the bile-pigment thus conveyed into the blood-vessels. That 
it also displays poisonous properties has been maintained by some investigators, 
but has not yet been absolutely proved. The presence of the bile-acids in the 
blood at any rate is of considerable clinical importance. Physiology has shown 
that these acids possess certain injurious qualities, and, among others, the power 
to destroy red blood-corpuscles. But in reality few if any blood-corpuscles are 
destroyed by the bile-acids in the blood, because they are too much diluted, and, 
besides, seem in large part to be quickly decomposed after absorption. These acids 
do really, however, excite certain nervous centers in a way to give rise to decided 
clinical symptoms. The most frequent effect is that produced by the cholate of 
sodium upon the cardiac ganglia, or possibly also upon the center for the vagus, 
and it is evinced by a slowing of the pulse. This is an almost invariable phenom- 
enon, provided there be no fever or other complication, and is seen not only in 
simple catarrhal jaundice but in all cases of hepatogenous icterus. The pulse-rate 
is from 64 to 50, or even less. Slight irregularity in the heart's action is not 
infrequent. There are certain other nervous disturbances often seen in jaundice, 
referable to the presence in the blood of biliary constituents, and in particular 
of biliary acids. Sometimes there is a striking languor and muscular weakness, 
or headache, or the patient is " out of sorts." Grave nervous symptoms, sometimes 
seen in jaundice and grouped under the name of cholcBmia, are discussed in 
another chapter. It also deserves a brief mention here that many cases with 
marked jaundice have a noticeable tendency to bleeding — that is, a sort of " hem- 
orrhagic diathesis." Haemorrhages into the skin and in the viscera are quite 
often seen, and also epistaxis and analogous occurrences. 



CATAKKHAL JAUNDICE 



539 



We come now to a consideration of those symptoms which arise because the 
bile does not reach the intestine. In this regard the standpoint of modern physi- 
ology is essentially different from the old views. Formerly the bile was valued as 
an important digestive secretion ; now it is regarded by many merely as an excre- 
tion, containing certain end-products of metabolism; but perhaps this view is 
extreme, for the very fact that the bile is discharged into the upper part of the 
intestine suggests that it has a certain significance in the processes to which the 
intestinal contents are subjected, and there is certainly one function of the bile 
which is indisputable — viz., that it promotes the absorption of fat. The bile both 
contributes to the emulsifying of fat, and also promotes the passage of the fat- 
drops through the intestinal walls into the lacteals. Now, in hepatogenous icterus 
this work remains undone, as is shown by the fatty stools. From time imme- 
morial the white clay-colored stools of jaundice have been well known, and are 
employed as the best measure of the completeness of biliary retention. The light 
color of the stools is due partly to the lack of biliary pigment, for it is that chiefly 
which imparts to normal fasces their dark-brown color; but the characteristic 
white clay color is due exclusively to the presence of undigested fat in large 
amounts. We have ourselves performed the experiment of putting a patient with 
extreme hepatogenous icterus upon a diet containing as little fat as possible, and 
have found that the stools then became light brown, and not at all like clay. 
Upon microscopic examination of the fasces in jaundice, sheaf -like aggregations 
of crystals are almost invariably observed. These were formerly supposed to be 
tyrosine, but Oesterlein has shown them to be in reality lime or magnesia soap. 

Besides this influence upon the absorption of fat, there have been two other 
properties ascribed to the bile, having apparent significance for the pathology of 
jaundice. In the first place, there is the antiseptic power of the bile ; this was said 
to explain the fact that in patients with biliary obstruction the fasces usually 
have a particularly bad odor, and also that there are often excessive tympanites 
and flatulence. Secondly, the bile was reputed to exert an influence upon intesti- 
nal peristalsis — hence, the constipation frequently seen in jaundice. Of late, how- 
ever, authorities have felt doubts about ascribing either of these properties to the 
bile. The foul odor of the fasces may be associated with the imperfect digestion 
of fat, and the constipation with the change in the diet and with other circum- 
stances. 

We must mention one other point : If the obstruction to the discharge of bile 
is actually situated at the papilla duodenalis — and this was formerly regarded 
as certain in catarrhal jaundice — then the discharge of pancreatic juice must also 
be affected, and we must also consider the results of the exclusion of this secretion 
from the intestinal contents; but we do not possess definite knowledge as to the 
actual effects of such an exclusion. 

We must now inquire what becomes of the absorbed bile. As to the biliary 
acids, we have already said that they probably undergo decomposition. Of the 
other constituents, including the taurine and cholesterine and the pigmentary 
matter, we know the fate of the last-named only — that is, we have learned how 
Nature seeks to rid herself of this foreign substance. As soon as the amount of 
bile-pigment in the blood and tissues becomes considerable, excretory efforts are 
made, in which the kidneys take the chief share. Certain changes take place in 
the urine almost simultaneously with the first appearance of a jaundiced hue in 
the skin ; and these changes are due to the urine containing excreted biliary color- 
ing matter. 

The urine of jaundice is generally recognizable from its color, which is dark 
brown, like beer. The foam caused by shaking it is not white, but decidedly 
yellow. A bit of white filter-paper dipped in the urine is stained yellow. If the 
urine is shaken with chloroform in a test-tube, the chloroform dissolves the pig- 



540 



DISEASES OF THE DIGESTIVE ORGANS 



ment, and, on being- allowed to collect at the bottom of the tube, displays a decided 
yellow color. This is known as the " chloroform test." Another reaction which 
usually gives a satisfactory result, but not always, is Gmelin's. If urine contain- 
ing* bile-pigment is slowly poured down the sides of a test-tube containing a few 
cubic centimetres of nitric acid, the zone between these two liquids exhibits a fine 
play of colors. The oxidizing effect of the acid upon the biliary pigment produces 
a number of colored rings, the highest and most characteristic of which is green ; 
next comes blue, then violet and red. Gmelin's test often shows very prettily if 
one filters the urine and then adds a drop of nitric acid to what remains upon the 
moist filter-paper. The characteristic colored rings form around this drop. In- 
stead of nitric acid, we may use tincture of iodine, diluted with nine parts of 
water. If a small amount of this solution is poured upon urine containing bile, 
in a test-tube, there is usually developed a ring of a beautiful green color between 
the two fluids. 

The biliary acids also may be detected in the urine of jaundice; but the pro- 
cess is somewhat tedious, and the knowledge gained is of no great practical im- 
portance. 

The urine very often contains morphological elements which are characteristic. 
ISTothnagel was the first to describe minutely the icteric casts — that is, hyaline 
casts which usually have a yellow tinge and quite often are completely covered 
with dark-yellow granules or with epithelium. The urine may contain a little 
albumen also, but thir. is not constant. If we add acetic acid, there may be an 
opacity developed which is said to be due to nucleine. All these changes in the 
urine point to a slight degree of damage done the renal parenchyma by the biliary 
pigment excreted. 

[The presence or absence of albumen depends largely on the amount of the 
biliary constituents and on the length of time they continue in action on the kid- 
neys ; their effect on these organs is more or less that of an irritant.] 

The sweat-glands also take part in the excretion of bile-pigment. The latter 
can be demonstrated in the perspiration of jaundiced persons, as well as in their 
urine. Not infrequently the patient's linen is colored yellow by the sweat. On 
the other hand, no bile-pigment is found in the tears, saliva, gastric juice, or secre- 
tions other than those mentioned. 

Having now considered the phenomena common to all cases of hepatogenous 
icterus, we revert to the subject of simple catarrhal jaundice. The prodromal 
gastric symptoms usually last a few days, more rarely a week or two, when the 
skin becomes evidently jaundiced and the other results of the icterus are also 
seen. The urine grows dark with biliary pigment, the stools become light-colored 
and more or less clay-colored. The nervous system is not usually seriously de- 
ranged, but still most patients feel very languid, and have anorexia and a tend- 
ency to constipation. The pulse often becomes somewhat slower than normal, and 
sometimes the temperature also is subnormal, 97° or 98° (36°-36.5° C), but 
there may be slight fever. 

In most cases the physical examination of the liver is of interest, the organ 
being, as already mentioned, enlarged from the retained bile. Accordingly, the 
lower boundary of hepatic dullness usually extends the breadth of two or three 
fingers below the edge of the ribs, and not infrequently the lower margin of 
the organ can be plainly felt. Often the gall-bladder is so distended, both by bile 
and possibly by the mucus which the bladder itself secretes, that it projects from 
under the edge of the liver. In such cases, as Gerhardt tells us, we may some- 
times make out by percussion a convexity in the lower line of hepatic dullness, 
which corresponds to the gall-bladder. If the abdominal walls are lax, we may even 
feel the distended viscus. As a rule, there is not much distress in the hepatic re- 
gion, although now and then there is a certain sensation of pressure or tension. 



CATARRHAL JAUNDICE 



The symptoms depicted seldom last longer than a few weeks. Usually a 
patient who takes proper care of himself begins to feel better in even less time. 
The urine grows lighter colored, the stools darker, and the pulse more rapid. The 
yellow color of the skin often remains visible for quite a while, although gradu- 
ally diminishing, even after the patient feels perfectly well; but at last the jaun- 
dice disappears also and recovery is complete. Eelapses are indeed possible, par- 
ticularly after errors in diet ; but they are rare. 

The termination of catarrhal jaundice is, therefore, almost invariably favor- 
able. The entire course of the disease occupies about three to six weeks, rarely a 
longer period. It is a very exceptional occurrence, but one which we must always 
think of as possible, for this apparently mild and secure condition to be suddenly 
merged into the grave, pernicious variety of jaundice. (See the chapter on acute 
yellow atrophy of the liver and pernicious jaundice.) 

Diagnosis, — Catarrhal jaundice is usually easily diagnosticated. The diag- 
nosis is made chiefly from the course of the disease — the development of jaundice, 
preceded by gastric symptoms, in a previously healthy person, and generally in a 
youthful individual. It is very important to exclude other conditions which 
might occasion jaundice. We must consider, therefore, whether the history of 
the case suggests the presence of gall-stones (pain, hepatic colic), and be vigilant 
in our physical examination to detect a possible cirrhosis or new growth. In the 
case of elderly patients, particularly, it is not rare for what was at first regarded 
as an attack of ordinary catarrhal jaundice eventually to disclose itself as a 
grave chronic disease, such as cancer of the gall-bladder. We should not make a 
diagnosis of catarrhal jaundice until we have carefully weighed all the rational 
and objective signs. 

Treatment. — Most cases of catarrhal jaundice terminate favorably and require 
no active treatment. Rest and prudence are indicated, and the diet should be 
carefully regulated, that the gastro-duodenal catarrh may not be aggravated. Fat 
must not be eaten, for, as we have seen, it is not assimilated, and only excites 
abnormal processes of decomposition in the intestinal canal. Lean meat, bread, 
soups, if not too rich, vegetables, cooked fruit, and lemonade or tamarind-water 
are allowable. Milk is to be avoided as a rule, because of the fat it contains, but 
yet it is often well borne. Alcohol is to be allowed very sparingly if at all. 

We should also employ internal remedies to mitigate the assumed gastric ca- 
tarrh. The various stomachic tonics are frequently prescribed. Rhubarb is a 
favorite drug. A very good medicine is Carlsbad water, or the artificial Carlsbad 
salts, of which latter the dose is half a tablespoonful to a tablespoonful, in a tum- 
bler of warm water, before breakfast, or twice a day. The alkalies are said to 
have a favorable influence upon the gastro-intestmal mucous membrane, and 
they are also laxative; that they furthermore promote the secretion of bile, as 
many assume, is doubtful; but there is no doubt that the flushing of the kidneys 
by an abundance of liquid is beneficial. If there is obstinate constipation we 
are obliged sometimes to resort to more powerful remedies, such as castor-oil, 
calomel, or rhubarb. 

Lately much enthusiasm has been displayed about the treatment of catarrhal 
jaundice by large enemata of cold water. The injections are said to overcome the 
biliary retention by exciting peristalsis, and possibly by also promoting the secre- 
tion of bile. Once a day a quart or two of water, ax 60° to 70° (12°— 18° R.), is 
injected, and is retained as long as possible. The good effect is said to be observ- 
able in a few days, both in the general condition of the patient and in the dimin- 
ished amount of bile-pigment in the urine, as well as the darker color of the 
stools. Other physicians recommend injections of a pint to a quart (J to 1 
litre) of lukewarm water several times a day. We have tried both methods re- 
peatedly without being able to convince ourselves that the course of the disease 



542 



DISEASES OE THE DIGESTIVE ORGANS 



is thus rendered much different from that under simple dietetic management; 
still, one may try irrigations, especially if the case is obstinate. Whether there 
are any internal remedies which promote the secretion of bile is very doubtful. 
The drug which is most recommended for this purpose, and is much employed in 
catarrhal jaundice, is salicylate of sodium, in the dose of eight to fifteen grains 
(gramme 0.5-1.0), several times a day. The biliary acids have also been tried, in 
the form of purified ox-gall, and also salol, podophyllin, and many others. We 
believe that all these remedies may be perfectly well dispensed with. 

The effort has also been made to empty the gall-bladder by manipulation. 
Gerhardt states that sometimes the distended viscus can not only be felt through 
the abdominal walls (vide supra), but it can be so firmly compressed as to squeeze 
its contents into the duodenum. Sometimes the obstruction is said to yield sud- 
denly, as if a plug were driven out. This method has not been extensively 
adopted. It seems applicable only in a limited number of cases, and is probably 
not free from danger. Several authorities have recommended external faradiza- 
tion as a means to stimulate the gall-bladder to contract and discharge its con- 
tents. We believe that few will adopt the suggestion. 

Among symptoms, the troublesome itching deserves particular attention. The 
remedies which may be recommended for this are bathing with cold water, rub- 
bing the skin with slices of lemon, or the application of a 2-per-cent. solution of 
carbolic acid, or of salicylic acid or thymol dissolved in alcohol (1 to 3 per cent.) ; 
also menthol (headache pencil) and chloroform mixed with olive-oil. Sometimes 
temporary relief is afforded by a dose of antipyrine or salicylate of soda internally. 



CHAPTER II 

ACUTE EEBRILE JAUNDICE 

{Infectious Jaundice. WeiVs Disease) 

There is a peculiar acute infectious disease which was first described by Weil, 
and then more fully by Eiedler and others, which seems to be always associated 
with an acute infectious inflammation of the gall-ducts, and, having jaundice for 
a symptom, it may properly be described in this connection. 

The disease is most frequent in the months of summer. It attacks by prefer- 
ence young and middle-aged men. Eiedler was struck by the frequency with 
which butchers suffered from it. The symptoms usually begin suddenly. Ex- 
treme chilliness, fever, headache, and malaise are almost always present at the 
onset. Jaundice usually appears on the second day, or soon after, and it may 
become severe. Its immediate cause is doubtless obstruction of bile, for the 
stools are colorless, and the urine contains an abundance of bile-pigment. The 
constitutional symptoms remain for several days quite severe. The patient com- 
plains of violent headache, wakefulness, and vertigo. Sometimes there is evident , 
stupor or mild delirium. Upon physical examination we not infrequently notice 
herpes on the lips, besides the icterus. The tongue is coated. There is nothing 
unusual about the lungs or heart, except that the pulse is apt to be quite rapid. 
The abdomen is not particularly distended. The liver is often enlarged, but not 
always. An acute splenic tumor is very often, but not invariably, present. There 
is usually diarrhoea. Vomiting may occur. The urine almost invariably^ con- 
tains albumen, and, as a rule, we find blood, epithelium, and casts, indicating a 
considerable amount of nephritis. In a few cases there are anuria and uraemia. 
Finally, a very characteristic symptom is the violent pain in the muscles, particu- 



BILIARY CALCULI 



543 



larly in the calves of the legs, of which most patients complain. Epistaxis and 
haemorrhages into the skin have also been repeatedly observed. 

With these symptoms the disease persists for from five to eight days, during 
which period the fever is often very considerable. Temperatures of 105°-107° 
(40°-41° C.) are not rare. Then the fever falls by crisis or rapid lysis, although 
seldom with perfect regularity. At the same time the other symptoms abate also, 
and convalescence ensues after an illness of ten to fourteen days in all. ^lany 
of the milder cases recover promptly, while others are prolonged by various 
sequelae and fresh exacerbations. An unfavorable termination seems to be excep- 
tional : it may result from uraemia. 

It is highly probable that this perfectly specific disease, the most important 
symptoms of which are, as we have seen, jaundice, fever, swelling of the spleen, 
albuminuria, and pain in the muscles, is an acute infectious process, with a spe- 
cial involvement of the biliary ducts ; but we do not yet possess any precise infor- 
mation as to its aetiology. Possibly we do not always have to deal with abso- 
lutely the same morbific process, but with several allied conditions. We have no 
information about the pathological anatomy, because the disease is too benign 
to furnish autopsies, and the few bacteriological examinations which have been 
thus far reported have led to no decisive conclusion. 

The treatment must be purely symptomatic. In the beginning calomel is 
useful. Later we prescribe antipyretics, hydrochloric acid, salicylate of sodium, 
and stomachics. The headache is often relieved by an ice-bag; the muscular 
pain by the inunction of chloroform oil. From the first the diet must be such 
as not to aggravate the nephritis (milk, simple soups). 



CHAPTER m 

BILIARY CALCULI 

{Hepatic Colic. Cholelithiasis) 

Etiology.- — Gall-stones are of very frequent occurrence; Riedel asserts that 
some two millions of the inhabitants of Germany have gall-stones, although this 
estimate seems to be very high. Despite their frequency, we have little positive 
knowledge of their causation. We can merely state certain circumstances which 
in all probability favor the formation of these concretions. 

Biliary retention certainly acts in this way, both directly and by leading to an 
increased consistency and increased concentration of the bile. As a result, certain 
constituents which were before held in solution are thrown down. And yet this 
cause, however potent (vide supra), can not be regarded as the only one. The 
chemical composition of gall-stones suggests that their formation must be pre- 
ceded by certain abnormal chemical processes of decomposition and of trans- 
formation. We can not otherwise explain why the constituents of gall-stones 
should differ, as they do in many ways, from the matters which normal bile holds 
in solution. Eor example, the pigment in gall-stones is never found unchanged, 
but invariably exists in composition with lime. ZSTow, normal bile contains only 
a trace of lime, so that long ago Frerichs expressed the opinion that the lime 
comes from the mucous membrane of the gall-bladder. It is an important fact, 
that the cholesterine, and probably also a portion of the pigmentary matters, are 
held in solution in normal bile by the combination of sodium with the biliary 
acids which it contains. If this sodium salt were decomposed from any cause, 
the matters named would naturally be precipitated. The decomposition of the 



DISEASES OE THE DIGESTIVE OKGAXS 



salts formed by the bile-acids is greatly promoted if the bile acquires an acid 
reaction ; but of the circumstances in which this last-mentioned change occurs we 
do not yet have any accurate knowledge. Lately N aunyn, after extensive inves- 
tigations, has propounded a theory that the formation of calculi is due in most 
cases to a primary disease of the mucous membrane of the gall-bladder and the 
bile-ducts. The disease causes the destruction of great numbers of the epithelial 
cells of the mucous membrane, with a resultant production of cholesterine, and of 
a compound of lime with bilirubine. Thus are formed friable masses of detritus, 
which are gradually changed into gall-stones, in the interior of which it is still 
possible at an early stage to demonstrate the original pultaceous mass. As the 
cholesterine and the compound of lime with bilirubine continue to form by crys- 
tallization, and fresh deposits of firm material take place, the stone gradually 
grows harder and larger. Very often also there is added at this stage a deposit of 
carbonate of lime. The cause of the original lithogenous catarrh is not known. 
Perhaps the mere mechanical obstruction of bile is causative, perhaps infection. 
In particular, the bacterium coli commune, which originates in the intestines, 
seems to be important — or at least, if not this, a very similar kind of bacillus. 
If the supposition were confirmed that infection of this sort is a factor, it would 
also be natural, as shown by what has been previously stated, to consider that 
such an infection would have an influence upon the bile itself. 

We have rather more knowledge as to predisposing causes than about the 
chemical processes involved in the formation of gall-stones. 

Age seems to be an important factor. The great majority of patients are over 
forty. Gall-stones are much less frequent between twenty and forty years of age ; 
and in children they are very rare, although they have been observed in the new- 
born. One reason why elderly people are so liable to this trouble is said to be the 
senile weakness of the muscular fibers of the gall-bladder. Thus stagnation and 
retention of bile are promoted. It has also been suggested that in old age the 
bile may contain an excessive amount of cholesterine and lime. It must be con- 
fessed that this explanation is not very satisfactory. 

Sex also has a decided influence. All authors agree that gall-stones are more 
frequent in females than in males, the proportion being about three to two. An 
explanation of this fact has been sought in the sedentary life of women, and par- 
ticularly in the mechanical effect of women's clothes and tight lacing, impeding 
the outflow of bile. It is a fact which certainly deserves consideration that we 
are very apt to find gall-stones and a corset-liver in the same individual. Also, 
the influence of pregnancy can not be denied. Gall-stones are found in women 
who have borne children much oftener than in others. 

Much has been said about certain peculiarities of constitution, in their rela- 
tion to the formation of gall-stones ; and it is asserted that the mode of life may 
favor their development — as when too much food is taken, particularly an 
excess of fat and meat, and when there is insufficient bodily exercise. In general, 
statements of this sort must be viewed with much suspicion; still, we can not 
deny that cholelithiasis is seen with striking frequency in obese women, and that 
the trouble seems to be somewhat more common among the favored classes than 
among the poor. There often seems to be a hereditary predisposition to gall- 
stones. It has been said that there is a relation between cholelithiasis and gout, 
arterio-sclerosis, and other diseases, but this is not at all certain. It is an inter- 
esting fact that sometimes the same individual has gall-stones and renal calculi. 

In many cases there may be disease of the liver and of the bile-ducts them- 
selves, leading to persistent obstruction, and thus causing gall-stones. It must be 
confessed that it is often very difficult to decide about this point, for gall-stones, 
as we shall see later, may themselves lead to secondary disease of the liver, such 
as biliarv cirrhosis and carcinoma; so that when gall-stones and some other 



BILIAKY CALCULI 



545 



hepatic disease are both present it is often impossible to decide which of the two 
lesions was primary. 

Occurrence, and Chemical and Physical Properties of Gall-stones. — The 

place where gall-stones are most frequently formed and found is the gall-bladder. 
We may find in it any number, from one or two up to a hundred and more. The 
size varies from that of a grain of sand to that of a hen's egg. The large 
stones may completely fill the gall-bladder ; and sometimes the smaller stones are 
numerous enough to fill it also. The stones usually lie free in the bladder, al- 
though exceptionally they may be found adherent to its walls. Rarely the blad- 
der presents a diverticulum, in which a stone has been formed. The lining mem- 
brane of the viscus often presents quite a severe catarrhal inflammation. This 
may have preceded the formation of the stone (vide supra), but, on the other 
hand, it may have developed as a result of the mechanical irritation of the mucous 
membrane occasioned by the concretions. Very often the wall of the gall-bladder 
and the neighboring tissues are affected by mild or even severe inflammatory pro- 
cesses, necrosis, perforation, and similar lesions (vide infra). 

Stones which are found in the larger bile-ducts are not formed in them, but 
they have become wedged in them while on their way to the intestine. Some- 
times, however, stones are formed in the liver itself ("hepatic calculi")- These 
are seldom primary, but are usually the result of biliary obstruction because of 
persistent stenosis of the common duct. Hepatic gall-stones of this sort may 
reach a diameter of a half to one centimetre. In such cases the small intra- 
hepatic bile-ducts are usually a good deal widened; or occasionally they present 
niches in which the stones lie. As a rule, the hepatic parenchyma surrounding the 
stone is in a state of chronic or acute purulent inflammation (vide infra). 

In form, gall-stones vary infinitely. The smallest are irregular masses, well 
described by the name of " gall-sand." The larger stones are more or less round, 
oval, or polyhedral. The polyhedra are usually due to the mutual rubbing and 
pressure of a number of stones upon one another. In color, the stones vary ac- 
cording to the amount of pigment they contain, from almost black or dark brown 
to a lighter greenish or bright yellow shade. A fresh gall-stone always sinks in 
water; but when dry, gall-stones contain air and generally float. On cross-sec- 
tion, the hard stones are found to be either homogeneous or composed of layers. 
As a rule, there is a nucleus, darkly pigmented, which is surrounded by a lighter- 
colored envelope, itself either made up of concentric layers or evidently crystalline. 
Often the outermost layers are still distinguishable as peculiar darker and harder 
strata. If we examine thin scales of gall-stones microscopically we shall find in 
them (as in renal calculi) an organic cement which holds the minute crystals 
together (Posner). 

As to chemical composition, gall-stones are usually divided into several 
groups. By far the most frequent variety is made up of cholesterine and pigment 
(bilirubine) mixed together in greatly varying proportions. The pigment is in 
great part combined with lime. On the average, stones contain about seventy 
to eighty per cent, of cholesterine. Besides these two chief ingredients, most 
stones also contain lime and magnesium. In color, they are light or dark ac- 
cording to the smaller or greater proportion of coloring matter they contain. 
Stones of pure cholesterine are less common. These are usually found singly, 
are soft, and often are almost transparent. Most cholesterine stones have a 
nucleus of pigment and lime in combination. Pure pigmentary concretions are 
rare, and are generally small, like coarse sand. A still greater rarity is a stone 
made up entirely of lime. Such a stone is small and very hard. 

Anatomical and Clinical Results of Gall-stones. — It is by no means rare 
for gall-stones to be present even in considerable number and size without caus- 
ing the slightest discomfort. This is proved by the fact that often at autopsy 
35 



546 



DISEASES OF THE DIGESTIVE ORGANS 



gall-stones are found by chance, although there had never been a symptom sug- 
gesting their presence. In such cases it is evident that the concretions have 
formed very gradually in the gall-bladder, and never have led to mechanical or 
inflammatory disturbance. 

In other cases, probably very numerous, the gall-stones occasion certain dis- 
turbances, but these are comparatively insignificant and not of such a character 
as to enable the physician to make an absolute diagnosis. Patients of this sort 
complain at times of slightly painful or disagreeable sensations in the stomach 
and liver, particularly after bodily exertion, and they may also have other symp- 
toms, such as slight dyspepsia. The objective examination yields nothing posi- 
tive. The physician suspects a gastric disorder, a floating kidney, or a neurosis. 
It is important that he should always in such cases, particularly in women, 
consider the possibility of gall-stones ; for it is possible, if there is an actual chole- 
lithiasis, that at any time there may be severe symptoms, the correct interpreta- 
tion of which will be rendered much easier if these mild prodromata have been 
duly appreciated. 

In a third class of cases the gall-stones cause severe and sometimes actually 
fatal illness. The symptoms may be very characteristic, so that they can be rec- 
ognized easily and absolutely; but not infrequently the condition is difficult to 
interpret, and misleading. 

The form of the disease which can be recognized most certainly and which 
has been longest known to clinicians is characterized by the occurrence of distinct 
and peculiar paroxysms. These are usually termed biliary colic. An attack of 
this sort may occur suddenly, while the patient is apparently in perfect health. 
More often, however, the first distinct attack is preceded for a long time by mild 
disturbances (vide supra), although these latter often receive little attention, 
and are apt to be misinterpreted. 

The typical attack of biliary colic begins either with absolute suddenness or 
after some slight prodromata, such as chilliness, nausea, and malaise. It may 
occur at any time, day or night. Usually there is no exciting cause to be dis- 
covered. Sometimes the paroxysm is preceded by a slight injury or some other 
apparently harmful influence, such as errors in diet and the like. The chief 
symptom of the attack is the pain. This may be extreme from the start, or it 
may begin mildly and then rapidly or slowly become extreme. Usually the 
patient refers the pain chiefly to the epigastrium and to the right hypochondrium, 
but from here it radiates into the left side, the back, the shoulders, and even the 
right arm, and sometimes again down into the hypogastrium and the thighs. 
In some paroxysms the pain increases to extreme severity ; and convulsive move- 
ments have been repeatedly observed, particularly in nervous persons, as a result 
of the pain. The pain may be accompanied by nausea, eructations, and repeated 
vomiting. The bowels are usually constipated, but sometimes there is diarrhoea. 
The constitutional disturbance is marked ; the patient feels extremely feeble and 
exhausted, and gives the impression of anguish and collapse. The pulse is small, 
usually accelerated, but sometimes infrequent. The bodily temperature is normal 
in a minority of the cases ; often there is slight fever, and sometimes a consider- 
able rise of temperature, to 104° (40° C.) and more. At the beginning of the 
attack, and also later, there is apt to be chilliness, or a well-marked rigor; and 
this is often, but not invariably, associated with high fever. 

Upon objective examination of the abdomen we find its upper portion, par- 
ticularly the region of the liver and gall-bladder, slightly prominent or even 
markedly so. The same region is sensitive to pressure, and this tenderness may 
be diffuse or localized. Sometimes an enlargement of the liver can be distinctly 
made out (vide infra), and sometimes when the abdominal walls are yielding we 
can, upon careful palpation, feel the enlarged, tense, and tender gall-bladder 



BILIARY CALCULI 



547 



(vide infra). In exceptional cases we can even feel the grating of the stones 
upon one another, and with a stethoscope hear the crepitation thus produced; 
but in other cases it is impossible to make out with certainty any change, either 
in the liver or the gall-bladder ; or the abdominal walls may be so thick and rigid 
that a good examination is impossible. In any case of this sort the physician looks 
with special attention for the appearance of jaundice. Even a slight icteric hue 
of the eyes and the skin is important, for the appearance of jaundice is often 
decisive in leading to an absolute diagnosis. Sometimes the jaundice is very 
marked; in such cases the urine contains an abundance of bile pigment. It 
can not, however, be too much insisted upon that it is by no means exceptional to 
have no jaundice at all in an attack of biliary colic (vide infra). With regard 
to finding gall-stones in the faeces, vide infra. 

The duration of an attack of biliary colic varies greatly. Extremely mild 
attacks may last merely a few hours or a day; more severe attacks continue 
two to four days and even much longer. It is equally impossible to establish 
any universal rule as to the frequency with which the attacks recur. Sometimes 
a second attack will come after a short interval; sometimes not until months or 
years have elapsed. ~Not infrequently there will be several attacks in close 
succession, and then none for a long time; or there may never be any more. 
Again, the early attacks of simple colic may be followed later by a complicated 
disorder, due to one of the numerous sequela? to which gall-stones may lead. 

We intend to discuss the remote results of gall-stones, but we must first answer 
the question, What abdominal processes occasion the attacks of biliary colic, of 
which we have just presented the clinical picture. Until within a few years the 
answer to this question seemed very simple. Almost all authorities conceived 
that the attack was due mainly to the moving about of the calculi and their 
expulsion. It was said that the stones moved into the cystic duct because of 
their own weight, the pressure of the diaphragm, and, above all, the contractions 
of the gall-bladder ; and being once in the duct, they were forced along through the 
cystic and the hepatic ducts. The attack was successfully ended when at last 
the concretion escaped from the common duct into the duodenum. The incar- 
ceration of the stone in the common duct necessitated jaundice. If the stone 
stopped in the cystic duct, or, as was often supposed to be the case, went back 
into the gall-bladder again, there would be no jaundice. 

This old doctrine of the causes of biliary colic is now known to be in large 
part incorrect, a better understanding having been obtained, incidentally to 
operations upon the gall-bladder and the bile-ducts. In particular, Riedel has 
made extensive and careful observations, and has contributed many new facts 
and views to the doctrine of cholelithiasis. Still, complete insight into all the 
conditions has been by no means attained. 

Even now it must be confessed that small stones can be driven from the gall- 
bladder through the cystic and common ducts into the intestine in the way above 
mentioned, but the progress of the small stone in this manner into the intestine 
usually causes no symptoms at all, or, if there are any, they are slight and 
ambiguous. It may be that now and then a somewhat larger stone is forced from 
the gall-bladder into the intestine and excites a genuine attack of biliary colic, 
in the old sense of the term; but in most cases the attack which we clinically 
term biliary colic is probably due, only to a very slight extent, to the incarcera- 
tion of a calculus, or to cramp-like contractions of the gall-bladder and biliary 
ducts, but it is rather an inflammatory process. So long as the stones in the gall- 
bladder remain there without exciting any secondary change, and so long as the 
bile flows freely around them, in and out, there are no clinical symptoms, although 
there is very often a gradual development of what is called dropsy of the gall- 
bladder. If a stone enters the neck of the bladder and there increases in size, or 



548 



DISEASES OE THE DIGESTIVE ORGANS 



if the cystic duct becomes obstructed by the swelling of its membrane, then the 
entrance of the bile into the gall-bladder is impeded. The constituents of the 
bile which is in it are absorbed, and the contents of the gall-bladder change to a 
yellowish serum, which may finally be almost colorless. This process often goes 
on without any symptoms, but frequently there are slight suggestions of chronic 
inflammation. The wall of the gall-bladder becomes thickened; there may be a 
gradual formation of manifold adhesions between the serous coat of the gall- 
bladder and the neighboring parts, such as the omentum, duodenum, or transverse 
colon ; and these adhesions are in many cases the cause of the mild and indefinite 
pains and other unpleasant sensations of which many patients with gall-stones 
complain for a long time previous to their first genuine attack. When a gall- 
bladder has been changed in this way, there is liability to frequent and sudden 
acute inflammatory symptoms; acute calculous cholecystitis is the true anatom- 
ical basis of biliary colic. 

We do not possess accurate knowledge as to the cause of these acute inflam- 
matory attacks or exacerbations. In our judgment, it is more probable that from 
the start infectious germs are factors in promoting the inflammation — perhaps the 
bacterium coli commune, perhaps other bacteria. These usually originate in the 
intestine, and opportunity for their pathogenic activity is afforded by the 
mechanical irritation and pressure of the gall-stones. The ordinary brief attacks 
of biliary colic are due to simple cholecystitis with a serous exudation, which 
usually gets well of itself in a few days. This serous or " catarrhal " chole- 
cystitis occasions swelling of the gall-bladder, pain, fever, and vomiting. The 
calculus caught in the neck of the gall-bladder may, of course, have many other 
stones behind it; but it is not pushed onward if it has reached a certain size; it 
remains till the inflammation passes away. We have in this case a so-called 
"unsuccessful attack of biliary colic" (Riedel). These attacks are, of course, 
as a rule not associated with jaundice. If, however, the stone is small and the 
cystic duct patent, the stone is pushed on by the pressure of the inflammatory 
exudation which collects behind it. We have now the pain due to the inflam- 
mation and also that due to the incarceration of the stone, and as soon as the 
stone reaches the common duct, and for a time blocks the discharge of bile, we 
almost invariably have obstructive jaundice. If the stone is successfully driven 
through the common duct into the duodenum, the pain and inflammation usually 
promptly cease. By careful search we may find one or more stones in the faeces. 
In brief, we have to deal with a so-called " successful " attack of biliary colic. 
The distinction between unsuccessful and successful attacks is, of course, not 
always self-evident ; but it should be noted that, according to Riedel, unsuccessful 
attacks are much more frequent than the successful. It is true that in the success- 
ful attacks there is always jaundice, and in the unsuccessful attacks there is usu- 
ally no jaundice, yet this criterion is not absolute, because, as Riedel was the first 
to point out, jaundice may occasionally be present in the unsuccessful attacks. 
In such a case the jaundice, of course, is not due to closure of the common duct 
by a stone — that is, it is not lithogenous, but it is inflammatory. The catarrhal 
inflammation of the gall-bladder may sometimes extend to the bile-ducts and pro- 
duce jaundice, because of inflammatory swelling of the common or hepatic duct. 

This simple cholecystitis or cholangitis (inflammation of the bile-ducts) does 
not by any means comprise all of the pathology of cholelithiasis. In many cases 
there is not a simple cholecystitis or cholangitis, but a purulent inflammation, 
which is either purulent from the start or a sequel to a serous exudation. That 
bacteria are factors in this process there can be no doubt, and it is the author's 
opinion that we can scarcely draw any sharp dividing line between serous and 
purulent inflammation of the bile-ducts. The danger of inflammation varies 
according to the power of the infecting bacteria, and the greater or less vulner- 



BILIARY CALCULI 



549 



ability of the infected tissue. It is certain, however, that the purulent inflam- 
mation will cause severer clinical symptoms. The condition now presented is no 
longer a simple attack of colic, but a far more severe and persistent constitu- 
tional disturbance, associated with pain in the hepatic region, vomiting, possibly 
jaundice, and very likely signs of enlargement of the gall-bladder and the liver. 
There are high fever (often accompanied with rigors), general prostration, and 
cerebral symptoms. In milder cases there is only a purulent cholecystitis. In 
the severer cases there is a purulent diffuse cholangitis alone, or combined with 
purulent inflammation of the gall-bladder. To enumerate here all the possi- 
bilities of the condition is impossible. Even severe derangement of this sort is 
not incompatible with spontaneous recovery, but in some cases, if it is too late 
for surgical aid, there is a general septic infection and death. 

We shall refer to a great number of other sequelae of gall-stones when we are 
considering the fate of the calculi after they have left the gall-bladder and 
reached the bile-ducts. As above mentioned, the smaller stones may be driven by 
a successful attack of biliary colic into the duodenum, but in other cases the- 
stones are stopped on the way, either in the cystic or in the common duct. If the- 
stone lodges in the common duct there is usually long-continued jaundice with 
secondary changes in the liver, with which we shall later become better acquainted 
(vide infra, biliary hepatic cirrhosis). The inflammation may, however, abate — 
the stone remaining quietly where it is lodged, and the duct gradually dilating 
and, in a certain measure, accommodating itself to the stone ; but the mechanical 
effect of the foreign body will be very likely eventually to occasion fresh attacks 
of inflammation and the gradual formation of chronic adhesions and distortions 
of the surrounding parts. There is special danger when there is a considerable 
pressure-necrosis of the underlying tissue. This immediately opens the door to 
inflammatory germs, and results in secondary suppuration, which may be either 
diffuse or localized. In the worst cases there may be -purulent phlebitis of an 
abdominal vein, with metastatic abscesses in other organs. 

Precisely similar consequences may, however, arise from stones which are 
situated in the gall-bladder itself (usually at its neck), with a consequent suppu- 
rative infection of the neighboring parts. Perforation into the abdominal cavity 
leads to purulent peritonitis. If adhesions have already been formed, as is 
usually the case, there may be perforation in any one of many directions, either 
outward with escape of the pus and often the gall-stones, and perhaps with the 
formation of a biliary fistula, or into the transverse colon, or more rarely into the 
stomach, the portal vein, or the urinary tract; but chief in relative frequency 
and importance is perforation from the neck of the gall-bladder into the duo- 
denum, for this, as Virchow and Fiedler have pointed out, is the most common 
way by which large gall-stones reach the intestine and come to be discharged with 
the faeces. Many of these processes may, under favorable circumstances, lead 
to spontaneous recovery from cholelithiasis. The gall-bladder, under the 
influence of suppuration, may finally completely shrivel up, perhaps retaining in 
its folds one or more calculi; but much oftener, if there is no prompt surgical 
intervention, the termination is unfavorable. The associated clinical conditions 
are manifold and they can not be sketched in detail, and the end may come in an 
acute and stormy manner, or after a long illness marked by many fluctuations. 
Still, we feel bound to emphasize, in closing, that the frequency of these manv 
grave results of cholelithiasis which we have mentioned must not be over-esti- 
mated. In comparison with the extremely great number of gall-stones which 
produce either no symptoms at all, or none which suggest danger to life, the 
severe cases of purulent inflammation after cholelithiasis are few. 

Diagnosis. — It is evident from what has been already said that often the diag- 
nosis of cholelithiasis is easy and indubitable, while in other cases the symptoms 



550 



DISEASES OF THE DIGESTIVE ORGANS 



and course of the disease are obscure and ambiguous. The attacks of colic are 
certainly the most characteristic symptom. We should therefore make it a rule, 
in case of severe paroxysmal pain in the region of the stomach or liver, particu- 
larly in middle-aged women, to think of the possibility of gall-stones. If an 
attack of this sort is associated in even a slight degree with jaundice, the diag- 
nosis is usually perfectly clear. If there is no jaundice — and frequently there is 
none — the diagnosis is less certain, but still it can often be made because of the 
general character of the painful attack; the indications of localized peritoneal 
irritation, such as slight swelling of the abdomen, tenderness on pressure, and 
vomiting; and finally because of the discovery on palpation of an enlarged gall- 
bladder. In every case importance must be laid upon a careful inquiry of the 
patient or his friends as to any previous attacks or any mild indefinite prodrom- 
ata, etc. In a certain number of cases, however, it will not be possible to get 
beyond a mere suspicion that there are gall-stones, and occasionally it will be 
impossible to avoid confusion with cardialgia, intestinal colic, renal colic, the 
pains of a movable kidney, and visceral neuralgia. This is particularly apt to 
happen when the attack is not a well-developed one with characteristic symptoms, 
but is more indefinite and suggests cardialgia, dyspepsia, and similar conditions. 
A careful and thorough examination of all the organs that might be involved, 
such as the stomach and kidneys, may in many cases aid us ; and often the truth 
is revealed by the further course of the disease; but many cases remain obscure. 
The hope that gall-stones might be recognized during life by means of the 
Roentgen rays has, unfortunately, not been fulfilled. 

We must say a word about finding the gall-stones in the faeces. Of course, 
the discovery of the corpus delicti in the evacuations after an attack of colic 
makes the diagnosis absolute. They are to be searched for by mixing the stools 
with water, and then passing them through a sieve. But, as we have pointed out 
above, the " unsuccessful " attacks of biliary colic are probably much more fre- 
quent than the " successful." We can not, therefore, be surprised that in many 
cases of cholelithiasis no stones can be found in the dejecta, and Riedel is right 
in maintaining that it is not worth while to search for the stones except in those 
attacks which are associated with jaundice, that is, those that are not unlikely to 
be " successful." It should be pointed out further that we should be on our 
guard not to mistake for gall-stones hardened portions of faeces — for instance, 
compacted vegetable matter. 

Often the diagnosis is very difficult in cases of severe purulent inflammation, 
originating from gall-stones. If there are such symptoms as indicate a peri- 
tonitis localized in the hepatic region, associated with fever and rigors, and 
suggesting circumscribed suppuration, we must always consider the possibility 
of gall-stones being the primary cause. We should make a careful local exami- 
nation and consider the general conditions, such as age and sex, and we shall 
often be greatly helped by inquiring carefully into the previous health of the 
patient — e. g., with regard to any characteristic colic. It must be confessed that 
it will not always be possible to avoid confusion between this and other suppura- 
tive processes, particularly those originating from an abnormally situated appen- 
dix, or from suppurating echinococci. No special diagnostic rules can be formu- 
lated, for the symptoms are peculiar in almost every single case. Even when we 
are able to make a correct diagnosis of cholelithiasis we are often unable to 
estimate the exact condition, the extent of the secondary inflammation, the 
number and the situation of the stones, or the presence of secondary adhesions. 

Prognosis. — The prognosis of gall-stones must really be termed doubtful in 
every case, that is, if we provisionally exclude the possibility of cure by surgical 
means. The presence of gall-stones, as the reader already knows, may entail a 
number of dangerous sequelae, and we can never foretell whether the patient will 



BILIARY CALCULI 



551 



suffer from these or escape them; still, there is no doubt that in many cases, 
particularly when the stones are small (vide supra), there may be a spontaneous 
and permanent recovery, while in other cases there may be disturbances of the 
most varied kind, persistent, or constantly recurrent, and yet never absolutely 
serious. There is no occasion for describing here a second time the numberless 
possibilities of cholelithiasis and their prognostic significance. 

There is one important symptom which is interesting from the standpoint of 
general pathology and which must be noted here — viz., the development, subse- 
quent to cholelithiasis, of cancer of the gall-bladder and bile-ducts. This possi- 
bility is, of course, of great clinical importance, and agrees with the general 
observation that persistent mechanical irritation of the mucous membrane and 
scar formations may occasion the development of carcinoma. The formation of 
secondary cancer after cholelithiasis is precisely analogous to the growth of cancer 
after ulcer of the stomach, or secondarily to stone in the kidney. 

Treatment. — Our means of efficient prophylaxis against the formation of 
gall-stones are very limited. The most we can assume is that an entirely suitable 
regimen, and particularly the avoidance of any tight lacing or similar mechanical 
interference with the excretion of bile, will prevent or at least delay the develop- 
ment of any tendency to the formation of calculi. If gall-stones have been once 
formed, our task as physicians consists merely in moderating the disturbance 
which they produce; in guiding, so far as possible, all sequelae to a favorable 
termination ; and finally in effecting the removal of the stones from the body, so 
far as this is necessary and within our power. 

If the symptoms of the patient remain comparatively slight, and especially if 
the diagnosis of gall-stones has not yet been absolutely established, energetic 
treatment is not demanded. We regard it as important that in such cases, as 
soon as we conceive the possibility of cholelithiasis, the patients should enter 
upon a proper rest-cure. Very often female patients of this sort are regarded 
as nervous, are sent into all sorts of health-resorts, and treated with electricity 
and massage, and, of course, without success. Instead we should induce such a 
patient to spend a few weeks of complete rest in bed, or at any rate, lying on a 
sofa with easy clothing; prescribe a cautious and nourishing diet, and the reg- 
ular application of warm poultices upon the hepatic region; and administer 
before breakfast and in the middle of the forenoon a half pint of warm Carlsbad 
Muhlbrunnen water. We may then hope for a satisfactory improvement in the 
symptoms due, in our judgment, to the cessation of the slight inflammatory 
irritation. Often patients of this sort are sent to Carlsbad. We will not deny 
that Carlsbad water may have some favorable influence upon cholelithiasis, but 
we believe that the exertion of the journey and the promenades and other activi- 
ties in which the patients are apt to indulge after their arrival, are often serious 
drawbacks. That Carlsbad water, as such, is of real value in expelling the stones 
or in actually dissolving ( !) them, we find difficult to believe. 

Whenever there is a well-marked attack of biliary colic we have special 
indications for treatment. Of course, in this case also, we must immediately 
enjoin complete rest in bed. 

The pain demands the prompt employment of narcotics, particularly of mor- 
phine or opium. If the suffering is extreme, a subcutaneous injection of 
morphine is by far the best and quickest remedy ; but the internal use of opium 
is also to be recommended. We may give every two or three hours fifteen or 
twenty drops of the tincture, or half a grain to a grain of powdered opium (gramme 
0.03-0.05).* Other narcotics, such as chloral or belladonna, are scarcely ever 



* [When giving repeated doses of opium for biliary or renal colic, it should be remembered that 
the pain will cease abruptly as soon as the stone ceases to obstruct the passage, and that severe toxic 



552 



DISEASES OF THE DIGESTIVE OKGANS 



necessary, but we may sometimes combine extract of belladonna, which is 
much praised by many physicians, with the opium. Of external applications 
upon the hepatic region the best is a warm or hot poultice. It is exceptional for 
the patient to prefer an ice-bag. Usually, gentle rubbing of the hepatic region 
with chloroform-oil (a mixture of equal parts of chloroform and olive-oil) does 
good. In a few cases the patient experiences relief from a prolonged warm bath. 
If there is violent vomiting we give tincture of opium, bromide of potash, cocaine, 
or bits of ice. If there is marked collapse, such stimulants must be employed as 
wine, strong black coffee, or even injections of ether and camphor. When the 
acute symptoms have ceased, we must still persist for some time in a cautious 
diet and in bodily quiet, and it is often well to prescribe a gentle laxative, such 
as Carlsbad salts or rhubarb. 

When the attack is completely over, the question arises how to guard against 
the occurrence of others. The answer to this question depends mainly upon the 
view we take of the present attack, whether we regard it as a " successful " or an 
" unsuccessful " one. If the attack was successful — that is, if calculi were found 
in the intestinal evacuations after it — we may hope that in case there are more 
stones present they also may be discharged. Whether we possess artificial means 
of insuring this discharge is extremely doubtful. Still, many remedies and 
methods of cure have been recommended as exerting a favorable influence in this 
direction. Here again we must mention first the use of Carlsbad and similar 
waters, such as Hamburg, Ems, and Vichy. Many physicians believe that they 
have seen good results from the persistent use of turpentine, particularly in the 
form of what is called Durande's remedy; that is, a mixture of ether and tur- 
pentine in the proportion of three to two, of which two or three times a day 
twenty to thirty drops are given ; and the same is true of salicylate of sodium, of 
which half a drachm to a drachm (grammes 2-4) is given daily for a consider- 
able period, either alone or in combination with bicarbonate of sodium. We 
should also mention in this connection the administration of large doses of olive- 
oiL This is extremely unpleasant for the patient, and very uncertain in its 
effect, but still is highly praised by many physicians. A mixture of six or seven 
ounces (grammes 200) of olive-oil, five drachms (grammes 20) of brandy, and the 
yolk of two eggs, with a few drops of oil of peppermint, is given in two portions 
at a short interval. [Most of the oil is passed in lumps, which have a super- 
ficial resemblance to gall-stones, and are sometimes called such.] Of course, we 
should also regulate the diet and the life of the patient in a suitable manner, and 
this may be the most important prescription of any. 

If, however, the attack was unsuccessful, or particularly if several unsuc- 
cessful attacks have occurred, there is scarcely room to hope that any internal 
remedy will result in expulsion of the stone. It may be too large. If, then, we 
do not choose to let the case take whatever course it will, there is only one remedy 
available, and that is the operative removal of the stones by opening the gall- 
bladder. If we consider the dangers which are entailed by the presence of stones 
that can not be evacuated by the natural passages, we must agree with Eiedel 
when he says a " single unsuccessful inflammation of the gall-bladder is a suffi- 
cient indication for immediate operation." To be sure, no one will fail to 
recognize that the circumstances in practice may prevail over purely theoretical 
considerations, however lucid the latter may be. Many patients will not consent 
to an operation after a single brief attack which, although painful, has ended in 
apparently complete recovery, and the conscientious physician will consider in 



effects of the drug may then appear. In bilious colic the distance to he traversed by the stone is 
relatively short, and in that affection especially the inhalation of ether or chloroform is sometimes the 
best, and, indeed, the imperative treatment.] 



SUPPURATIVE HEPATITIS 



553 



any actual case the indisputable dangers of the operation, and the possible doubt 
as to diagnosis. It is a very different matter when the unsuccessful attacks are 
frequently repeated or when there is persistent discomfort, so that the patient is 
deprived of all joy in life and all personal activity. Then we ought not and dare 
not longer delay in urging him to operation. The surgical treatment of chole- 
lithiasis in such cases already possesses a record of many brilliant successes. 

There is likewise an urgent indication for prompt operation when the symp- 
toms indicate a purulent cholecystitis or a localized abscess, due to gall-stones. 
It would probably be better if such complications of cholelithiasis were avoided 
by anticipatory surgical interference, but this desirable result will never be 
attained in practice, because in many cases the purulent infection of the gall- 
bladder or the bile-ducts occurs without having been preceded by any marked 
symptoms. In these suppurative cases, surgical intervention often not only saves 
life but works a permanent cure, unless the purulent infection has already 
extended to the bile-ducts of the liver itself, or has led to general pyaemia. We 
can not in this place enter into the particulars of the surgical treatment of gall- 
stones, or the removal by operation of stones fixed in the cystic or common ducts. 
Complete information will be found in surgical monographs. 



CHAPTER IV 

SUPPURATIVE HEPATITIS 

{Hepatic Abscess) 

-Etiology. — Exclusive of traumatism there are two ways by which bacteria 
may penetrate into the liver, there to excite a suppurative inflammation — namely, 
by the blood and through the bile-ducts. In the circulatory system the main 
route is by way of the portal vein, by which pyogenic organisms from the intes- 
tines reach the liver. This explains why many ulcerative processes in the intes- 
tine, such as severe dysentery, are followed by hepatic abscess ; and why purulent 
pylephlebitis (q. v.) and other suppurative processes within the portal system may 
have a similar sequel. In general pysemia, the germs must take a very circuitous 
route in order to reach the liver. They must, on leaving the primary abscesses, 
first enter the veins and the lungs, and then gain the liver by way of the hepatic 
artery. It has been well known for a long time that suppurating wounds of the 
head are followed by hepatic abscess with comparative frequency. Perhaps it 
may exceptionally happen that infectious matter enters the hepatic veins by 
" retrogressive embolism " from the vena cava. 

The germs which make their way into the liver from the bile-ducts invariably 
originate in the intestine. In these cases the hepatic inflammation is almost 
always preceded by disease of the biliary passages. The most frequent cause 
by far of this variety of hepatic abscess is the formation of gall-stones in the 
gall-bladder and in the liver. This has been fully discussed in the preceding 
chapter. 

Among us, hepatic abscesses are rarely occasioned in other ways than those 
indicated; but in the tropics it is said that quite a large number of apparently 
primary hepatic abscesses are met with. Their origin is not yet explained, 
although in this case also there is most probably an invasion of pyogenic bacteria 
from the intestine. 

Pathology. — The smallest and as yet imperfectly developed embolic abscesses 
best illustrate the mode of formation. We find the blood-vessels choked with 



554 



DISEASES OF THE DIGESTIVE ORGANS 



micrococci, and the cells of the surrounding parenchyma void of nuclei and in 
process of disintegration. Along the course of the blood-vessels nuclei are very 
abundant. These are due to white corpuscles which have escaped through the 
vascular walls. The cells and the liquid exudation rapidly increase, and there is 
complete destruction of the hepatic parenchyma, and the formation of an abscess 
in its place. This extends in all directions. Large abscesses may at last involve 
an entire lobe. In other cases the suppurative process is limited by encapsulation. 
Sometimes quite large portions of the liver become necrotic and slough off, under 
the influence of what is called " sequestrating " suppuration. We almost invari- 
ably find some shreds of hepatic tissue in the pus of hepatic abscesses. When 
hepatic abscess has been occasioned by gall-stones, the suppuration has usually 
been due to direct extension of the process from the bile-ducts to the parenchyma 
of the liver. Not infrequently gall-stones are found in the pus of such cases. 

Small abscesses may perhaps be absorbed, but they are in most cases merely 
symptomatic of pyaemia or some such disease, which is itself incurable. Larger 
abscesses may point into neighboring organs. If they are discharged into the 
abdominal cavity, diffuse peritonitis follows. The most favorable termination, 
and one repeatedly observed, is perforation through the abdominal walls, after 
these walls and the liver have been joined by adhesions. They may also break 
into the pleural cavity, the pericardium, the intestine, and the pelvis of the right 
kidney. 

Clinical History. — An absolutely complete clinical description of hepatic 
abscess is impossible, because, as we have seen, it may be a symptom of such 
diverse pathological processes. Hepatic abscesses are often found post mortem 
which had given no previous indication of their presence ; this is frequently true 
in pyaemia. In other cases there are symptoms, in part directly referable to the 
seat of inflammation, and in part due to its influence upon neighboring organs. 

Enlargement of the liver can often be made out by percussion or even by pal- 
pation. It is the result of swelling and hyperemia involving the entire organ. 
Extensive abscesses may give much more definite signs of their presence, however, 
if situated on the anterior surface of the organ. They are sometimes felt 
through the abdominal walls as hemispherical and actually fluctuating tumors. 
It is not so very rare for tropical hepatic abscess to attain these dimensions. 

Pain in the right hypochondrium, although it may be entirely absent when 
the abscesses are small, even if they are numerous, is often violent and persistent 
when the abscess is large. It is excited by the tension of the peritoneal covering 
of the liver, or by perihepatitis. The pain often radiates — and with especial 
frequency, it is said, into the neighborhood of the right shoulder. 

The course of the fever may prove a strong diagnostic point. When the 
abscess is chronic and encapsulated there may, it is true, be no fever whatever; 
but, as a rule, fever does exist, and it often presents a very characteristic inter- 
mittent character. There are great elevations, usually ushered in by a chill, 
and succeeded by deep depressions of temperature accompanied by perspiration. 
If the hepatic trouble is merely a symptom of general pyaemia, then the fever is 
to be ascribed to the latter ; but if there are signs of a severe local hepatic disease, 
such as pain, enlargement, and perhaps jaundice, and if these febrile attacks 
come on at irregular intervals, we should always consider the possibility of 
abscess of the liver. In the cases of large tropical abscess this sort of fever is the 
rule. It is most frequent with us in cases of purulent pylephlebitis and of abscess 
excited by gall-stones. The " fievre inter mitt ente hepatique " of the Erench is 
in most instances due to the presence of gall-stones in the liver, with secondary 
suppuration and abscess formation. 

Among the secondary symptoms of hepatic abscess jaundice is prominent. It 
is not invariably present, however, occurring only when the abscess has com- 



CIRRHOSIS OF THE LIVER 



555 



pressed some large biliary duct, and has thus given occasion to the absorption of 
bile by the lymphatics, or when an extensive cholangitis has simultaneously 
developed, sufficient to cause jaundice. In rare instances the abscess compresses 
the portal vein and thus causes ascites. There may be pulmonary symptoms of 
considerable importance, even when there are no actual pulmonary complications. 
This is because the right half of the diaphragm is crowded up by abscesses pro- 
jecting from the convex surface of the liver. Hiccough is sometimes a source 
of distress, and it may be due to the pressure of the abscess upon the stomach. 
Vomiting is also a rather common and often very troublesome symptom. 

There is almost always great constitutional disturbance. The patient has no 
appetite, and loses flesh, particularly if there are frequent febrile exacerbations. 
Often there are severe nervous attacks. Very exceptionally, the disease remains 
latent for a long time, and does not disturb the general health to any great 
extent. 

The course of the disease depends mainly upon the nature of the original dis- 
turbance. Severe pyemic cases, in which hepatic abscesses develop, are generally 
brief, and are almost invariably fatal. Abscesses due to gall-stones, and the large 
abscesses which are apparently idiopathic, are generally chronic, lasting for 
weeks, or even for many months. Cases exhibit manifold diversities, according 
to the position, size, number, and sequelae of the abscesses. Among the possible 
results, we would once more call attention to perforation into neighboring organs. 
If the pus is discharged externally, recovery may ensue; as also if the pus 
reaches the intestinal canal or the bronchi, which seldom happens. Perforation 
into the abdominal cavity always excites a fatal acute peritonitis. As a general 
rule, hepatic abscess finally proves fatal, recovery being exceptional. Death is 
due either to the gradual loss of strength or to some complication. 

Treatment. — Local bleeding, counter-irritation, purgatives, and emetics are 
among the remedies which are advocated, but we can hardly expect them to exert 
much influence upon a hepatic abscess. The best way is to treat the case purely 
symptomatically, seeking to keep up the patient's strength and mitigate his suf- 
fering until, if we are very fortunate, we have a chance for operative interfer- 
ence. When once the other symptoms are re-enforced by the discovery on palpa- 
tion of a fluctuating tumor, the diagnosis is established, and the pus should be 
evacuated and the cavity drained. Particulars about the operation should be 
sought in works on surgery. More than one case of the large tropical abscess 
have been cured in this way; but the cases which are most common among us — 
namely, embolic abscesses and those excited by gall-stones — hardly ever afford 
any opportunity for surgical interference. 



CHAPTEE V 

CIHHHOSIS OP THE LIVER 

(Chronic Diffuse Interstitial Hepatitis. Laennecs Cirrhosis. Gin-drinker's Liver. Hob-nailed Liver) 

iEtiology and Pathology —Cirrhosis of the liver is usually denned as a 
diffuse interstitial inflammation, chronic in duration, and resulting in a secondary 
atrophy of the true hepatic parenchyma. This conception makes the disease per- 
fectly analogous to u chronic interstitial inflammation " of the kidney and many 
other organs. Weigert's careful study of the processes of " chronic interstitial 
nephritis " has shown that at least a large part of the changes which take place 
in the connective tissue are not primary, but secondary, and the consequence of 



556 



DISEASES OF THE DIGESTIVE OKGANS 



a primary destruction of the genuine renal parenchyma. The question naturally 
suggests itself, whether the same may not he true of the apparently closely allied 
phenomena of hepatic cirrhosis. We feel, therefore, that in most cases of hepatic 
cirrhosis the origin of the disease consists of a primary injury and consequent 
partial destruction of the hepatic cells, whereupon follow a secondary prolifera- 
tion and final contraction of the interstitial tissue, just as is seen in lesions of 
the parenchyma of the kidneys, spinal cord, and heart. 

Such a conception would be extremely compatible with one fact about the 
aetiology of the disease — namely, that chronic alcoholism is universally regarded 
as a potent predisposing cause. Hence the English name, " gin-drinker's liver.' 7 
The harmful influence of alcohol can be appreciated if we remember that on being 
absorbed it is carried directly by the blood-vessels through the portal vein to the 
liver. According to the usual view of the disease, the poison excites a chronic in- 
flammation of the connective tissue ; while, according to the new view, the alcohol 
exerts a specific injurious influence upon the hepatic cells proper, impairing their 
nutrition, and finally causing their destruction. That the disease attacks the 
periphery of the lobules and the interlobular connective tissue is equally conso- 
nant with either theory. It is well known that the capillary anastomoses of the 
portal vein are situated between the lobules. 

Hepatic cirrhosis is most common in those who drink distilled liquors, while 
excessive indulgence in less strongly alcoholic beverages, such as wine and beer, 
leads less frequently to cirrhosis. Still, we have repeatedly seen the disease in 
beer drinkers. 

The abuse of alcohol is surely the chief but by no means the only cause of 
cirrhosis, for quite often the disease attacks persons in whose case no such 
aetiology is possible. In such instances we are seldom able to demonstrate the 
real cause. The excessive use of spices, and other analogous substances, has some- 
times been regarded as causative. It is also said that malaria and the acute 
infectious diseases sometimes leave behind them a tendency to cirrhosis. In our 
opinion such cases are due to the long-continued action of chemical agents and 
bacteria, about which we do not as yet possess any accurate knowledge, which 
are conveyed from the intestine to the liver. These cases of " genuine hepatic 
cirrhosis " are analogous to the not infrequent cases of " genuine interstitial 
nephritis " of unknown origin. Perhaps in many instances, also, there is a con- 
stitutional and excessive sensitiveness of the hepatic cells to the injurious influ- 
ences to which they are exposed while performing their normal functions. — The 
form of cirrhosis which follows diseases of the bile-ducts, and also " syphilitic 
cirrhosis," will receive separate consideration. 

Cirrhosis of the liver is seen much oftener in men than in women, and usually 
occurs in middle life. This is in harmony with the fact that the chief cause 
is the abuse of alcohol. 

The anatomical changes are generally divided, without regard to the way in 
which they are brought about, into two stages. In the first stage the liver is 
uniformly enlarged, resistant, with its edge blunt, and its surface at first per- 
fectly smooth, but later presenting little dimples. On section, the increased con- 
sistency, or " interstitial induration " of the liver, can be readily perceived. The 
acini are separated from one another by a relatively thick band of grayish-red 
interstitial tissue, and are at first readily distinguishable. Later on, the inter- 
stitial hyperplasia invades the acini themselves, and they cease to be discernible. 
The microscope shows that the cause of this increase in size and firmness of the 
organ is due exclusively to the abundant cellular infiltration and the new forma- 
tion of connective tissue between the individual lobules. The neighboring cells 
of the parenchyma exhibit signs of disintegration, undergoing either simple 
atrophy or else fatty degeneration. 



CIRRHOSIS OF THE LIVER 



557 



The second stage corresponds with the process of contraction of the newly 
formed connective tissue, but in this stage the destruction of the proper hepatic 
tissue has already assumed grave proportions. On the old theory, the paren- 
chyma perishes because of the great disturbance of circulation in the portal 
capillaries, great numbers of which are obliterated by the shrinking of the con- 
nective tissue. We ourselves, as we have already intimated, incline rather to 
Weigert's view, that the atrophy of the hepatic cells is, as a rule, the direct result 
of a primary pathological lesion of the hepatic tissue. Under this process of 
contraction the liver undergoes progressive atrophy, and its surface becomes 
mammillated. The size of the nodules varies. The size of the whole organ may 
be reduced one half, or even more. Frequently its general contour is consider- 
ably modified. Often the diminution of the size of the liver is confined mainly to 
the left lobe. The serous coat of the liver is usually thickened and rendered 
opaque ; the hepatic tissue feels very resistant and cuts with difficulty, often with 
a grating sound; the color of the cut surface is usually a rather light yellow 
(icippos = yellow). Upon microscopic examination, we find merely vestiges of 
parenchyma, embracing which are wide, firm bands of connective tissue. Even 
within the acini there is decided interstitial hyperplasia along the blood-vessels. 
The hepatic cells exhibit various stages of fatty degeneration and simple atrophy. 
Brown masses of pigment are often found here and there, which have been left 
behind by the hepatic cells now destroyed. Regenerative changes can also be de- 
tected quite frequently. The most common of these is the formation of small 
biliary passages in the broad bands of interstitial tissue. 

The division of hepatic cirrhosis into two stages is somewhat schematic, 
for there is really no sharp dividing line between them. The same liver may in 
different places illustrate both stages simultaneously. Thus, the surface is often 
distinctly granular, while the liver as a whole remains hypertrophic. In many 
cases there seems to be no so-called " first stage " at all, and the previously normal 
liver is directly transformed into a contracted liver, perhaps comparable to the 
kidney of genuine interstitial nephritis. 

Clinical History, — The onset of the disease is usually insidious. At autop- 
sies quite an advanced stage of cirrhosis is sometimes found, to which not a 
single clinical symptom had pointed ; and it is often observed that the duration 
of unambiguous symptoms is much shorter than the degree of anatomical change 
discovered post mortem would have led us to expect. 

It is, however, true that certain prodromata may appear long before the genu- 
ine cirrhotic symptoms ; but there is generally room for doubt whether these pro- 
dromata are excited by the incipient hepatic disease or whether they are not due 
to other coincident affections, such as the chronic gastric or intestinal catarrh 
which drunkards so often have. There are anorexia, nausea, epigastric uneasi- 
ness, eructations, constipation, and sometimes vomiting. There is evident con- 
stitutional disturbance in many cases, but in others the strength is unimpaired. 
The severer symptoms usually date from the time when disturbance of the portal 
circulation arises. We have already stated that the diseased process is most 
active in the interlobular connective tissue — that is, where the portal capillaries 
are situated. When the contraction of the connective tissue has resulted in the 
destruction of a large number of these portal capillaries and the minute veins 
from which they spring, the portal circulation is inevitably impeded, and there 
arises a passive congestion of the whole portal system. The signs of this are soon 
manifest. 

The stasis in the veins of the peritoneum is, as a rule, the first to attract atten- 
tion, from the ascites which it occasions. The distention of the abdomen and the 
sensation of weight and pressure due to this effusion, are often the first things 
which excite the patient's attention and lead him to seek medical advice. Later 



558 



DISEASES OE THE DIGESTIVE OKGANS 



on, the ascites sometimes becomes enormous, causing immense swelling and 
extreme tension of the abdominal walls, and, of course, proportionate discomfort. 
Proper nursing and internal treatment may diminish the ascitic effusion, but 
they will seldom wholly remove it. It quite often remains nearly uniform, until 
finally, for some reason, there is a change for the worse. 

Next to ascites, the most important symptom of portal obstruction is enlarge- 
ment of the spleen, which is due both to the increased amount of blood in the 
organ and to a diffuse hyperplasia of its tissues. As a rule, the increase in size is 
considerable, amounting sometimes to two or three times the normal dimensions. 
It is not very exceptional to find a well-marked splenic tumor in hepatic cirrho- 
sis, even before there is any ascites. In such cases the splenic tumor is not due 
at all to portal congestion but to other, perhaps toxic, influences, just as in biliary 
cirrhosis (vide infra). At any rate, the discovery of splenic tumor is invariably 
of great diagnostic importance, although it is often no easy matter to make out 
the size of the spleen, inasmuch as both percussion and palpation are rendered 
very difficult by the presence of ascites. On the whole, palpation is the more 
reliable. Pain or other subjective symptoms are rarely observed. Exceptionally, 
there is no enlargement of the spleen. This may be due to the firmness and thick- 
ness of its capsule, or to the general marantic condition of the patient. 

The venous congestion of the stomach and intestines excites catarrh, which is 
evinced by anorexia, nausea, and irregularity of the bowels. Usually there is 
quite obstinate constipation, but there may be persistent diarrhoea. None of these 
symptoms occupies the foreground of the clinical picture, however, both because 
such symptoms are frequent in all grave chronic diseases and because many pa- 
tients have had digestive derangements long before these severer troubles began. 
A more significant symptom, if it occurs, is haemorrhage. This is now and then 
occasioned by the extreme gastro-intestinal congestion. If the haemorrhage is 
slight and comes from capillaries, there is diarrhoea with blood-stained stools, or 
vomiting, the vomitus being dark-colored. Probably the tendency to haemorrhage 
is aggravated by the general cachexia or by the alcoholism. Of more importance 
is the vomiting of large amounts of pure blood. This, as the author knows from 
repeated observations, may be sufficient of itself to endanger life. Such cases 
have more than once led to the incorrect diagnosis of gastric ulcer, but at autopsy 
we usually find well-marked varices in the oesophagus, due to passive congestion. 
The severe haemorrhage is occasioned by the bursting of a varix. We surmise 
that similar conditions, probably mostly in the rectum, cause the severe intestinal 
haemorrhages which are sometimes seen. 

There is sometimes a slight jaundice in ordinary cirrhosis, which is due to the 
existence of duodenal catarrh, or perhaps to catarrh of the smaller bile-ducts. In 
many cases, however, there is no jaundice at all, or the skin shows merely a slight 
yellowish tinge. There is also a peculiar dark or dirty-grayish color, which is 
tolerably characteristic of cirrhosis. 

The above signs of portal obstruction will often render the diagnosis of 
hepatic disease extremely probable, but we should always endeavor to confirm our 
opinion by physical examination of the liver. In the later stages of the disease, 
and particularly if there be great ascites, our efforts may be fruitless ; but at first, 
or after paracentesis has been performed, percussion and palpation may yield 
valuable information. In the earliest stages the liver is usually large. Hepatic 
dullness reaches some way below the edge of the ribs, and we can often feel the 
lower edge and anterior surface of the organ. Later on we find the surface irreg- 
ular and rough. If we can feel these little nodules or prominences through the 
abdominal walls, as we sometimes can, of course the diagnosis of cirrhosis of the 
liver is nearly certain. As already mentioned, it often happens that irregular- 
ities are already to be felt upon the surface of the organ while it still remains 



CIRRHOSIS OF THE LIVER 



559 



hypertrophic. The demonstration of atrophy by percussion in the later stages of 
the disease is less reliable. The ascites often interferes with such an attempt. 
We may also be misled by coils of intestine distended with gas and perhaps lying 
in front of the liver. If, however, after guarding against error, we constantly 
find the area of hepatic dullness diminished, the sign has some value. Moreover, 
it is not infrequently possible to make out by palpation that the liver, although 
reduced in size, is hard and uneven. This is easier after the removal of ascitic 
fluid, when the abdominal walls are lax, and also if the attachments of the liver 
have been loosened so that it sinks downward. 

General nutrition is usually much impaired in the later stages of the disease. 
At first the patient may retain vestiges of his former corpulence, but finally he 
grows emaciated. Anasarca may exceptionally occur toward the close ; but there 
is frequently considerable oedema of the lower extremities, and even of the scro- 
tum and the dependent portions of the abdominal walls. The cause of this is a 
purely local one — the pressure of the ascites impedes the return of blood from the 
lower limbs to the heart. Thus arises a condition which is characteristic of portal 
obstruction in general, and hepatic cirrhosis in particular, and has been termed 
" oedema of the lower half of the body." There is ascites with oedema of the loins, 
the scrotum, and the lower extremities; while the upper extremities, the upper 
half of the trunk, and the face are entirely free from oedema. 

Occasionally there are ecchymoses into the skin, the mucous membranes, the 
retina, and other parts. These are probably due to malnutrition of the vascular 
walls. The gastric and intestinal haemorrhages have been already discussed. 

In uncomplicated cases of the disease there is no fever. The pulse, even 
when there are no cardiac complications, is small and often somewhat rapid. 
Respiration may be much embarrassed, as a result of the upward pressure of the 
diaphragm. 

At first the urine presents no characteristic changes. When the ascites has 
become considerable and there is oedema, the urine grows scanty, dark, and con- 
centrated, and often has an abundant sediment of urates. It should be men- 
tioned that some observers have found a diminished excretion of urea. This is 
perhaps due to a disturbance of the urea-generating function of the liver, about 
which both earlier and more recent investigators agree. In a few instances the 
urine has been found to contain a trace of sugar. As a rule, however, the urine 
contains no sugar whatever, not even when an attempt is made to induce an 
alimentary glycosuria. 

It remains for us to describe briefly the collateral circulation which may be 
developed in cirrhosis, so as to enable the blood of the portal system to reach the 
systemic veins. The clinical history of the disease does not indicate that this 
attempt at compensation is very successful. We may have : 1. Communications 
between the veins of the mesentery and of the abdominal walls. 2. Communica- 
tions between the coronary vein of the stomach and the veins of Glisson's capsule 
on the one hand, and the phrenic veins on the other. 3. Anastomoses between 
the internal hemorrhoidal and the hypogastric veins. 4. As pointed out by 
Baumgarten, enlargement of the not yet completely obliterated umbilical vein in 
the ligamentum teres. Through all these the blood may flow from the portal 
system into the veins of the abdominal walls — that is, in the reverse of the normal 
direction. Then in a few exceptional cases the veins around the navel become 
varicose, a phenomenon which has been termed the " caput Medusa?" Much more 
frequent and more important is the finding of unnaturally distended and tortuous 
veins in the skin of the abdominal walls, when there is ascites. These veins 
usually extend upward from the neighborhood of Poupart's ligament. This phe- 
nomenon is due to the fact that because of the ascites the flow of venous blood 
from the lower extremities through the iliac veins is impeded (vide supra), and 



560 



DISEASES OE THE DIGESTIVE OEGANS 



consequently a part of the venous blood takes its course through, the inferior and 
superior epigastric veins to the mammary veins. 

The complications which are seen in many cases are probably due in part to 
the same influences which occasion the cirrhosis. In this list belong, for exam- 
ple, cardiac hypertrophy, intestinal nephritis, and chronic pachymeningitis. Of 
special interest, because of its diagnostic and therapeutic importance, is the 
combination of hepatic cirrhosis with tubercular peritonitis. As we have already 
seen Cpage 531), hepatic cirrhosis is probably in most cases the primary disease, 
and occasions a predisposition to the development of tubercular peritonitis. The 
clinical picture in these cases is a combination of the symptoms of hepatic cirrho- 
sis, such as a palpable granular liver, splenic tumor, and yellowish complexion, 
with the symptoms of tuberculosis, such as irregular distention and tenderness 
of the abdomen, persistent fever, and emaciation. If we consider the aetiology 
(alcoholism), we may, therefore, sometimes make a complete diagnosis of this 
combination, particularly if at the same time the tuberculous inflammation at- 
tacks other serous membranes, such as the pleura. 

As to the general course of cirrhosis, its duration can not easily be determired 
because the onset is usually insidious. As a rule, the disease lasts one to three 
years, or rarely longer. In many cases the symptoms are insignificant for the 
first six to eighteen months. Then the disorder takes on a severer form, perhaps 
rather suddenly. Ascites appears, for example. These graver symptoms persist, 
until after a few months the patient dies. The course of the disease reminds one 
of cardiac cases, where for a long while the compensatory changes avert any dis- 
tress, until on a sudden the circulatory disturbances become pronounced and per- 
sist to the end. 

The prognosis is always unfavorable, at least when the symptoms have once 
become well marked. It may be that in the earlier stages the disease can be 
checked or even permanently cured; but even this is open to doubt. "No case 
recovers in which the diagnosis of cirrhosis is certain. 

Death is due either to intercurrent disease, or more often to gradually increas- 
ing exhaustion. In some few cases severe cerebral symptoms suddenly appear: 
there are coma, general convulsions, and delirium; and these usually are soon 
fatal. Just how these nervous phenomena originate we do not certainly know 
(see the chapter on acute yellow atrophy of the liver). 

Diagnosis. — The diagnosis of hepatic cirrhosis is not usually self-evident. It 
may be made with some positiveness if a patient who has a previous history of 
alcoholic excess gradually develops ascites and splenic tumor, and if upon palpa- 
tion we find the liver unnaturally firm and hard, either enlarged or shrunken, 
perhaps with a roughened surface, and in any case distinctly to be felt; yet in 
palpating the granular surface one is very liable to errors, and particularly the 
separate kernels of fat in the panniculus adiposus of the abdomen are apt to be 
mistaken by inexperienced observers for irregularities in the surface of the liver. 
The difficulties in the percussion of the liver have been already indicated. Often 
a patient does not come under observation until a considerable ascitic effusion 
has already taken place, so that physical examination of the liver and spleen is 
rendered very difficult, if not impossible. Then we must first exclude any general 
disturbance of circulation as a cause of the ascites. If the heart, lungs, and 
kidneys are found to be normal, and if there is no cedema in the upper half of 
the body, it is very probable that there is a local derangement of the portal circu- 
lation, particularly if the patient is positive that the abdominal enlargement was 
the first evidence of dropsy; but we have still to determine whether the cause of 
this derangement is cirrhosis of the liver. This may be assumed to be the case 
if the whole course of the disease warrants the assumption, and if the history 
furnishes that most frequent of all ^etiological factors, chronic alcoholism. Oth- 



CIRRHOSIS OF THE LIVER 



56 L 



erwise we must be cautious, for portal obstruction with precisely similar results 
may be due to other causes — such as the external pressure of tumors or portal 
thrombosis. Many forms of hepatic syphilis (q. v.) can not be differentiated from 
cirrhosis by mere clinical observation of the hepatic disorder. Here it is only the 
aetiology and the demonstration of other signs of syphilis that can justify the 
assumption that the disease in hand is of specific origin. It is often a great aid 
in diagnosis to examine the liver directly after tapping. The abdominal walls are 
then relaxed and soft, so that the liver may be made out very distinctly. It 
should be borne in mind that irregularities of considerable size are more frequent 
in hepatic syphilis (" lobulated liver"), while cirrhosis is suggested by a more 
uniform granulation. 

It is also very difficult in many instances to exclude chronic peritonitis. The 
aetiology may aid us. Other points are, that in chronic peritonitis there may be 
tenderness on pressure, the abdominal distention is less uniform, and there is no 
enlargement of the spleen. Another point is that the specific gravity of a simple 
ascites due to passive congestion is often below 1015, while an inflammatory exu- 
dation usually reaches higher figures. Haemorrhagic ascites, as a rule, indicates 
tuberculous or cancerous peritonitis. The combination of hepatic cirrhosis and 
chronic peritoneal tuberculosis (vide supra) may be diagnosticated with a certain 
probability if, besides symptoms of cirrhosis and peritoneal disturbance, there are 
definite indications of a tuberculous affection; such are a phthisical constitu- 
tion, persistent fever, and the existence of a tuberculous disease in some other 
organ, particularly the pleura. 

Treatment. — In treating hepatic cirrhosis the first necessity is a strict regu- 
lation of the diet. The earlier in the disease proper diagnostic rules are fol- 
lowed, the more likelihood of benefit. The most important principle in regulat- 
ing the diet is to avoid all ingesta which in any way might irritate or damage the 
hepatic cells. We forbid, therefore, all alcoholic beverages, or at most allow very 
small amounts merely to stimulate the appetite. We likewise forbid sharp spices, 
pepper, mustard, horse-radish, onions, and similar articles. In general, the 
amount of meat should be limited. We may allow milk, buttermilk, eggs, 
vegetables, and cereals. In suitable cases we may try the prescription of an 
exclusive milk diet for some weeks. Quite a number of authors report favorable 
results from a milk-cure of this sort, but the individual peculiarities of every case 
must be considered. 

If the disease has already developed we must resign ourselves to merely symp- 
tomatic treatment ; at least, the specific benefit which iodide of potassium is said 
to exercise in hepatic cirrhosis is very doubtful, and is probably based merely 
upon cases of syphilitic disease of the liver. 

The symptomatic treatment of hepatic cirrhosis has to deal mainly with the 
disturbances due to portal congestion, and the associated gastro-intestinal ca- 
tarrh. In such cases experience shows that the best results are obtained by the 
cautious use for a considerable time of laxatives. In early cases we should resort 
first to salines, particularly Carlsbad salts. We may prescribe artificial Carlsbad 
salts, dissolved in warm water, or the genuine Carlsbad water to be drunk at all 
times. If the patient's circumstances permit we may even recommend in suitable 
cases a visit to Carlsbad. Other appropriate health-resorts are Marienbad, Kis- 
singen, Ems, and ISTeuenahr. If the saline remedies are ill-borne we employ vege- 
table laxatives, such as rhubarb and aloes. In case there is already a consider- 
able degree of ascites, good results may sometimes be obtained by administering 
drastic purgatives, among which gamboge has earned a special reputation. Many 
observers have seen benefit from calomel, giving three times a day three grains 
(gramme 0.2) for a period of two to three days. Calomel may be given repeatedly 
in this way at intervals of from five to eight days. Of course, caution is necessary 
36 



562 



DISEASES OE THE DIGESTIVE OEGAXS 



in its employment. Probably it does good both as a laxative and also as a diuretic 
(vide infra). Sasaki, in Japan, has seen excellent results in hepatic cirrhosis 
from the administration of cream of tartar in considerable doses, two to four 
drachms (grammes 10 to 15) a day, associated with a nourishing diet, including 
milk and scraped raw meat. After all, however, laxatives should not be employed 
if they disturb the digestive apparatus. 

If ascites has already developed, we may administer diuretics besides the 
drastic purgatives ; trial may be made of acetate of potassium or sodium, squills, 
diuretine, and the species diureticas of the German Pharmacopoeia (containing 
lovage, rest-harrow, licorice-root, and juniper berries). English authorities rec- 
ommend the balsam and the resin of copaiba as particularly efficient in the vari- 
ous forms of ascites. The dose is about fifteen minims (gramme 1) a day. 
The best mode of administration is in gelatine capsules. This remedy occasions 
in some cases a rapid increase in diuresis, and a consequent diminution in the 
ascites. Sometimes, also, pure urea (2.5-4 drachms, grammes 10-15, daily, dis- 
solved in water) acts as a good diuretic. If the heart is feeble, digitalis may 
cause a decided increase in the amount of urine, and it is also worth while to 
try a combination of digitalis with calomel. 

If the ascites is so excessive as to occasion much local discomfort and to im- 
pede respiration, the removal of the fluid by paracentesis may afford relief. The 
details of this proceeding were given in the last section. Many physicians recom- 
mend tapping as early as possible, before it is absolutely necessary. The relief 
is said to be more lasting in that case; but this proposal has by no means met 
with universal assent, and, as a rule, the physician will not tap until the abdom- 
inal tension, the dyspnoea, and other symptoms occasioned by the ascites render 
it necessary. Unfortunately, the relief is only temporary, for the fluid collects 
again with great rapidity after tapping ; yet it is sometimes possible to delay the 
reaccumulation for a considerable time by compressing the abdomen with an 
elastic bandage, and by using the above-mentioned remedies (diuretics and digi- 
talis) directly after tapping. 

[In 1896 Drummond and Morison proposed an operation to relieve the venous 
stasis, by producing adhesions between the liver, spleen, and omentum and the 
parietal peritoneum. A few successful cases have been reported. Three known 
to one of the translators all died. — V.] 



CHAPTER VI 

BILIARY CIRRHOSIS AND HYPERTROPHIC CIRRHOSIS OF THE 

LIVER 

There are two forms of cirrhosis which differ in many respects from the dis- 
ease just described : they are called biliary cirrhosis and hypertrophic cirrhosis of 
the liver. Charcot and Hanot were the first to call attention to them. Since 
then the literature of the subject has become quite extensive, but all doubts 
and differences of opinion are not yet settled. 

1. Secondary Biliary Cirrhosis of the Liver. — Whenever there is retention of 
bile in the liver for any length of time, no matter what causes it, certain changes 
may result. The small and the medium-sized bile-ducts become distended, and 
granules of pigment are deposited, both in the interlobular connective tissue and 
within the acini themselves. Besides this, however, and undoubtedly because of 
the noxious influence of the retained bile, the hepatic cells not infrequently un- 



BILIARY CIRRHOSIS 



563 



dergo destructive changes. In accordance with the general rule, connective tis- 
sue gradually fills the gaps thus left in the parenchyma, and, more than this, the 
interstitial hyperplasia is so great as to increase the size of the organ. If, there- 
fore, there is persistent obstruction of the common duct by a gall-stone, or a cica- 
tricial stenosis, or a tumor pressing from without upon the duct, the liver will, in 
all such cases, be found to be larger, firmer, and richer in fibrous tissue than nor- 
mal — in a word, " cirrhotic." Hence this condition does not represent an inde- 
pendent disease, but is a result of chronic biliary retention, in whatever way 
occasioned. It is appropriately termed " secondary biliary cirrhosis." That re- 
tention is really the cause of this change has been proved by experiments, for it 
has been shown that ligature of the common duct in animals causes well-marked 
biliary cirrhosis. 

2. Primary Hypertrophic or Biliary Cirrhosis. — The secondary cirrhosis just 
described is due to occlusion of the large bile-ducts. There is also a not very 
common primary form of biliary cirrhosis, usually known as hypertrophic cirrho- 
sis. French authors have given it the name of " cirrhose hypertrophique sans 
ascite avec ictere," out of regard to its most important clinical symptom. That 
there is an essential difference between this form and the ordinary " atrophic " 
cirrhosis of Laennec is manifested by the clinical behavior of the disease. 

The specific cause of hypertrophic bilious hepatic cirrhosis is as yet entirely 
unknown. We can merely surmise that we have to do with a chronic inflamma- 
tory process, excited by some toxic or infectious agent, and that the process prob- 
ably originates in the small bile-ducts of the liver. 

Often this disorder attacks hard drinkers, but they are not by any means its 
only victims. While, in the common form of cirrhosis, ascites is usually the 
earliest grave symptom of disease, in hypertrophic cirrhosis a slight jaundice gen- 
erally appears simultaneously with the first indefinite symptoms of pressure in 
the region of the liver, languor, and anorexia. This jaundice rapidly increases, 
and persists throughout the illness. In ordinary cirrhosis there may be, as we 
have said, hardly any jaundice, or, at any rate, it is a rather late symptom, and 
even then it is seldom extreme. On the other hand, ascites, as a rule, is slight or 
absent in hypertrophic cirrhosis. It is true that there have been cases with great 
ascitic effusion, but it never comes till the disease is quite far advanced. 

On physical examination the liver is usually found to be considerably en- 
larged, and its surface is smooth, as a rule, or rarely it displays some low eleva- 
tions, due perhaps to variations in the fullness of the blood-vessels. In general 
there is said to be this important difference between the ordinary and the hyper- 
trophic forms, that in the latter the newly formed connective tissue evinces little 
tendency to contraction, so that the liver remains large, even late in the course 
of the disease, and does not shrink. This is certainly true of the majority of 
cases, so that after an illness of two or three years the liver is still found to be 
large and smooth; but further observations are necessary in order to determine 
whether there may not sometimes be contraction toward the end of the disease. 

Along with the chronic jaundice and the marked enlargement of the liver 
there is a third important symptom — viz., chronic splenic tumor, usually of con- 
siderable size. As there are no indications of portal obstruction, we must con- 
clude that the spleen is not enlarged from passive congestion, as is usually the 
case in ordinary alcoholic cirrhosis, but as the result of hyperplasia; and post- 
mortem examinations confirm this conclusion. The origin of the hyperplasia is 
not clear. In one case we found not only splenic tumor but a distinct hyper- 
plasia of many mesenteric and peritoneal lymph-glands ; which suggests the pos- 
sibility of infectious influences. A corroborative fact is that not infrequently 
the entire course of the disease will be marked by slight elevations of temperature. 
The other symptoms of the disease are in part the direct result of the jaundice, 



564 



DISEASES OF THE DIGESTIVE OKGANS 



such as the slow pulse, the itching, and the changes in the urine; while others, 
such as languor and weakness, are the results of the constitutional disturbance. 
The dejections are not always colorless and fatty, as in case of obstruction of the 
large bile-ducts. Many patients have a noticeable tendency to haemorrhage, par- 
ticularly to haematemesis. In the case mentioned above, the fatal termination 
was due to constantly repeated and profuse hEemorrhages from the stomach, for 
which the autopsy disclosed no anatomical cause in the stomach or intestine. It 
seemed as if the haemorrhages had taken place by diapedesis. 

The entire duration of the disease is about one or two years; but it may last 
much longer. The prognosis is almost always bad. Occasionally a case will 
exhibit marked temporary improvement or an apparent arrest of the disease, so 
that, in spite of the size of the liver, the patient is able to do light work. Death 
comes, when there are none of the above-mentioned haemorrhages, as a result of 
gradual exhaustion, or is suddenly ushered in by coma, convulsions, and other 
grave nervous symptoms, usually ascribed to cholaemia (vide infra). 

That a chronic hepatic disease of so peculiar a nature should be marked by 
peculiar anatomical changes would seem certain, even from clinical observation. 
In general, this view is confirmed, although further and careful investigations are 
much needed. Upon microscopic examination there is always found an abundant 
new growth of a tissue containing many cellular elements, surrounding the small 
bile-ducts of the liver. In other particulars the histological changes are very 
similar to those of ordinary hepatic cirrhosis. The new growth of connective 
tissue is found in the interior of the hepatic lobules, but this can scarcely be 
regarded as a radical difference. Still, one gets the impression that the entire 
pathological process of hypertrophic cirrhosis originates in the bile-ducts and the 
tissues surrounding them, while the changes of ordinary alcoholic hepatic cirrho- 
sis start from the branches of the portal vein. The absence of contraction in the 
new tissue of hypertrophic cirrhosis seems to be consonant with the fact that the 
anatomical changes suggest hyperplasia rather than inflammation (compare the 
changes in the spleen and the lymph-glands). 

The diagnosis of hypertrophic cirrhosis can sometimes be made with consider- 
able positiveness, and sometimes can merely be regarded as probable. The grad- 
ual development and persistence of jaundice and the presence of an enlarged liver 
and spleen, but usually without marked ascites, would suggest the disease strongly, 
especially if long-continued observation enabled us to exclude carcinoma and 
other diseases. Sometimes, however, it is very difficult to decide whether the 
biliary cirrhosis is primary or secondary, for the conditions giving rise to sec- 
ondary biliary cirrhosis (occlusion of the bile-ducts from scars, new growths, or 
calculi) may be obscure. A careful investigation into the history of the case 
with regard to biliary colic and similar symptoms might be decisive. Other fac- 
tors are the general course of the disease and the presence of a splenic tumor, 
unaccompanied by ascites. An enlarged spleen is scarcely ever seen in this way 
in ordinary chronic jaundice of obstructive origin. 

The treatment should conform to the principles laid down in the chapters on 
jaundice and ordinary cirrhosis of the liver. Sacharjin has lately recommended 
the persistent use of small doses of calomel — one grain (gramme 0.06) several 
times a day. 



ACUTE YELLOW ATROPHY OF THE LIVER 565 



CHAPTER VII 
ACUTE YELLOW ATROPHY 03? THE LIVES, 

Etiology. — Acute fatty degeneration of the liver occurs both as a primary dis- 
ease and as secondary to other hepatic disorders, or as a symptom of constitu- 
tional diseases. Secondary acute fatty degeneration in rare instances accom- 
panies severe acute infectious diseases, such as typhoid fever, recurrent fever, 
septicaemia, and puerperal disease. It also appears, with equal rarity, in the 
course of cirrhosis of the liver or of persistent biliary retention; and it is a con- 
stant phenomenon in acute phosphorus poisoning. Indeed, the effects of phos- 
phorus resemble the symptoms of primary acute yellow atrophy in many ways so 
closely, even post mortem, that formerly the two were often confounded. 

Primary acute yellow atrophy of the liver is a very rare but extremely severe 
disease which almost invariably leads to speedy death. There is generally no 
determinable cause, and its victims are struck down in blooming health. It is 
most common in young adult life between the fifteenth and thirty-fifth year. 
Children and elderly people have been occasionally attacked. Females are much 
more liable to the disease than males; and pregnancy increases the predisposi- 
tion to it. 

As we have said, we can not as a rule find any exciting cause. It is stated that 
sometimes the onset has been preceded by some violent emotional excitement, or 
excess in alcohol, or the like ; but how important these factors may be is not at 
all clear. 

It is an interesting fact that sometimes the disease becomes rather more fre- 
quent than usual, and endemic. For instance, several members of one family 
may be attacked. This favours a theory as to the nature of acute yellow atrophy 
which a majority of the present investigators seem inclined to adopt. The theory 
referred to is suggested not only by the whole course of the disease, but by the 
pathological appearances, and places it in the category of acute infectious dis- 
eases. It must be confessed that as yet we know nothing about the intimate 
nature of the infection. 

Pathology. — The chief change found post mortem is in the liver, and it has 
determined the name given to the disease. 

The liver is much atrophied, sometimes being only one half or one third its 
normal size. This makes its capsule often seem contracted and wrinkled. The 
organ is usually soft and flabby, so that in some places it seems as if the finger 
could be pressed into it. The color of the surface, and for the most part of the 
cross-section also, is yellow, like ochre or saffron; but the cut surface may be 
parti-colored, having red and yellow spots interspersed. Hence the names " red 
atrophy " and " yellow atrophy." The arrangement and relative extent of these 
patches may vary exceedingly. The red places look as if they had collapsed, and 
seem tougher than the yellow. They correspond, as we shall soon see, to the 
more advanced stages of the affection, while the yellow spots have undergone 
less change. The lobules are, as a rule, no longer distinguishable by the naked 
eye. Such lobules as can still be made out seem abnormally small and have a 
gray periphery. 

On microscopic examination, we find that the essential change is an intense 
and uniform fatty degeneration of the hepatic cells, affecting the entire paren- 
chyma. Only a few cells still retain their normal condition. The others are filled 
with large and small fat-globules, and many are already suffering evident disin- 
tegration and absorption. Where the degeneration is furthest advanced, fat, 
detritus, and pigment alone remain. Inasmuch as the lymphatics rapidly absorb 



566 



DISEASES OE THE DIGESTIVE OKGANS 



and remove the fatty and albuminoid grannies, there is finally little left except 
blood-vessels and connective tissue. The blood-vessels are frequently quite con- 
gested, and thus occasion that red color which the naked eye detects in the more 
advanced, broken-down portions. Ererichs made an interesting discovery, which 
deserves mention, of the existence of leucine and tyrosine crystals both in the 
parenchyma and in the blood-vessels. Bilirubine crystals also are sometimes 
found in the detritus, and more rarely in the interior of the hepatic cells. 

]STot only the liver, but many other organs present fatty degeneration: the 
heart in particular, the kidneys, and rarely the muscles ; but the process is always 
most intense in the liver. The skin (vide infra) and most of the viscera are evi- 
dently tinged with jaundice. 

Acute splenic tumor is invariably present. This suggests that the disease may 
be infectious. That the disease is a constitutional one is also to be inferred from 
the numerous ecchymoses in the skin and the interior of the body, especially in 
the mucous membrane of the stomach and intestines, in the serous membranes, 
in the pelvis of the kidneys and the kidneys themselves, and more rarely in the 
brain and heart. This, again, is like the grave septic diseases. The blood itself 
is dark, with few clots. Leucine and tyrosine have repeatedly been detected in it. 
The peritoneum and other serous cavities sometimes contain a considerable 
amount of serum. 

Clinical History. — The disease is usually divided into two stages, the first of 
which corresponds to the milder prodromal symptoms, the second to those severe 
symptoms which are alone characteristic. In many instances, however, the first 
period is wanting, or is so brief that the patient is plunged almost without warn- 
ing into the gravest condition. 

The prodromata in most cases consist of constitutional disturbances and mild 
gastro-intestinal symptoms. The patient is languid, without appetite, and disin- 
clined to exertion. There are headache, nausea, vomiting, slight pains in the gas- 
tro-hepatic region, and sometimes moderate fever. In a few days jaundice usually 
appears. This is almost invariably taken for an ordinary catarrhal attack. 

After some days, or it may be weeks, the second stage begins. The chief 
characteristic of this is the occurrence of grave nervous symptoms. First thera 
is violent headache, with sleeplessness and marked restlessness. The intellect is 
usually somewhat dulled even now, and articulation is slow and clumsy. The 
mental confusion usually advances very rapidly to a noisy and violent delirium. 
The excitement becomes at times maniacal. The patient screams and storms, and 
he can hardly be kept in bed. Often there are convulsive twitchings of individual 
muscles ; and there may be typical epileptiform attacks, but this is not common. 
After one or two days, or rarely longer, the excitement abates, and is followed by 
sopor, which soon passes into deep coma. At death the patient is usually per- 
fectly unconscious. It is exceptional for the excited stage to be wanting; in such 
cases the first nervous symptom is sopor. 

The cause of the nervous symptoms has not yet been explained in a way to 
silence discussion. The same theories which have been set up to account for the 
grave form of jaundice in general (see appendix to this chapter) have also been 
employed to elucidate the nervous phenomena of acute yellow atrophy. Thus, 
some refer them to cholaamia, some to acholia. In acute yellow atrophy of the 
liver it might also be that the primary specific processes of infection or intoxica- 
tion are factors in the development of the severe cerebral symptoms. 

The jaundice, which is present even in the first stage, afterward usually deep- 
ens. The urine contains bile-pigment, and many investigators have also found 
bile-acids in it. If these latter are present, it suggests that the jaundice is not 
(as was formerly believed) hematogenous — that is, the result of a destruction of 
red blood-corpuscles and the transformation of their pigment into biliary color- 



ACUTE YELLOW ATROPHY OE THE LIVER 



567 



ing matter — but is due rather to a retention of bile. ' Just how this retention 
arises we do not yet know definitely. The obstruction can not be in the large 
bile-ducts, for the gall-bladder is usually found empty. Hence the cause of the 
retention of bile and of the jaundice is probably a derangement of the smaller 
biliary passages within the liver. We should add that in a few rare cases there 
has been little or no jaundice. 

On physical examination of the liver during the last stage of the disease, there 
is usually a striking diminution of hepatic dullness, corresponding to the atrophy 
of the organ. Generally the first change to be detected is a contraction of the 
left lobe, as shown by the development of tympanitic resonance in the epigastrium. 
At the co mm encement of the illness, the hepatic dullness is normal or slightly 
increased in area. If the disease proves very rapidly fatal, the organ may never 
become very small. In most cases, though by no means in all, there are pain and 
tenderness in the hepatic region, but these are seldom so great as in phosphorus 
poisoning. 

The enlargement of the spleen has been already mentioned as an almost con- 
stant symptom of the disease. Even during life some increase of the area of 
splenic dullness can usually be made out, and some- 
times the spleen can be felt under the edge of the || . ^ 
Tibs. 

The occurrence of the haemorrhages, which have 
already been referred to under the pathological le- % X ? w/> 
sions, can often be demonstrated during life. The x.MMz ■ ' v 
cutaneous ecchymoses can, of course, be -eon. and ~ < 
the haemorrhages in the mucous membranes may 
give rise to haematemesis, bloody stools, bleeding W 
from the female genitals, or epistaxis. The litem- ij^^lt 1 H 
orrhages are due probably to the impaired nutri- ^liP 
tion and diminished resisting power of the vascular _ M , 

,, . , , . . , ,. . Fig. 63.— a. Leucine ervstals. b. 

walls occasioned by the grave constitutional disturb- Tyrosine crystals, 

ance. 

The condition of the urine in acute yellow atrophy is very interesting. The 
amount is either normal or slightly diminished, and the specific gravity is some- 
what increased. Often there is a trace of albumen. We have already mentioned 
the presence of bile-pigment. The point of chief interest, however, is one that 
Ererichs discovered and various others have since confirmed — namely, the great 
diminution of urea and the appearance in its place of several other substances, 
which are likewise the products of the decomposition of albuminoid matter, and 
represent, in all probability, the first steps in the formation of urea. Of these sub- 
stances, the most important are leucine and tyrosine. Their characteristic crys- 
tals can sometimes be detected by the microscope in the urinary sediment (see 
Eig. 63). The crystals may also sometimes be obtained by allowing a drop of 
the fresh urine to evaporate slowly upon an object-glass. The proper way, how- 
ever, to demonstrate these crystals is to precipitate the urine with basic acetate 
of lead, to remove the lead from the filtrate by means of sulphuretted hydrogen, 
and then to evaporate the filtrate thus obtained to the point of crystallization. 
There are some other abnormal constituents to be found in the urine besides 
leucine and tyrosine; but what their significance is we do not know. Among 
these are sarcolactic acid, oxymandelic (paraoxyphenylglycolic) acid, peptonoid 
substances, and large amounts of kreatine. 

It at once suggests itself that this disappearance of urea and appearance of 
leucine and tyrosine, which are regarded as preparatory stages in the formation 
of urea, gives valuable support to Meissner's and Von Schroder^ idea that this 
substance is manufactured in the liver. 



568 



DISEASES OE THE DIGESTIVE ORGANS 



As to the other organs little need be said. Vomiting is very frequent in the 
second stage, as well as in the first. It usually ushers in the severe cerebral symp- 
toms. The stools are, as a rule, clay-colored, as is usual in jaundice. There is 
generally constipation. The pulse is rapid, often reaching 140 to 160 beats per 
minute, and is also small and compressible. It is this acceleration of the pulse, 
contrasting with its usual slowness during the first stage, which, along with the 
vomiting, announces the onset of dangerous symptoms. The pulmonary signs 
are seldom marked, although there may be bronchitis or a pneumonia due to 
the inhalation of foreign substances. During the coma which precedes death 
respiration is usually hurried, and often deep and noisy. Sometimes it is 
irregular. 

The temperature is generally approximately normal. Toward the fatal termi- 
nation there may be a subnormal temperature. Still more frequently the tem- 
perature rises before death, and even sometimes grows higher after death, reach- 
ing 107.5° (42° C.) or more. 

In case the disease attacks a pregnant woman, abortion or premature delivery 
is almost certain to occur. 

The entire duration of the disease depends mainly upon the length of the first 
stage. This may be wholly absent, or may be brief, or may occupy several weeks. 
The duration of the second stage, reckoning from the occurrence of grave cere- 
bral symptoms, is generally only a few days (two to four), rarely a week. The 
termination is almost invariably fatal. In a few cases recovery has been ob- 
served. 

The diagnosis can not be made till the second stage. The symptoms of the 
first stage are indistinguishable from those of simple catarrhal jaundice. "With 
the development of the grave symptoms all doubt usually vanishes. The general 
course of the disease, the deep jaundice, the cerebral disturbances, the cutaneous 
ecchymoses, and the character of the urine, form a clinical picture resembling no 
other disease. The only cases where there can be any uncertainty about the diag- 
nosis are the exceptional ones in which there is no jaundice. It is of practical 
importance to distinguish this disease from acute phosphorus poisoning (q. v.). 
The differential diagnosis is to be made from the history of the case and from 
the following factors : 



Acute Yellow Atrophy of the Liver 

1. Prodromes are usually present, but 
may be absent. 

2. Jaundice develops early, sometimes be- 
comes marked. 

3. Liver seldom enlarged, becomes atro- 
phic from the start; pain in hepatic region 
not the rule. 

4. Maniacal delirium very frequent. 

5. Not infrequently fever, sometimes 
high fever. 

6. Leucine and tyrosine often found in 
the urine. 

7. Spleen often enlarged. 



Phosphorus Poisoxtng 

1. Prodromes are almost always present. 

2. Jaundice does not appear until rather 
late, and it may be slight to the end. 

3. Liver much enlarged until death, and 
very painful. 

4. Seldom marked delirium. 

5. Not infrequently fever is absent 
throughout. 

6. Leucine and tyrosine found in urine 
exceptionally. 

7. Usually no enlargement of the spleen. 



After what has been said, we need hardly add that treatment is unavailing. 
Usually laxatives are employed, particularly calomel. The nervous symptoms are 
combated by an ice-cap and baths and narcotics ; the vomiting, by opium and bits 
of ice; and the cardiac weakness, by stimulants. 



PERNICIOUS JAUXDICE. CHOL.EMIA AXD ACHOLIA 569 



APPEXDIX 

PEEXICIOUS JAUNDICE. CHOL.EMIA AND ACHOLIA 

Reference has been repeatedly made in the preceding chapters to the possibil- 
ity of the sndden supervention of grave nervous derangements in the course of 
various hepatic diseases. These nervous symptoms resemble one another so much 
in the different instances of their occurrence that we are forced to believe them 
always due to the same cause. 

These symptoms are relatively most frequent when there is chronic biliary 
retention. Whether this retention be the result, for example, of obstruction of the 
common or the hepatic duct, or of stenosis of the biliary passages from a carci- 
noma involving the opening of the common duct into the duodenum or that duct 
itself, the patient may quite suddenly fall into a condition which in many respects 
corresponds to the second stage of acute yellow atrophy just described. Grave 
cerebral disturbances declare themselves, with delirium, convulsions, and coma. 
There are haemorrhages into the skin and into the mucous membranes, and in a 
few days the patient dies. Usually the end is attended with high fever. We have 
ourselves seen a temperature of 107.4° (41.9° C.) in a case of cancer at the duo- 
denal extremity of the common duct. It is this group of symptoms which is usu- 
ally termed pernicious jaundice; but almost precisely similar phenomena may 
suddenly appear in hepatic cirrhosis, when there is no great degree of jaundice, 
if any. 

Exactly what produces these grave results in acute yellow atrophy and the 
other disorders just enumerated, we are not certain. In the main three theories 
have been propounded in explanation. The first theory, the latest champion of 
which is Leyden, attributes pernicious jaundice to cholaemia — that is, to the accu- 
mulation in the blood of the constituents of bile, and in particular of the biliary 
acids, as a result of absorption. This accumulation, it is said, is promoted by the 
paralyzing effect of the jaundice upon the activity of the kidneys. Opposed to 
this theory is the fact that these same symptoms may occur when there is no 
marked hepatogenous jaundice. 

Bouchard and other Erench physicians ascribe to the liver the function of 
rendering harmless the products of the decay of albuminous matters developing 
in the intestine, which may be absorbed and enter the circulation. Destruction of 
the hepatic cells would consequently lead to auto-intoxication with these intes- 
tinal ptomaines. In Germany this doctrine has gained few adherents. 

The view which we are most inclined to accept is that of Ererichs. He has 
given to the group of symptoms under discussion the name of acholia. These 
symptoms he ascribes to the pernicious influence of those substances which under 
normal conditions are manufactured by the liver into bile, but which in such cases 
accumulate in the blood and the tissues. As Ererichs himself has said, and we 
believe very justly, this view should be extended to include all other metabolic 
functions of the liver, and especially the production of urea. There is no doubt 
that the processes of metamorphosis are very active in the liver. That these 
should be incomplete when there is a severe anatomical lesion of the liver, or 
when there is persistent biliary obstruction, is very likely, and this limitation of 
activity might occasion an accumulation of all sorts of material in the blood. 
We may, therefore, regard acholia, using the word as Ererichs does, as entirely 
analogous to uraemia, which latter appears not only in diseases of the kidney but 
also when the ureters are obstructed. In this sense the name cholaeinia would 
be preferable to the term acholia, to represent a condition analogous to uraemia — 
taking the word cholaemia to mean the intoxication of the blood with all sorts of 



570 



DISEASES OF THE DIGESTIVE ORGANS 



substances due to the imperfect metamorphosis going- on in the liver, and not, as 
Leyden formerly held, the saturation of the blood with the completely formed 
components of the bile. 

The termination of cholsemia or acholia is almost always unfavorable. In 
cases of this kind there is usually marked fatty degeneration of the hepatic par- 
enchyma to be found post-mortem, as the anatomical expression of its suspended 
function. . 



CHAPTER VIII 

ICTERUS NEONATORUM 

{Jaundice of the New-oorri) 

Frequently the normal red color of the skin in children changes on the sec- 
ond, third, or fourth day after birth to a distinctly yellow, jaundiced hue. The 
yellow tinge is deeper on the face and trunk than on the extremities. There are 
no special digestive or constitutional disturbances. Still it may be taken for the 
rule that weaklings and premature infants more often present this jaundice than 
do vigorous babes. The abnormal hue is almost certain to vanish in a week or 
two, and leave no sequelae. The termination is unfavorable in those instances 
alone where there is some special complication, not directly connected with the 
jaundice as such. 

The aetiology is a disputed matter. A large number of theories of all sorts 
have been set up, no one of which to this day has gained universal acceptance. 
Formerly there was considerable tendency to regard the jaundice as hematoge- 
nous — that is, as due to the transformation of the pigment of broken-down blood- 
corpuscles into bile-pigment. Points which seemed to support this view are the 
light (not jaundiced) color of the urine and the yellow color of the stools (from 
bile). But more accurate examination has shown that the urine does contain 
biliary pigment, as do also the kidneys of such infants as happen to die during 
the existence of the jaundice; and the biliary acids have been clearly shown to 
be present in the serous transudations. It is therefore assumed at present by 
most authors that icterus neonatorum is hepatogenous; but how the biliary 
retention and consequent absorption are caused we do not know. Perhaps the bile 
is not ejected properly, from weakness, or the ducts may be narrow, or temporarily 
plugged by desquamated epithelium. Birch-Hirschfeld has called attention to 
the fact that after birth there is a tendency to considerable passive congestion of 
the liver, with resultant oedema of Glisson's capsule and pressure upon the inter- 
lobular bile-ducts. Probably more importance, however, attaches to a circum- 
stance which Hofmeier has noted, that in the first days after birth many red cor- 
puscles are disintegrated, and consequently there is a comparatively large secre- 
tion of bile. This might easily lead to congestion of the smallest bile-ducts and 
so to icterus; but it should be said this view has its opponents. Quincke has 
an entirely different explanation of icterus neonatorum. He goes back to an old 
theory enunciated by Peter Frank. According to this, the jaundice of the new- 
born is due to the absorption by the intestine of a large amount of biliary color- 
ing matter from the meconium in the large intestine. ISTow, if the ductus venosus 
remains open for some little time after birth, as it often does, this biliary pigment 
is carried not to the liver, but by means of the vena cava inferior directly into 
the systemic circulation. The meconium is rich in bile pigment, and moreover 
there is an abundant secretion of biliary coloring matter in the new-born, and 
in them bilirubine is not changed into urobiline in the intestine, and finally the 



SYPHILIS OF THE LIVER 



571 



renal secretion of the new-born is at first very scanty. Consequently, the absorp- 
tion of the bile-pigment from the intestine results in jaundice. 

It is well to mention in conclusion that in very rare instances there is complete 
congenital stenosis, or even entire absence, of the larger bile-ducts. Then deep 
jaundice comes on soon after birth, and is persistent. The children become ex- 
tremely emaciated, and, after a few weeks, inevitably perish. 



CHAPTER IX 
SYPHILIS OF THE LIVER 

^Etiology and Pathology. — Syphilitic disease of the liver occurs both when 
the syphilis is acquired and when it is congenital. Congenital syphilitic disease 
of the liver may be diffuse or localized, and it causes a cellular infiltration in 
either case. If the changes are extensive, the organ is hard and considerably 
enlarged; or, if the newly formed connective tissue has undergone contraction, 
the liver is smaller than normal, and its surface is uneven. In some cases of 
hereditary syphilis, distinct gummata of considerable size have been observed. 

In acquired syphilis, hepatic disease is one of the so-called tertiary symptoms, 
and does not usually develop, at least to any great extent, until several years after 
infection. Indeed, it may be a very late result. It may take the form either of 
a diffuse syphilitic hepatitis, or of circumscribed gummata or syphilomata. The 
diffuse hepatatis does not present essentially different anatomical appearances 
from those of ordinary cirrhosis, although in syphilis the changes are seldom so 
uniformly distributed throughout the organ. The gummata are the most char- 
acteristic, and the most important clinically. They may form separate tumors 
the size of an apple or even larger. The convex surface of the organ, particularly 
that portion near the suspensory ligament, seems to be a favorite location for the 
new growth. The same is true of the porta hepatis, where Glisson's capsule enters 
the liver. At the autopsy the gummata have in most cases already begun to 
undergo contraction. If so, the liver is usually smaller than normal, and trav- 
ersed in various directions by deep furrows, which divide it into lobes. These 
furrows are due to firm cicatricial bands, among the fibers of which we may 
sometimes find necrotic and cheesy vestiges of the gumma proper. Often there is 
evident syphilitic endarteritis in the smaller and sometimes also in the larger 
branches of the hepatic artery and portal vein. 

Clinical History. — Circumscribed syphilitic changes in the liver often give rise 
to no symptoms whatever. It is only when the disease comes to disturb the portal 
circulation that a series of symptoms result, which, for evident reasons, may be 
analogous in all essential points to the effects of ordinary cirrhosis. Whenever 
the syphilitic growths contract so as to obliterate a large number of branches of 
the portal vein, or whenever a gumma happens to be so situated as to compress 
the trunk of the portal vein itself, then the well-known results of portal obstruc- 
tion are inevitable, the chief being ascites and enlargement of the spleen. The 
disturbance of circulation often gives rise also to anorexia and digestive disorders. 
Experience shows jaundice to be rare in hepatic syphilis, but it may appear when 
the lesions involve the larger bile-ducts or a considerable number of the smaller 
biliary passages. 

On physical examination, the results vary according to the form and the stage 
of the disorder. Sometimes the larger gummata may be plainly felt through the 
abdominal walls, usually as flattened hemispheres. Frequently, also, we can feel 



572 



DISEASES OF THE DIGESTIVE ORGANS 



the edge of the enlarged organ, and can detect that the edge is less sharp than nor- 
mal. In other instances the separate elevations and prominences can be made 
out. The area of dullness on percussion of course varies in different cases. 

It deserves mention that hepatic syphilis quite often causes severe pain, some- 
times over the entire region of the liver and sometimes in just one spot. Pain is 
by no means felt in every case. With the pain there may be great tenderness 
on pressure. 

The course of the disease is usually tedious, and it may occupy many years. 
Probably, too, lesions exist in many cases long before there are any symptoms. 
Just as in cirrhosis, ascites is usually the first thing to attract the patient's atten- 
tion. Improvement and temporary arrest of the disease are more frequent than 
in ordinary cirrhosis. Still, in most cases, if the lesions are at all extensive, 
the termination is unfavorable. 

The diagnosis is not always easy. Usually the objective changes in the liver, 
the ascites, and the enlarged spleen, ind^ate hepatic trouble, but we are often 
unable to determine just what the trouble is. Naturally, the setiological factors 
are of great importance. In a toper we would think rather of the common form 
of cirrhosis. If there is a syphilitic history, or if we find scars in the throat, 
irregularities in the surface of the bones, or other signs of a specific dyscrasia, 
we would naturally ascribe the hepatic disorder to the same cause. As to special 
signs, if the prominences on the liver are rather large in contrast to the smaller 
granulations of common cirrhosis, syphilis is somewhat more probable. Severe 
pain in the right hypochondrium also suggests syphilis rather than cirrhosis. It 
should also be considered that the course of hepatic syphilis is usually much more 
protracted than that of ordinary hepatic cirrhosis. 

Treatment. — Whether we feel certain that syphilitic hepatitis exists, or merely 
suspect it, specific treatment should be tried. Mercury and potassic iodide should 
both be given, but probably the iodide is the more valuable of the two. These 
remedies can be successful only when the gummata are still in process of forma- 
tion. Our therapeutic efforts produce no impression upon the cicatricial bands, 
the contraction of which is the main cause of derangement. Indeed, even the 
absorption of gummata may not always have a favorable influence upon the 
patient, because of the mechanical disturbance due to the consequent cicatricial 
change. Hence, in general, the results of antisyphilitic treatment are not very 
favorable. 

For symptomatic treatment, the reader is referred to the chapter on cirrhosis 
of the liver. 



CHAPTER X 
CANCER OF THE LIVER AND BILE-DUCTS 

etiology and Pathology. — Primary cancer of the liver is very rare, but sec- 
ondary or metastatic cancer of this organ is met with often. The chief explana- 
tion of this latter fact is the slowness of the blood-current in the liver, which 
favors the deposition of the cancerous germs suspended in the blood. 

Secondary hepatic cancer may be a sequel to primary cancer of any organ. It 
is most often seen, however, when the primary growth lies within the portal sys- 
tem, in the stomach, intestines, rectum, oesophagus, or pancreas. In some in- 
stances the projection of the primary growth into the lumen of a branch of the 
portal vein has been directly demonstrated, thus furnishing an obvious source for 
metastasis. The secondary cancers in the liver may be very numerous. They are 



CAXCEE OF THE LIVER AXD BILE-DUCTS 



573 



found both within the organ and upon its surface. If superficial, they form flat- 
tened protuberances, which are often dimpled in the middle. If the new growth 
is extensive, the liver may be greatly enlarged, so as to occupy a great part of the 
abdominal cavity. 

As we have said, primary cancer of the liver is very unusual. It may occur 
either in the form of separate large nodules, or as a more diffuse cancerous infil- 
tration pervading the greater part of the organ. Histologically considered, the 
primary growths are of cylindrical-cell carcinoma, apparently originating from 
the epithelium of the minute bile-ducts, but also, according to some authors, some- 
times starting from the cells of the parenchyma. 

Primary cancer of the larger bile-ducts is of more frequent occurrence than 
genuine primary hepatic cancer, and therefore it is of more importance clinically. 
The gall-bladder may also be the seat of primary carcinoma. Erom these sources 
may proceed abundant metastatic growths in the liver itself. 

As to the aetiology of hepatic cancer we can be brief. The disease is most fre- 
quent in advanced life, from forty to sixty, following in this the general rule for 
cancer. Of special exciting causes, there is only one to be mentioned — that is, 
biliary calculi. As we have already remarked (see page 551), the formation of 
cancer subsequent to cholelithiasis has been observed so many times that mere 
coincidence is out of the question. 

Clinical History— Diagnosis. — Many small nodules of cancer, as well as large 
masses which are favorably situated, may exist in the liver without exciting any 
symptoms. If there is an undoubted primary cancer in another organ, such as 
the stomach, we must always remember the possibility of metastatic growths in 
the liver; but they can not be proved to exist, unless they alter appreciably the 
size or shape of the organ. Sometimes their existence may be inferred, when we 
observe either ascites and enlargement of the spleen from pressure on the portal 
vein, or jaundice from pressure on the bile-ducts. 

On palpation, we are often able to make out plainly one or more tumors in 
hepatic cancer. These tumors are in the region of the liver, and they are directly 
connected with it, as we can prove by marking out its limits by percussion and 
palpation. Another characterstic sign is that almost all hepatic tumors can be 
felt to move with respiration, on account of the inspiratory depression of the dia- 
phragm pushing down the liver and all that is joined to it. Percussion over a 
hepatic tumor almost invariably gives flatness, in contrast to the muffled tym- 
panitic resonance of many gastric tumors. 

The most characteristic condition is not a very rare one ; in it the liver is the 
seat of a very large number of cancerous nodules. In such cases the organ is 
usually much enlarged. Often we can detect by mere inspection a great, irregular 
prominence in the hepatic region, pressing forward the flabby, atrophied Walls of 
the abdomen, reaching down to the level of the umbilicus, or even lower, and 
moving with respiration. On palpation, we can feel most of the anterior surface 
of the liver, and the separate cancerous nodules scattered over it. These usually 
are as large as walnuts, or even apples, and they are often umbilicated. The 
lower or anterior margin of the liver can often be made out plainly, and it also is 
often the seat of nodules ; and we can sometimes feel nodules on the lower surface 
of the organ. 

The other clinical phenomena in hepatic cancer have several causes : (1) The 
primary disease, such as cancer of the stomach; (2) the general cancerous ca- 
chexia, as shown by languor, emaciation, and possibly a slight oedema of the 
ankles; and (3) the possible compression of the blood-vessels or bile-ducts. This 
compression is not infrequent, and produces a moderate or even a large ascitic 
effusion. Even in these instances the spleen is seldom much enlarged as a result 
of the passive congestion, because the universal emaciation and anaemia counter- 



571 



DISEASES OF THE DIGESTIVE ORGANS 



act the tendency to increase in size. Jaundice is relatively more frequent in 
cancer of the liver than is ascites. It is caused by compression either of the 
hepatic duct or of the minuter bile-ducts. On the other hand, however, we can 
easily see that hepatic cancer may exist without producing either icterus or 
ascites. 

The differential diagnosis of hepatic cancer from cancer in other organs is 
sometimes extremely difficult. This is particularly true of pyloric cancer, and 
especially so when the pylorus has become adherent to the liver, which often is the 
case. Cancers of the omentum and of the colon sometimes simulate hepatic 
cancer, but they seldom move so decidedly in respiration as do hepatic tumors. 
Given a new growth in the liver, it is usually comparatively easy to distinguish 
between carcinoma and other tumors. In case of syphilitic new growths, we have 
to consider the previous history and other signs of syphilis, also the eventual con- 
tractions and diminution in size of the liver, the usually longer duration of the 
disease, and the general condition of the patient. Echinococci have, as a rule, a 
much more regular shape, like a flattened ball; they seldom occasion marked 
cachexia, and also have a much longer clinical history. Large abscesses are very 
rare in our climate and they can usually be recognized by special objective condi- 
tions. Moreover, they cause fever (rigors), which is exceptional in carcinoma. 
Other primary tumors of the liver, such as sarcoma and adenoma, are very rare, 
and therefore of no great clinical importance. There is, however, one rare but im- 
portant tumor of the liver which we must mention — viz., melanotic sarcoma, which 
may appear as a secondary growth in the liver. It may be of enormous extent, 
either diffuse or nodular, and secondary to melanotic sarcoma of the choroid or 
of the skin. 

When we have decided that cancer of the liver is present, the question arises, 
Is it primary or secondary ? In the first place, primary cancer here is so rare that 
the probabilities are in favor of a secondary growth. Not infrequently the 
primary tumor can not be detected during life. Thus a small cancer of the 
stomach, or a flat oesophageal cancer, or carcinoma of the pancreas, are all easily 
overlooked. Cancer in the rectum may be detected by digital examination. If 
we find many nodules in the liver and no primary trouble elsewhere, then there 
comes the possibility that there is primary cancer in the gall-bladder or the bile- 
ducts. In rare instances palpation may discover the gall-bladder in a state of 
cancerous degeneration close underneath the liver ; but usually the viscus will be 
small and contracted, and the flat and ulcerating growth is not noticeable, except 
from the inside. It is particularly in those cases of hepatic cancer in which there 
is at an early period great and persistent icterus, without evidence of carcinoma 
in any other organ, that we should be most apt to think of primary cancer of 
the bile-ducts. 

The duration of hepatic cancer is usually not prolonged. The first decided 
evidences of its existence no sooner present themselves than marasmus and ca- 
chexia rapidly develop. The fatal end comes in a few months, or at latest within 
a year. i 

The prognosis is hopeless. Treatment can avail only to alleviate somewhat 
the patient's sufferings. 



ECHINOCOCCUS OF THE LIVER 



575 



CHAPTER XI 
ECHINOCOCCUS OF THE LIVER 

Natural History and Pathology. — Inasmuch as it is the liver which suffers 
most frequently from invasions of the echinococcus, we will here state the main 
general points relative to the troubles produced by this parasite. 

The taenia echinococcus (see Eig. 64) is a small tape-worm about four milli- 
metres long, and composed of four Joints. It inhabits the intestinal canal of the 
dog. The head is small and bears a beak which is provided with some thirty to 
forty hooklets, arranged in two rows. Behind the circle of hooklets are four 
suckers. The last joint of the taenia is by far the largest, 
and contains some five hundred eggs. Man is infected by 
ingestion of the eggs. The great frequency of the echino- 
coccus in Iceland is explained by the close intimacy of the 
Icelanders with their dogs. In Germany the echinococcus 
is most frequent in Mecklenburg and Pomerania. 

If a human being has become infected, the embryo 
pierces the intestinal wall, and is carried with the blood- 
current or the lymph-current to some remote organ. Most 
of the eggs no doubt are destroyed in the stomach, as may 
be inferred from the fact that multiple echinococci are 
much less frequent than solitary individuals. In a great 
majority of cases the embryo passes through a branch of the 
portal vein into the liver and there fastens itself; but the 
echinococcus may be developed in other organs — including 
the lungs (vide page 278), the bones, the brain, the kidneys, 
and the heart. A hydatid cyst develops from the embryo, 
and is filled with a non-albuminous fluid. The cyst is com- 
posed of an external cuticle of laminated structure, and 
an inner, parenchymatous layer, which contains muscular 
fibers and blood-vessels. Surrounding the cyst, as it lies in 
the infested organ, there is gradually developed a thick 
capsule of connective tissue. 

After the cyst has continued its growth for some four 
to six months, being now about the size of a walnut, there 
are generated upon the inner surface of the capsule, from 
the parenchymatous layer, so-called breeding capsules, con- 
taining numbers of echinococcus-heads, or " scolices. 7 ' 
Each scolex has four suckers and a circlet of hooks. It 
can draw itself into the breeding capsule and also produce a prominence upon the 
outer surface of the latter (see Eigs. 65, 66, and 67). The number of new-formed 
scolices in an echinococcus is very great. The sac grows very slowly up to about 
the size of a fist, or even larger ; its wall has a pale, yellow color, is transparent, 
and displays an extremely characteristic laminated structure. The firmly at- 
tached breeding capsules are visible from the outside through the walls, as minute 
points. 

The primary cyst often gives rise to secondary " daughter vesicles," and these 
to "granddaughter vesicles." Some of these are formed in the cuticle, others 
from the breeding capsules. In man they generally grow inward — that is, are 
endogenous (echinococcus hydatidosus) — and finally become detached. Hun- 
dreds of them may sometimes be found free in the liquid contents of the cyst. 
In animals the daughter vesicles are more often exogenous (echinococcus veteri- 



Fig. 64.— (From Heller.^ 
Taenia echinococcus, 
enlarged. Above, at 
the right, echinococ- 
cus, of natural size. 



576 



DISEASES OF THE DIGESTIVE OEGAKS 



novum seu granulosus). A peculiar kind of echinococcus, which was formerly 
regarded as a kind of new growth, is that called by Virchow echinocoocus multi- 
locularis. This is a resistant tumor containing much connective tissue, and per- 




Fig. 65. Fig. 66. Fig. 67. 

Figs. 65 and 66.— (From Heller.) Echinococcus scolices, free, drawn in and turned outward. 
Fig. 67.— Echinococcus hooklets. 



meated with numerous small alveoli. The gelatinous contents of the alveoli con- 
sist of echinococcus vesicles. The growth probably originates from a single germ, 
which by persistent exogenous proliferation invades the lymph-vessels (perhaps 
also the blood-vessels and the bile-ducts). 

The growth of a hydatid cyst is very slow, and it may continue for years. At 
lastj however, the echinococcus dies. The cyst then undergoes considerable 
though gradual contraction, and both walls and contents become fatty-degener- 
ated and calcined. In the mortar-like detritus it is usually possible to find some 
characteristic hooklets. 

Clinical Symptoms. — As long as the cyst in the liver retains moderate dimen- 
sions, there is usually no discomfort. Frequently the cysts perish and become 
calcified, without having ever attracted attention, and are found post-mortem 
merely by accident. 

If the cyst becomes very large, it causes a sensation of pressure and pain in the 
hepatic region. In rare instances, unusually large cysts, if situated on the convex 
surface of the liver, may crowd up the diaphragm so as to compress the lower 
portions of the lung and induce dyspnoea. In such cases we find on the anterior 
or posterior wall of the thorax an abnormal protuberance, with dullness and 
diminished respiratory murmur. If a large echinococcus grows downward into 
the abdominal cavity it occasions pressure, tension, and pain in the abdomen. 
Compression of the portal vein may lead to ascites, and compression of the bile 
duct, in rare cases, to jaundice. The tumor can usually be made out with ease 
by inspection and palpation. It is approximately hemispherical, smooth, not 
tender, and feels rather firm and elastic. There is often a sense of fluctuation, 
while the so-called hydatid thrill — to be elicited by quick pushes with the flat of 
the hand — is recognized distinctly in but few cases. 

The condition may be complicated (1) ^by rupture of the echinococcus-sac 
into neighboring parts, and (2) by secondary suppuration. Both occurrences 
may be apparently spontaneous, or the result of traumatic influences. 

Of the possible directions in which rupture may take place, penetration of the 
pleural cavity should be particularly mentioned. It usually results in an acute 
empyema. Here we have to do partly with secondary infection occasioned by 
pyogenic bacteria, and partly also, as it seems, with the influence of toxic sub- 
stances (toxalbumens) which are present in the echinococcus fluid {vide infra). 
Penetration into the lungs with rupture of the echinococcus-sac leads to severe 
pulmonary symptoms. The patient may cough up constituents of the bile and 
small echinococcus vesicles, or portions of the same. Perforation into the abdom- 
inal cavity occasions purulent peritonitis. If viable daughter-vesicles are set free 



ECHINOCOCCUS OF THE LIVER 



577 



in the abdominal cavity, they may settle on some fresh spot and continue to grow. 
As extreme exceptions are to be mentioned rupture of the echinococcus-sac into 
the pericardium, the bile-ducts, the intestine, the vena cava, and the pelvis of the 
kidney. 

Suppuration of an echinococcus in the liver leads to the clinical symptoms of 
hepatic abscess — increasing tenderness and fluctuation of the tumor, fever, aggra- 
vation of the constitutional symptoms, etc. Perforation of the abscess into 
neighboring structures may occur, in the same way as above mentioned. Spon- 
taneous recovery is possible but infrequent. In general, suppuration of an 
echinococcus-sac is a dangerous condition, unless there is surgical interference. 

We must devote a few words to echinococcus multilocularis of the liver. As 
has been said, the tumor in this case is large, very firm and hard, and with a 
surface which is either smooth or rough. Tenderness on pressure is exceptional. 
On the other hand there is a feeling of painful distention in the hepatic region. 
Comparatively often (H. Yierordt) there is jaundice, which may be extreme. 
The spleen is usually enlarged. The bodily condition is fairly good for a long 
while, but later marasmus develops, particularly if ascites or oedema occurs. 
Secondary suppuration in the interior of the tumor also leads to fever and rapid 
loss of strength. The disease lasts one to two years, sometimes much longer. 

Diagnosis. — The diagnosis of echinococcus of the liver depends chiefly upon 
the demonstration of a very slowly developing tumor in the liver, hemispherical, 
fluctuating, and painless, with no marked influence at first upon the general 
health. If the patient comes from a country where the echinococcus is particu- 
larly frequent, of course this renders the diagnosis easier. Formerly it was the 
custom to aspirate the tumor for diagnostic purposes. In this way we can, in 
many cases, obtain from the interior of the sac a light yellow non-albuminous 
fluid, which often contains sugar and succinic acid; and in it sometimes, but 
of course not invariably, are found upon microscopic examination the charac- 
teristic hooklets, or little pieces of the laminated membrane. Lately, however, 
physicians have become much more cautious about puncturing echinococcus-cysts, 
because the procedure is sometimes followed by symptoms which are probably due 
to the poisonous influence of the escaping contents of the cyst {vide supra). 
Not infrequently after puncture there occurs urticaria or severe toxic symptoms, 
such as collapse, vomiting, dyspnoea, diarrhoea, chills, and epileptiform attacks; 
and these may even prove quickly fatal, although occurrences of this sort are 
infrequent. They have brought great discredit upon the practice of aspiration 
for diagnostic purposes in case of echinococcus. 

The diagnosis of the multilocular echinococcus of the liver is always very 
difficult. If made at all, it demands a careful consideration of all the separate 
symptoms, and particularly of the general course of the disease, in order to dis- 
tinguish the condition from hepatic carcinoma, cirrhosis, or syphilis. 

Treatment. — Inasmuch as internal remedies, such as iodine and mercury, are 
absolutely useless, the only treatment of echinococcus is by surgical means. In 
case the echinococcus tumor causes little if any discomfort, the patient is usually 
loath to consent to an operation, but it should be recommended in all cases, for it 
protects the patient from the possibility of later dangerous developments, and in 
itself is no grave matter. A description of the many methods of surgical treat- 
ment will be found in the text-books on surgery. 



37 



578 DISEASES OF THE DIGESTIVE ORGANS 



CHAPTER XII 
CIRCULATORY DISTURBANCES IN" THE LIVER 

1. Hepatic anaemia is seldom extreme except in cases of profound general 
anaemia, and it has no clinical importance, so far as we are aware. 

2. Passive congestion of the liver is of frequent occurrence and is of impor- 
tance. It may arise in any disorder which disturbs the systemic circulation. It 
is oftenest seen in connection with heart disease, particularly mitral disease. It 
also follows pulmonary emphysema and chronic processes which result in con- 
traction of the lungs. The liver is enlarged and engorged. The hepatic veins 
being situated in the center of the lobules, this central portion becomes darkly 
pigmented, while the periphery of the lobules seems lighter colored. The periph- 
eral cells may even appear distinctly yellow, from a fatty infiltration which is not 
infrequent. In this way the cut surface comes to present that variegated appear- 
ance which has led to the name of " nutmeg liver." If the venous stasis be per- 
sistent, there is considerable atrophy of the hepatic parenchyma, involving espe- 
cially the cells near the center of each lobule. Thus the liver is somewhat re- 
duced in size in spite of the secondary increase of connective tissue, and its 
surface may become slightly granular. This is the " atrophic nutmeg liver " or 
" contracted liver due to passive congestion." 

The clinical phenomena are chiefly those caused by the hepatic enlargement. 
If chronic cardiac disease, emphysema, or some analogous trouble has occasioned 
congestion of the liver, the area of hepatic dullness is increased, and frequently 
we can feel the edge or even a portion of the anterior surface. In well-developed 
cases the liver reaches a hand's-breadth or more below the ribs on the right side. 
If there is also tricuspid regurgitation (q. v.), the liver is usually much en- 
larged and can be felt to pulsate distinctly if the palm of the hand is laid upon it. 
ISTot infrequently in passive congestion of the liver there is jaundice, which may 
be slight or quite well-marked. This is perhaps due to the pressure exerted by the 
distended blood-vessels upon the small bile-ducts in the liver, and perhaps also to 
the secretion of a particularly viscid bile containing less water than normal, and 
tending to stagnate. As we have already mentioned, the peculiar mixture of 
jaundice and cyanosis in the complexion of many cardiac patients is very char- 
acteristic. The secondary cirrhosis of the congested liver leads to ascites. We 
may suspect this condition of the liver in all cases of heart disease in which 
ascites is particularly well marked, in comparison with the slight oedema in other 
portions of the body. 

Quite often the congestion, if great, produces subjective disturbances. There 
is a feeling of pressure and weight in the hepatic region ; and if the capsule of the 
organ is tightly stretched, there may be actual pain. ' 

The prognosis and treatment depend, of course, upon the primary disorder. 

3. About active hyperaemia of the liver we have little definite information. 
Formerly there was a great deal said about it, as one of the conditions in " ab- 
dominal plethora." Active hyperaemia is most frequently assumed to exist in 
case of those who are good livers and of sedentary habit. In such, we are told, 
the temporary physiological hyperaemia which attends digestion passes on into a 
permanent congestion of the liver. Thereby the organ is enlarged, there are pain- 
ful sensations in the right hypochondrium, digestive disturbances, and occasional 
slight jaundice. The abnormal condition just described is certainly often met 
with in practice, but it would seem hardly possible to draw a clear dividing-line 



ATEOPHY AND HYPEETEOPHY OF THE LIVEE 



579 



between active hyperemia of the liver and other disturbances which give rise to 
similar symptoms. Such are chronic gastric and intestinal catarrhs; cardiac 
hypertrophy and functional cardiac derangement, with passive congestion of the 
liver ; fatty liver ; and incipient cirrhosis. 

A prominent factor in the production of active hypersemia of the liver is also 
ascribed to the ingestion of such matters as are said to " irritate " the liver, like 
the various spices, coffee, and, above all, alcohol. 

It should also be noted that the liver may be much engorged in many acute 
infectious diseases, particularly in pernicious malarial diseases and in typhus or 
typhoid fever. 

It is also maintained that the hypersemia may result from the cessation of 
haemorrhages elsewhere, such as the catamenia or bleeding from haemorrhoids. 
The facts that have been brought forward to sustain this view are none of them 
conclusive. We will mention that the " menstrual jaundice " which occasionally 
appears when the menses are scanty or absent has been referred to a vicarious 
hypersemia of the liver. 

It is, of course, impossible to make general statements about the course and 
duration of active hypersemia of the liver. The treatment of the first variety 
mentioned — namely, that arising from an improper mode of life — demands care- 
ful regulation of the diet, abundant exercise in the open air, such as horseback- 
riding, and laxatives. We may order rhubarb, aloes, or a course of the waters at 
Carlsbad, Marienbad, Kissingen, or Homburg. 



CIIAPTEE XIII 

ATROPHY, HYPERTROPHY, AID DEGENERATIONS OE THE LIVER 

1. Simple Atrophy of the Liver,— Simple atrophy is not of rare occurrence, 
being seen in senile marasmus, and in malnutrition from almost any cause. The 
degree of atrophy varies. The borders of the organ are much wrinkled. The 
lobules seem decidedly smaller than normal, and even the individual cells that 
still remain are atrophied and also usually deeply pigmented. 

The condition does not of itself give rise to any special symptoms. The area of 
hepatic dullness is usually lessened, but this sign is too ambiguous ever to justify 
us in making from it a diagnosis of hepatic atrophy. Perhaps there is some value in 
the alleged lighter color of the stools, as indicating a diminished secretion of bile. 

2. Hypertrophy of the Liver. — Even under normal circumstances the liver 
undergoes quite marked alterations in size. The exact point, therefore, where an 
abnormal hypertrophy begins can not be set. Sometimes the autopsy reveals an 

1 unusually large liver, of which there had been no indications during life, and for 
which no cause can be made out. 

There are certain diseases in which enlargement of the liver is found with 
comparative frequency: diabetes mellitus, chronic malarial poisoning, leukaemia, 
and sometimes rachitis. Topers quite often have enlarged livers, which as a rule 
present simple hypertrophic changes. Occasionally a liver has been reported as 
showing spots of localized hyperplasia, which may form flattened prominences 
upon the surface of the organ. 

Hypertrophy is to be diagnosticated only when palpation and percussion give 
proof of an enlargement, and yet amyloid, hypertrophic cirrhosis, and other dis- 



580 



DISEASES OE THE DIGESTIVE ORGANS 



eases which cause an increase in the size of the liver, can be excluded. The aeti- 
ology of the case should also be considered. 

3. Fatty Liver. — This name is applied to excessive, diffuse, fatty infiltration 
of the hepatic cells. The size of the organ is increased. It is firm, anaemic, and of 
a uniform yellow color, both externally and upon section. The microscope shows 
that the cells of the parenchyma are filled with large and small globules of fat. 
The fat is most abundant toward the periphery of the lobules. 

The causes of fatty liver are by no means clear. Sometimes it is found in 
cases of general obesity, where we may assume that the amount of fat which the 
liver receives as nourishment is abnormally great; but often we find a liver that 
contains comparatively little fat in those who have a well-developed panniculus 
adiposus and much fat in other organs. Topers may have a decidedly fatty liver. 
The occurrence of fatty liver in the cachectic, and particularly in the consump- 
tive, is remarkable; and individuals suffering from cancer, or marantic children, 
may also exhibit the same change. We have no intimate knowledge of the condi- 
tions that prevent, in such cases, the oxygenation of the fat which comes to the 
liver from the ingesta or from other organs. 

We do not know that the fatty liver is in any way functionally impaired. The 
only clinical indication, therefore, of its existence is the increased bulk of the 
organ. In phthisis we may sometimes feel pretty certain that the liver is fatty, if 
an increase in bulk can be demonstrated, and if other causes for this enlargement, 
such as amyloid degeneration, appear improbable. If the anterior edge of a fatty 
liver can be felt, it is usually found to be noticeably thick and blunt. 

The treatment of fatty liver is to combat the original disease. 

4. Amyloid Liver (Waxy Liver). — Amyloid degeneration of the liver is al- 
most invariably a part of extensive amyloid disease, involving also the spleen, 
kidneys, intestine, and other organs. The disease occurs chiefly in certain cachec- 
tic conditions, such as chronic suppuration, as in caries and persistent empyema, 
and also in chronic pulmonary tuberculosis, and constitutional syphilis. 

The amyloid liver is usually increased in bulk. The organ may even become 
almost double its normal size. It feels very firm and hard, its surface is perfectly 
smooth, and its edge is slightly thickened. The cut surface presents a character- 
istic grayish-brown " waxy " appearance. 

The microscope shows that the degenerative process attacks chiefly the walls of 
the hepatic capillaries, the hepatic cells proper showing infrequent and slight 
amyloid changes. Very often the cells of the parenchyma are atrophied and 
somewhat infiltrated with fat. 

The diagnosis of amyloid liver requires (1) the demonstration by palpation 
and percussion of hepatic enlargement. We can often feel a large part of the 
anterior surface and the margin of the hard and firm organ. The liver may reach 
as low as the level of the umbilicus. The diagnosis further demands (2) that 
some disease which predisposes to amyloid be present, and (3) that there be evi- 
dence of the degenerative process in other organs : the spleen should be enlarged, 
and the kidneys secrete an abundance of albuminous urine. 

The other symptoms, as well as the prognosis and treatment, are determined 
mainly by the nature of the causative affection. The use of iodide of iron, iodide 
of potassium, the alkaline carbonates, and ammonic chloride, respectively, has 
been recommended as particularly efficient, but therapeutic claims of this sort do 
not withstand a rigorous criticism. The chief point is the general improvement 
of nutrition by careful diet and nursing. Further particulars about amyloid 
disease in general will be found in the chapter on amyloid degeneration of the 
kidney. 



ANOMALIES IN THE SHAPE AND POSITION OF LIVEK 581 



CHAPTER XIV 

ANOMALIES IN THE SHAPE AND POSITION OF THE LIVEE, 

1. Corset Liver. — The constant pressure of the lower ribs against the liver, as 
a result of tight lacing, often produces an atrophy of the hepatic parenchyma 
from pressure, as shown by a deep furrow crossing transversely the anterior sur- 
face of the organ. This " corset furrow " lies chiefly in the right lobe. Its usual 
situation corresponds to the margin of the ribs, and the atrophy may be so extreme 
that the liver is divided into a large upper part and a small, usually roundish, 
lower portion, connected by a narrow isthmus of tissue. At the atrophic place, the 
connective-tissue capsule of the liver is almost always much thickened. Often 
the lower section can be bent upward as if attached by a hinge. 

This deformity of the liver is found quite often in elderly females, and rarely 
in men, as in soldiers. Unless extreme, it can not be detected during life, and it 
causes no discomfort. Even the bad cases do not, as a rule, occasion any special 
symptoms; but they can be clearly made out if the abdominal walls are lax. The 
deep transverse furrow can be felt, and also the lower section, with its usually 
blunt edge. Particularly in the case of old women we must bear this condition 
in mind, else we might easily confound it with some enlargement of the liver, 
such as amyloid or passive congestion, or even new growths. 

In some few cases a well-marked corset liver seems to cause especial symptoms. 
It occasions a constant feeling of pressure and tugging in the region of the liver. 
Sometimes there are attacks of violent pain, with peritoneal irritation and vomit- 
ing, and a mild degree of collapse. These have been regarded as the result of tem- 
porary congestion and swelling in the portion of the liver below the constriction, 
but we should view this explanation with reserve, and should bear in mind that 
in corset liver gall-stones are remarkably frequent (vide supra, page 544), and 
that consequently the symptoms mentioned may also be connected with chole- 
lithiasis. The treatment of such attacks, even when the diagnosis is doubtful, 
will in every case consist chiefly in absolute rest in bed, the employment of poul- 
tices or perhaps of an ice-bag, and a restricted diet. If there is violent pain, we 
must resort to narcotics. 

2. Movable Liver. — This name has been applied to a condition exceptionally 
seen in women with very lax abdominal walls, in which the liver sinks deep down 
into the lower portions of the abdominal cavity, probably as a result of an unnat- 
ural length of the suspensory ligament. The organ can be distinctly felt in its 
new situation, and can usually be brought back to a normal position with toler- 
able ease by means of external pressure. It is invariably very movable and it can 
be seen to change its place when the patient lies upon the side. In most cases 
there are at the same time the indications of universal enteroptosis, with which 
we have already become acquainted (see page 462). The interpretation of the 
symptoms present, such as pain and digestive disturbance, is consequently diffi- 
cult in most cases, especially if the patient is also neurasthenic and hysterical, 
which is not infrequently the case. The reader may compare on this point the 
chapter on movable kidney. Treatment is governed by the same principles as in 
the other forms of enteroptosis. Above all, trial should be made of a suitably 
applied and well-fitting bandage. 



582 



DISEASES OF THE DIGESTIVE ORGANS 



CHAPTER XV 

SUPPURATIVE PYLEPHLEBITIS 

{Purulent Inflammation of the Portal Vein and its Brandies) 

iEtiology.— -Purulent pylephlebitis is seldom a primary, idiopathic disease. In 
most instances it is due to the propagation of a suppurative inflammation of 
neighboring tissues to the walls of the vein. The main trunk of the portal vein 
is rarely directly attacked. Usually the process originates in the hepatic branches 
of the vein or in the veins of the portal system, and thence extends to the larger 
vessel. 

Perityphlitie abscess is the most frequent source of suppurative pylephlebitis. 
The inflammation involves a mesenteric vein, and thence extends upward. Other 
causes are gastric ulcer, intestinal ulcers, as in dysentery, splenic abscess, and 
purulent inflammation at the porta hepatis or within the liver itself, as in abscess 
due to gall-stones. The mode of production in these cases is precisely analogous 
to that in perityphlitie abscess ; but they are rare. 

A special form of pylephlebitis is observed in the new-born. Here the inflam- 
mation originates in the umbilical vein, and we need hardly say that the cause is 
a suppurative infection through the navel. 

In rare instances it has been found that pylephlebitis has resulted from the 
penetration into a vein of some foreign body that had been swallowed, such as a 
pin. Here, too, the true factors in producing the inflammation are, of course, 
the bacteria which adhere to the foreign body. 

Pathology. — Where the inflammation has attacked the vascular walls, the 
vein is thickened, and often the surrounding connective tissue is infiltrated with 
pus-cells and mottled with minute ecchymoses. If the vein is cut open, the intima 
is seen to be opaque and often superficially ulcerated. The lumen of the vessel 
is filled with a thrombus, which is usually to a great extent in a state of purulent 
softening, so that offensive purulent fluid flows out. The course of events is as 
follows : First, the wall of the vein becomes inflamed. As a consequence of this, a 
thrombus forms at the same place. The bacteria penetrate this thrombus and 
occasion its purulent softening. 

The extent of a pylephlebitis naturally varies in different cases. As a rule, 
little fragments become detached from the thrombus and enter the liver, produc- 
ing metastatic abscesses. Secondary suppuration may occur also in the lungs, 
kidneys, brain, and joints, so that we have all the anatomical characteristics of a 
general pyaemia. 

Clinical History. — Inasmuch as the primary, causative disease may be very 
different in different cases, it is impossible to delineate the disease comprehen- 
sively. It is, however, frequently ushered in by a number of symptoms, which 
render a diagnosis possible, at least in some cases, if the original disease has 
been recognized. 

The symptoms of suppurative pylephlebitis are in part due directly to the local 
disease itself, and in part are occasioned by the general pyaemia. One of the local 
symptoms is pain in the epigastrium. This is rare. It may radiate downward or 
laterally, according to the starting-place and extent of the inflammation. An 
inevitable result of the portal thrombosis is portal obstruction. The spleen be- 
comes considerably swollen, and, if the disease be not too quickly fatal, there 
is an evident effusion into the peritoneal cavity. The splenic enlargement can 
not be regarded as due merely to venous stasis, but is in part the " acute splenic 
tumor" of constitutional septic conditions. If the inflammation spreads from 
the branches of the portal vein to the neighboring bile-ducts, jaundice results. 



THKOMBOSIS OF THE POETAL VEIN" 



583 



This is seen quite often. Sometimes it is due also to the hepatic abscesses, or to a 
gall-stone which happens to cause trouble simultaneously. ISTow and then there is 
no jaundice whatever. 

Of the pyemic symptoms, hepatic abscesses come first. They are due, as we 
have said, to the conveyance of infectious matter directly into the liver by emboli. 
The one almost constant sign of their occurrence is a decided enlargement of the 
liver. When there are no hepatic abscesses, the organ usually retains its normal 
bulk. 

The course of the fever is very characteristic. As in other pysemic conditions, 
there are almost invariably great elevations, to 106° (41° C), or higher, accom- 
panied by rigors, and followed by marked remissions, with profuse perspiration. 
These onsets of fever occur at irregular intervals, either daily, or every two or 
three days. 

There are at the same time indications of constitutional septic infection, 
which keep increasing in severity. The pulse grows rapid and small. Intelligence 
is impaired. Somnolence and delirium come on, and the strength rapidly fails. 

There are other symptoms. Vomiting is frequently seen. The bowels are sel- 
dom constipated, but usually relaxed. The dejections may contain blood, because 
of the venous stasis. In some cases the inflammation extends so as to produce a 
fatal general peritonitis. It is noticeable that the urine is generally scanty, and 
the amount of urea is strikingly diminished. 

The disease usually runs a rather acute course. On the average, it lasts about 
two weeks, but it may occupy three or four weeks, or even a longer period. It is 
invariably fatal. At least, no cases of recovery are known. 

The diagnosis can sometimes be made with considerable positiveness. In other 
instances it is impossible to exclude other pyagmic conditions, or abscess due to 
gall-stones, etc. Important factors are the origin of the trouble — if it can be 
made out — the pysemic rigors, the enlargement of the spleen and liver, jaundice, 
epigastric pain, and the evidences of general sepsis. 

Treatment is unfortunately almost entirely useless. The fever is not affected 
even by large doses of quinine. All we can aim at is to support and relieve the 
sufferer as far as possible. 



CHAPTEE XVI 

THROMBOSIS OF THE PORTAL VEIN 

(Chronic Adhesive Pylephlebitis. Pylethrombosis) 

Etiology and Pathology. — Like suppurative pylephlebitis, chronic portal 
thrombosis is not an independent disease, but is the sequel of a great variety of 
pathological conditions. Marantic thrombosis is of rare occurrence, and is usu- 
ally formed toward the close of life, so as not to be of practical interest. Apart 
from this, almost all cases of thrombosis of the portal vein are due to a compres- 
sion and constriction of the trunk of that vessel or one of its main branches. This 
most often occurs in certain chronic hepatic diseases which involve a mechanical 
stenosis, either of the smaller branches of the portal vein within the liver, or of the 
vein itself, with resulting coagulation of the "blood within it. Chief among these 
diseases are cirrhosis and syphilis of the liver, which have repeatedly been ob- 
served to entail portal thrombosis ; but other diseases in the neighborhood of the 
vein may produce a similar effect. ISTew growths of various kinds may press upon 
the vessel, or chronic inflammatory hyperplasia of the connective tissue at the 
porta hepatis may act in the same way. This is illustrated in chronic peritonitis, 



584 



DISEASES OF THE DIGESTIVE OKGA^S 



whether circumscribed or diffuse, an example of the former being sometimes seen 
as an effect of duodenal ulcer. 

It was formerly held that many forms of so-called " lobulated liver " were due 
to a primary adhesive pylephlebitis. This is erroneous. These cases are probably 
all due to some primary hepatic disease, usually syphilitic. The size of the liver 
is little influenced by obstruction of the portal vein, even if long continued, for 
the hepatic artery suffices to supply all the blood required by the organ. 

The anatomical changes in pylethrombosis do not differ essentially from those 
seen in thrombosis of any other vein. If fresh, the thrombus is still red; later 
it grows harder, paler, and more friable. If the thrombosis has existed a long 
while, the clot becomes completely organized. We have observed this even in the 
main trunk of the portal vein. 

Clinical History. — The symptoms of portal thrombosis are those occasioned by 
the obstruction, and therefore such as we have already repeatedly met with, in 
connection with various hepatic diseases. The intensity and extent of these re- 
sults, as well as the time occupied in their development, depend, of course, upon 
the place and size of the clot. If it is the portal vein itself which is attacked, and 
if the thrombus is extensive enough to obstruct the flow of blood, then the signs 
of venous stasis are evident throughout the portal system. The spleen becomes 
much enlarged, as can be easily demonstrated by percussion and palpation. Soon 
ascites appears, as a result of the passive congestion of the peritoneal veins ; and 
from a similar condition of the gastro-intestinal veins arise catarrhal disorders, 
such as diarrhoea ; or, not so very exceptionally, there is repeated gastric and in- 
testinal haemorrhage. 

As we have seen, a collateral circulation may be developed (vide page 559), by 
which the venous blood of the portal system is enabled to reach the systemic 
veins. This explains why some of the symptoms of venous stasis may temporarily 
(perhaps permanently) vanish. We saw one case of portal thrombosis, the sequel 
to what was apparently a syphilitic disease of the liver, in which quite a large 
ascitic effusion appeared some six or seven times at intervals of three to six 
months, and under proper nursing and treatment, without aspiration, as often 
disappeared. The patient did not die till the illness had continued six years, 
and tapping had been required in all some fifteen times. At the autopsy the 
trunk of the portal vein was found to be converted into a fibrous cord, with a 
lumen which barely admitted a knitting-needle. 

In simple pylethrombosis there are no local symptoms such as pain. The con- 
dition of the liver depends upon the primary disease. It is possible that a moder- 
ate atrophy of the entire organ might at length ensue if the portal blood were 
permanently cut off from it. But, as we have said, any cirrhotic changes, or any 
" lobulation," are not to be regarded as the result, but as the cause of the throm- 
bosis, or at least as related to the cause. 

The course and duration of the disease are according to the nature of the 
original, causative trouble. ~No general statements can be made. 

The diagnosis of thrombosis of the portal vein is usually extremely difficult, 
and it can really hardly ever be made with absolute certainty. We may, indeed, 
recognize readily that there is some decided obstruction to the portal circulation ; 
but whether this be due to a thrombus, or to compression of the portal vein, or to 
the obliteration of a large number of the smaller branches of that vein within the 
liver, we can very seldom determine. Pylethrombosis may be regarded as prob- 
able, if no other possible cause of the portal obstruction seems likely, and if we 
are able to discover a cause for thrombosis. 

The prognosis is always unfavorable, although there may be, as we have said, 
great temporary improvement. Treatment must be symptomatic, and it follows 
in the main the principles set forth under cirrhosis of the liver. 



DISEASES OF THE PANCREAS 



585 



APPENDIX 
DISEASES OF THE PANCREAS 

The few facts of clinical importance that are known about the pathology of 
the pancreas are given below. 

1. Haemorrhages into the Pancreas. — Small haemorrhages occur in the pan- 
creas in cases of general haemorrhagic diathesis, marked passive congestion, severe 
acute constitutional infection, and trauma of the abdomen. These do not, as a 
rule, cause marked clinical symptoms. On the other hand, Klebs, Zenker, and 
others describe cases in which a more or less extensive pancreatic haemorrhage has 
been found at autopsy as the only demonstrable cause of death. The patients 
were previously in apparently perfect health and were vigorous, although usually 
corpulent individuals; and they died suddenly. Perhaps it was the influence of 
the haemorrhage upon the semilunar ganglia or the solar plexus which occasioned 
the speedy death. At any rate, we find in such cases the cavities of the heart of 
usual size and empty, while the abdominal vessels are distended with blood. The 
special causes which lead to the haemorrhage are not aways clear. In general, we 
probably must surmise a primary disease of the blood-vessels (syphilis, atheroma). 
It is noteworthy that a comparatively large number of cases have occurred in 
hard drinkers. Many cases also seem to be similar to those first described by 
Balser. These have an uncertain aetiology, perhaps infectious, and exhibit a mul- 
tiple necrosis of fat and of the pancreatic tissue — there being numerous minute 
necrotic foci in the pancreas and in the fat tissue of the mesentery. Extensive 
disorder of this kind is observed particularly in obese persons, but is not con- 
fined to them. Sometimes in cases of pancreatic haemorrhage death is extremely 
sudden and apoplectiform. In other cases the symptoms last from twelve to 
twenty-four hours before the fatal termination. The patient suffers from violent 
abdominal pain, vomiting, abdominal distention, and general collapse ; treatment 
is purely symptomatic. 

2. Atrophy of the Pancreas. — The organ may share in a general marasmus. 
There is sometimes also extreme atrophy of the pancreas in those who have died of 
diabetes mellitus (q. v.). 

3. Pancreatitis. — A few cases have been reported of what would seem to be a 
primary acute pancreatitis, usually haemorrhagic. The disease is certainly very 
rare. It begins with violent colicky pains in the epigastrium. Vomiting and 
collapse soon follow. The pulse grows small, the extremities become cool, and 
death is speedy. At the autopsy the pancreas is found to be much enlarged, and 
mottled with ecchymoses, or it even presents scattered foci of suppuration. The 
aetiology is unknown. It is most likely that the germs which excite the inflamma- 
tion originate in the intestines. Apparently there should be a sharp distinction 
made between primary pancreatic haemorrhage and acute haemorrhagic pancrea- 
titis, but formerly these two conditions seem often to have been confounded. 
Secondary abscesses of the pancreas are not infrequent in pyaemia. 

[Fitz, in the Middleton-Goldsmith lecture for 1889, threw much light on the 
aetiology and diagnosis of acute pancreatitis, which he subdivides into three ana- 
tomical forms — the haemorrhagic, the suppurative, and the gangrenous. He shows 
that the affection is not so rare as has been supposed ; that its victims are usually 
in middle life, fat, and good livers ; that it commonly originates by the extension 
of a gastro-duodenal inflammation along the pancreatic duct. 

" If the case does not end fatally in the course of a few days, recovery is pos- 
sible, or a recurrence of the symptoms in a milder form takes place, and the char- 
acteristics of a subacute peritonitis are developed." 



586 



DISEASES OE THE DIGESTIVE ORGANS 



In the differential diagnosis irritant poisoning, perforation of the digestive or 
biliary tracts, and acute intestinal obstruction are to be considered. The location 
of peritonitic symptoms, their suddenness of onset, the absence of apparently 
sufficient cause, and the age and habit of the individual are important points.] 

Chronic interstitial pancreatitis sometimes results from the extension of 
chronic inflammatory processes affecting neighboring parts. Eriedreich states 
that it sometimes is a primary disease in topers. Syphilitic lesions of the pan- 
creas have been observed, occasioning contraction and induration. 

There are no characteristic clinical symptoms which correspond to these vari- 
ous changes. The symptoms observed in the cases belonging in this category are 
digestive disturbances, indefinite pain, bodily weakness, emaciation, and anaemia, 
and they are so ambiguous that a diagnosis of the true condition is scarcely ever 
possible. If there were a single distinctive symptom, it would be one common to 
all sorts of grave pancreatic disorder — namely, the appearance of a large amount 
of fat in the stools. As we know, the pancreatic juice is an important factor in 
the digestion of fat, so that it is very natural for any great derangement of the 
organ to have this result; and yet the bile alone may render the ingested fat 
capable of absorption, so that in repeated instances there have been no fatty stools 
when the pancreas has been completely atrophied or degenerated. 

4. Cysts of the Pancreas. — After closure of Wirsung's duct by scars, concre- 
tions, or the like, cysts of the pancreas may form, as a result of the dammiog up 
of the secretion. These may become so large as to be felt as great tumors through 
the abdominal walls. In some instances they have been operated upon with 
success. Rarely, spaces are found in the neighborhood of the pancreas filled 
with a thick, slimy fluid. These seem to be associated with the above-mentioned 
peculiar multiple necrosis of fat and pancreatic tissue, but with regard to them 
further observations are desirable. 

5. Cancer of the Pancreas. — Primary cancer is the most frequent, and there- 
fore clinically the most important disease of this organ. As a rule, the new 
growth is situated in the head of the pancreas. It is usually of the medullary 
variety, though occasionally colloid. It may involve neighboring parts by direct 
extension, and a great many organs by metastasis; for example, the liver, peri- 
toneum, and lymph-glands. 

The clinical symptoms of cancer of the pancreas are very seldom so decided as 
to justify a positive diagnosis. Sometimes the secondary nodules can be detected 
in the liver, peritoneum, and elsewhere. Then we are left in doubt about the seat 
of the primary growth. Or the primary tumor may be plainly felt through the 
abdominal walls ; but then we can hardly ever exclude cancer of the stomach or 
of the omentum, and neighboring parts. 

The symptoms of pancreatic cancer, as a whole, resemble closely those occa- 
sioned by most cancers of abdominal organs. Usually the patient is elderly. The 
first symptoms are weakness, emaciation, and indigestion, or they are the result of 
compression. Often there is complaint of a persistent dull pain in the epigas- 
trium. If the portal vein is pressed upon by the tumor, ascites appears. If the 
common duct is compressed, there is jaundice. Icterus is an especially frequent 
symptom of pancreatic carcinoma. The dejections have repeatedly been observed 
to contain a large amount of fat (vide supra), but there may be none whatever. 
Osier remarks the noticeable frequency and large amount of the dejections, 
and the quantity of undigested muscular fiber which they contain, because the 
pancreas no longer performs its part in the digestion of albuminoids. Sugar is 
sometimes present in the urine, but by no means in every case. Marasmus in- 
creases, and usually at the end of six months or a year the patient dies. 

The diagnosis is difficult. It can be made with a certain degree of probability 
when there is a slowly growing tumor in the region of the pancreas, without 



DISEASES OE THE PANCKEAS 



587 



enlargement of the liver, but accompanied by jaundice, deeply-seated epigastric 
pain, glycosuria, and the above-mentioned abnormalities in the faeces. Usually, 
however, the clinical picture is by no means so characteristic, and it is often im- 
possible to avoid confusing cancer of the pancreas with cancer of the stomach, 
duodenum, gall-bladder, or other organs. 

The prognosis is absolutely bad. The treatment is merely symptomatic, with 
the aim of lessening the patient's suffering. 

6. Pancreatic Calculi.- — In the excretory ducts of the pancreas are sometimes 
found calculi of small or moderate size, consisting essentially of carbonate and 
phosphate of lime. The cause of their formation is as little settled as that of 
gall-stones (which see). Because of the obstruction caused by these calculi we 
have secondary dilatation of the ducts, secondary contraction and atrophy, and in 
some cases secondary inflammation and suppuration; these probably result from 
processes similar to those with which we have become acquainted, while consid- 
ering biliary calculi. There may be no symptoms. Sometimes, however, there is 
violent pain, either continuous or paroxysmal, also digestive disturbances, and 
occasionally the above-mentioned changes in the dejecta, and glycosuria. In only 
a very few cases has it been possible to find pancreatic calculi in the fasces. An 
absolute diagnosis can rarely be made. As a therapeutic measure Eichhorst has 
recommended the stimulation of the pancreatic secretion by means of injections 
of pilocarpine ; as a rule, treatment will be purely symptomatic. 



DISEASES OF THE URINARY ORGANS 



SECTION I 
Diseases of the Kidneys 
CHAPTER I 

GENERAL PRELIMINARY REMARKS UPON THE PATHOLOGY 
OF RENAL DISEASE 

Although some knowledge of the occurrence and significance of renal affec- 
tions had been acquired even by the older physicians, still the service of having 
pointed out the frequency of these diseases, and of having clearly recognized their 
most important anatomical forms and their chief clinical symptoms, belongs 
undoubtedly to the English physician Richard Bright, who was born in 1788 and 
died in 1858, as physicion in ordinary to Queen Victoria. Bright's first work on 
this subject appeared in the year 1827. In this he brought forward the special 
discovery that, in many cases of general dropsy, which are associated with the 
secretion of an albuminous urine, a primary affection of the kidneys must be 
regarded as the true cause of the disease. Since then, the disease described by 
him has been almost universally called " Bright's disease " (" Morbus Brightii "), 
a name still much employed, but in whose stead the anatomical terms would be 
more proper, since many forms were previously classed under it which, according 
to our more accurate present knowledge, must be separated. 

Bright's statements were either confirmed or expanded in subsequent times by 
many other observers. Christison, Osborne, and R. Willis in England, and Rayer 
and M. Solon in Prance, were the chief students of renal diseases. Ererichs pub- 
lished the first great work in Germany in the year 1851. His division of Bright's 
disease into three different " stages," based on Reinhardt's histological investiga- 
tions, was for a long time quite generally accepted, until gradually further clin- 
ical experience showed that it was untenable. A more accurate division of renal 
diseases was substituted for it first in England (Johnson, S. Wilks, and others), 
and then in Germany (Traube, Bartels). However admirable these labors, espe- 
cially the work of Bartels in 1871, renal pathology fell into subjection to the- 
ories, with which the facts of experience could be harmonized only by force. 
Only of late years has a natural theory of renal diseases, derived from general 
pathological observations, at last become accepted — a theory which is based chiefly 
upon the anatomical work of Weigert. 

The following presentation of renal pathology is intended to show that, from 
a clinical standpoint as well, the renal diseases may be viewed comprehensively as 
a unit, and this not in a schematic way, but with due regard to actual conditions. 

The chief reason why the kidneys are so often diseased, either alone or in con- 
junction with other organs, is to be found in the fact that the body must eliminate 
all forms of injurious matter, which circulate in the blood, in great part by the 
kidneys. Consequently the action of any injurious substance is often manifested 
588 



REMARKS UPON THE PATHOLOGY OF RENAL DISEASE 589 



chiefly in the kidneys, and they must, in a certain measure, suffer for the service 
which they do the rest of the body. According to their nature and character, the 
injurious substances, which are here to be considered, are divided chiefly into two 
great groups — the chemico-toxic and the organized infectious substances. At the 
same time, it should be noted that in case of infection it is comparatively excep- 
tional for the germs themselves to reach the kidneys and there fix themselves. 
Most cases are referable to toxines, which are formed in the body as the result 
of the infectious process, and, being excreted through the kidneys, produce a 
nephritis. In this way the kidneys may be involved sympathetically after the 
ingestion of many poisons, both organic and inorganic, and also in the great 
majority of all the infectious diseases. In these cases, of course, as we shall see 
later, certain chemical and infectious poisons exert their action in a particularly 
frequent and in a particularly severe or definitely characterized fashion. Resides 
these forms of origin for many renal diseases, which are the chief ones to be con- 
sidered, we must consider other causes of disease which are much rarer. One way 
in which the morbific agents may also enter is especially important — namely, 
from the lower urinary passages, the bladder, and pelvis of the kidney, upward 
into the kidney. In this way those renal diseases arise which come on secondarily 
to cystitis, pyelitis, etc. Finally, of course, disturbances of circulation and 
mechanical injuries may also make themselves manifest in the kidneys. 

The clinical symptoms which are caused by the different forms of renal dis- 
ease are referable only in very small part directly to the diseased organ itself. In 
renal diseases characteristic subjective local symptoms — such as local pain — are 
rare, and the anatomical position and the physiological conditions of the kidneys 
make it almost impossible to discover any changes in their size, their physical 
consistency, etc., by a direct objective examination. In the diagnosis of renal dis- 
eases we are therefore confined chiefly to the investigation of two groups of symp- 
toms : in the first place, to the examination of the secretion from the kidneys, the 
urine, whose character, as we know by experience, may be materially altered when 
there is renal disease; and, in the second place, to the discovery of certain phe- 
nomena in other portions of the body, which are immediately dependent upon 
the renal affection. Since both the pathological changes in the urine, and the 
symptoms in other organs occurring in renal affections, have much in common 
in almost all the forms of renal disease, it is advisable first to describe the main 
features, at least, of the general symptomatology of renal diseases. We shall then 
be obliged, in the following chapters, to mention only the precise circumstances 
of the occurrence and onset of each symptom — the general significance of the 
symptoms being already known. 

1. Albuminuria 

The most constant symptom, which in many cases, even by itself, renders 
the diagnosis of a renal affection possible with complete certainty, is albuminuria 
— that is, the appearance of albumen, and especially of serum albumen and serum 
globuline (paraglobuline) , in the urine. From recent investigations (Leube, 
Fiirbringer, and others) we know that in some cases the urine may contain a very 
slight amount of albumen even in healthy persons, especially after physical exer- 
tion, emotional disturbance, a cold bath, a hearty meal, etc. Indeed, we find occa- 
sionally in some few individuals, particularly in early years, marked albuminuria, 
especially in the urine of the daytime, while the night urine never contains a 
trace of albumen; and yet these persons are apparently in perfect health. This 
has been called intermittent or functional albuminuria (vide infra). Yet it is 
at least questionable if such a condition, even if no symptoms are associated with 
it, can be regarded as physiological, and these facts do not impair the justice of 
the dictum that every case of persistent excretion of albumen in the urine, which 



590 



DISEASES OF THE UEESTAEY OKGAJSTS 



can be demonstrated clearly by ordinary methods, is to be regarded as somewhat 
pathological. 

The detection of albumen in the urine for clinical purposes, wherein no regard 
need be paid to the separation of serum albumen and serum globuline, is per- 
formed almost exclusively by means of the so-called heat test. If the urine is 
cloudy, it must be filtered before heating. The reaction of the urine must always 
be tested first. If the reaction of the urine is acid, as it ordinarily is, it is heated 
in the test-tube without any further addition. If the urine is neutral or alkaline, 
then, and only then, we acidify it slightly before boiling, by means of a few drops 
of dilute acetic acid. If the urine contains albumen there will appear, upon boil- 
ing, a distinct flocculent precipitate of coagulated albumen. The possibility of an 
error lies in the fact that sometimes, with a neutral or faintly acid urine, upon 
heating there appears a cloudiness because of the phosphates and carbonates 
which are precipitated. These are salts of lime and magnesia. In order to avoid 
confounding such phosphatic deposit with a deposit of albumen, we must in every 
case after the urine has boiled for a short time, if there is any deposit formed, add 
a few drops of nitric or acetic acid. By this means the deposit of phosphate or 
carbonate is immediately dissolved, while a deposit of albumen is not affected. 
The change in the color of the urine, which is sometimes caused by the addi- 
tion of nitric acid, is due to the action of the acid upon the urinary pigments. 
We can measure the amount of albumen contained in the urine approximately 
by the height of the settled precipitate in the test-tube. We often speak of 
" one-half or one-fourth of the volume being albumen," but we can not state 
any definite relation between this estimate of the volume and the precise amount 
of albumen. Approximately, however, a deposit of albumen, which upon settling 
occupies about half the volume of the urine, corresponds to about one per cent, by 
weight of albumen ; a deposit of about one-third of the volume to about one-half 
per cent, of albumen, and so on. 

Besides the test by boiling there is a very distinct test which can be highly 
recommended to practitioners, in which acetic acid and ferrocyanide of potassium 
are employed. A rather large amount, perhaps one-tenth of the volume, of acetic 
acid is added to the urine, and then a few drops of a ten-per-cent. solution of 
ferrocyanide of potassium are added to the mixture. If the urine contains albu- 
men there is formed a distinct deposit. This reaction usually takes place at 
once, but if the amount of albumen is very small, it may be somewhat delayed. 

If we have found out that the urine certainly contains albumen, we must then 
decide whether we have really a true renal albuminuria — that is, whether a urine 
already albuminous is secreted in the kidneys, or whether the albumen is not 
mixed with a perfectly normal or at least non-albuminous urine later, in the kid- 
neys themselves or in the urinary passages, the pelvis of the kidney, or the bladder 
(spurious, accidental albuminuria). Such a spurious albuminuria occurs when 
the urine is contaminated with blood (as in haemorrhages from the kidneys, the 
pelvis of the kidney, the bladder, or the urethra), or with pus (in pyelitis, cystitis, 
etc.). In these cases, of course, the albumen contained in t]ae serum of the blood 
or pus is found in the urine. Spurious albuminuria is usually easily recognized, 
since the presence of pus or blood in the urine, which is shown by the appear- 
ance of the urine or upon microscopic examination (red blood-corpuscles, pus-cor- 
puscles), points with immediate certainty to the origin of the albuminuria. 
Moreover, the amount of albumen in these cases is usually but slight, and corre- 
sponds to the amount of pus or blood in the urine. A disproportion in this respect 
must excite the suspicion whether, beside the spurious albuminuria, there is not 
perhaps at the same time an affection of the kidneys causing a true renal albu- 
minuria. The determination of this point is not always perfectly easy, but we 
can usually come to a decision by finding abnormal morphological constituents 



REMARKS UPON THE PATHOLOGY OF RENAL DISEASE 591 



in the urine, the so-called urinary casts (vide infra), which give indubitable evi- 
dence of the existence of a disease of the kidneys. 

What general pathological significance has the true renal albuminuria, and 
what are the causes of its origin ? According to our present theories, the answer 
to these questions is simply this : In every case of genuine albuminuria there is 
an abnormal transudation of the albumen of the blood into the urine. The 
place of this transudation is chiefly the glomeruli, and its immediate cause is the 
abnormal permeability of the walls of the glomeruli, due to disease of those struc- 
tures, and particularly of their epithelium. The fact that the easily filtrated 
serum albumen of the blood, as well as the water, does not pass through the 
vascular loops of the glomeruli, even under normal conditions, is due entirely to 
the circumstance that the capillaries of the MalpigMan bodies are not inserted 
bare into the beginning of the uriniferous tubules, but that they are covered with 
epithelium. This epithelium of the glomeruli has the physiological task and the 
power of providing for the retention of the albumen in the blood. If it suffers a 
pathological change in any way, it loses this power, and then the albumen passes 
into the urine (Heidenhain). The inflammatory changes which the walls of the 
blood-vessels themselves undergo probably facilitate the transudation of serum 
albumen, as is suggested by what we know about inflammatory exudations in 
other parts of the body. The best experimental proof of the theory that the 
changes in the walls of the glomeruli are the chief cause of the appearance of 
albumen in the urine is furnished by the albuminuria which appears whenever 
the supply of arterial blood to the kidney is checked by a temporary constriction 
of the renal artery. The epithelium of the glomeruli thereby suffers a visible 
microscopic change. If the kidneys in this condition are removed as rapidly as 
possible and boiled, according to Posner's suggestion, we can discover under the 
microscope in the capsules of the glomeruli the albumen that is thus coagulated 
(Pibbert) — a most certain sign that the passage of the albumen from the blood- 
vessels into the urinary passages has in fact taken place in the glomeruli. 

Almost all cases of albuminuria may readily be referred to analogous disturb- 
ances of nutrition in the epithelium of the glomeruli, whether they be excited by 
anomalies of the circulation, such as arterial anaemia or venous stasis, by toxic or 
infectious influences which have reached the glomeruli, or by any other circum- 
stances. In these cases the changes in the glomeruli need not always be of a 
very severe or irreparable nature; for we often see a slight albuminuria appear 
under the most different conditions, and rapidly pass off again. This is the so- 
called "transitory albuminuria," which is seen, for example, in various febrile 
affections, after slight intoxications, after epileptic attacks or in other severe 
nervous conditions, in lead-colic, etc. We will show later how the anatomical 
changes in tl\e glomerular epithelium explain the occurrence of albuminuria in 
severe renal diseases. 

The other factors, which have also been made answerable for the origin of 
albuminuria, are without doubt quite subordinate to the changes in the epithe- 
lium of the glomeruli, and at most they can affect merely the amount of albumen 
eliminated. The changes in the composition of the blood, on which formerly, and 
again by some investigators recently, great stress has been laid, especially the hy- 
draemia and hypalbuminosis (the diminished amount of albumen) of the blood, 
have probably only an indirect significance, since the nutrition of the walls of 
the glomeruli suffers from such a faulty condition of the blood, and this circum- 
stance again is the true cause of elimination of the albumen. 

The significance of the blood-pressure with regard to the occurrence of albu- 
minuria was also formerly very much overrated. According to the older hypoth- 
esis, it was believed that, in an increase of the blood-pressure, the molecules of 
albumen in the blood could be pressed through the filter formed by the membrane 



592 



DISEASES OF THE TTRISTARY ORGANS 



of the glomeruli. This hypothesis has heen disproved, especially by the experi- 
ments of Runeberg ; these experiments showed that, in the filtration of solutions 
of albumen through animal membranes, a rise in the filtration pressure was fol- 
lowed by a decrease, and a fall in the pressure by an increase of the percentage of 
albumen in the filtrate. 

Although in the preceding paragraphs only the Malpighian bodies have been 
regarded as the spot where the transudation of the albumen of the blood into the 
urine takes place, we must also note that, under some circumstances, we may 
admit the possibility of a passage of albumen directly into the tubules from the 
capillaries that encircle the uriniferous tubules; but we must also necessarily 
assume in such cases that there is a disturbance of nutrition in the membranse 
propriss, or at least in the epithelium of the uriniferous tubules. Such an assump- 
tion seems to explain the albuminuria, according to Senator's experiments, in 
venous stasis in the kidneys, although in these cases the epithelium of the glome- 
ruli also suffers soon, and then becomes pervious to albumen. 

2. Casts and other Abnormal Morphological Constituents of the Urine in 

Renal Disease 

Beside albuminuria, certain peculiar morphological constituents of the urine, 
visible under the microscope, are of especial importance for the diagnosis of renal 
affections — the urinary casts, whose significance was first correctly recognized by 

Henle in 1842. These are cylindri- 
cal bodies, whose breadth corre- 
sponds to the width of the urinif- 
erous tubule, and whose length only 
exceptionally reaches a millimetre, 
which must be regarded in their 
chemical nature as consisting main- 
ly of a coagulated albuminous sub- 
stance. To the latter circumstance 
we owe their old name of " fibrine 
casts," or " fibrous casts," a name 
which is obsolete, and properly so, 
since the coagulated albuminous 
substance of casts is certainly not 
identical with fibrine. 

Since the precise conditions of 
the occurrence and the character of 
the renal casts, in the different dis- 
eases of the kidneys, will be spoken 
of later, we need discuss here only 
the general properties, the origin, and the significance of casts (see Fig. 68). 

1. Hyaline Casts. — The hyaline casts are the commonest and most important 
form of casts, and, to a certain extent, are the ground-form for different varieties. 
They are perfectly homogeneous, clear as glass, colorless, soft, and flexible. \Ye 
find them either wide or narrow, sometimes broken off short, sometimes quite long, 
usually straight, but in many cases partly curved. They are easily stained with 
carmine or gentian-violet. On heating the urine, they are dissolved, but they are 
quite resistant to acids. 

The hyaline casts are very often covered to a greater or less extent with all 
sorts of deposits, which are usually affixed to the soft substance of the cast in the 
kidney itself, but which may often be attached to it later. These deposits are as 
follows: First, red blood-corpuscles. This condition is important, because it 
points with certainty to the existence of haemorrhages in the kidneys themselves. 




Fig. 68.— Different forms of casts, a. Hyaline cast with 
occasional granules, b. Hyaline cast with fat-drops 
and granular cells, c. H3 T aline cast with red blood- 
corpuscles attached, d. Hyaline cast with white 
blood-corpuscles attached, e. Cast with a large 
number of fat-drops. 



EEAIAEKS UPOX THE PATHOLOGY OP EEXAL DISEASE 593 



Ssecona. ca w 
we must gut 

linm tt4 



blood-corpuscles. These are often considerably swollen, so that 
gainst mistaking them for epithelium, Third, of renai epithe- 
may be recognized by its size., its more angular shape, and its nuclei, 
■we often find the epithelium cloudy and gTanular, or shriveled and 
of fatty granu- ^ lar globules — that is, both fatty-de- 
white blood-corpuscles which are filled 
generated cells. Fifth, of little gran- 
always be easilv recosrnized. They 



a 1 



bumen, or 




hseinatoidine, 



fat-drops, or urates, or 
which have come from 




Ut ecu 

atrophied. Fourth, of fatty granu- 
generated epithelium and also 
with fat-drops from the fatty-de- 
ular masses whose nature can not 
are either coagulated granules of 
bacteria, or, finally, granules of 
the destruction of red blood-cor- 
puscles, and are usually easily rec- 
ognized by their dark, brownish- 
yellow color. Sixth, we rarely find 
in the casts drops like myeline, as / 
to whose precise significance noth- 
ing is known. j 

As to the origin of hyaline 
casts, despite many investigations . 
the question has not been fully 
answered. Probably they are due 
to the coagulation of the excreted 
albumen occasioned by the dying 
epithelial cells and the escaped leu- 
cocytes. It may be questionable 
whether, in this process of coagula- ■ 
tion, the albumen excreted with 
the urine by the glomeruli is in- 
volved, or the albumen due to the 
inflammatory exudation and origi- 
nating from the other renal blood- 
vessels. From analogy with other 

inflammations which lead to coagulable exudates.we regard the latter as the 
more probable supposition. Furthermore, many investigators assume that the 
desquamated and disintegrating epithelium is transformed into hyaline casts. 

2. The epithelial casts are composed exclusively of renal epithelium, although 
probably hyaline casts not infrequently form a basis to which the epithelial cells 
adhere. Epithelial casts are usually easily recognized, and always indicate an 
excessive desquamation of epithelium in the diseased kidneys. One must be on 
one's guard, as already mentioned, not to confound renal epithelium with swollen 
white blood-corpuscles. The separate epithelial cells and the epithelial casts may 
present various changes, such as granular opacity, fatty degeneration, and 
atrophy. 

3. The so-called waxy casts are almost always rather broad and usually yellow- 
ish-colored, opaque casts, of evidently a much tougher consistency than hyaline 
casts. TVe have found them most frequently in severe acute nephritis, either 




F.&. 



Fit 



b 

Fig. 69. 
-a. Waxy east. 
iC-ic oxalate, c. 

fFroi 
• v.; i ■ " 



Fig. 



b. Waxx ca 
Fras-Trents 



half. 



primary, or secondary to scarlet fever, but they also appear in the severer forms 
of chronic diffuse nephritis. As to their origin, we are convinced that they cer- 
tainly in many cases are formed out of epithelial casts. The closely apposed renal 
epithelial cells degenerate into waxy flakes, and gradually coalesce. One can, in 
fact, observe all stages of transition between the epithelial casts and the almost 
completely homogeneous waxy casts. Fiirbringer. therefore, terms waxy casts 
" metamorphosed " ; and he insists, correctly, that they always indicate severe dis- 
ease of the kidney. 
33 



594 



DISEASES OE THE URINARY ORGANS 



4, Granular Casts. — A kind of cast which is composed of coarse, yellowish, 
flaky granules represents the just-mentioned transition of epithelial casts into 
waxy casts. In other cases the waxy casts are nothing but hyaline casts com- 
pletely covered with the above-mentioned granules of various kinds. Sometimes, 
also, coagulated masses of albumen or granules of hsematoidine may themselves 
be formed into cylindrical shapes. 

Genuine blood casts are not very frequent. They consist of coagulated blood 
and represent casts of the renal canals into which haemorrhage has taken place. • 

The clinical diagnostic significance of renal casts is very great. They are, in 
the first place, always a sure sign of the existence of some renal disease, since in 
normal urine casts are not found at all, or, at most, they are exceptional and are 
present in small numbers. The consideration of the special forms of casts, and 
of the deposit upon them, is also of great diagnostic importance, although from it 
we can never decide immediately upon the general form of the renal disease, but 
we can recognize with certainty the type of special pathological processes in the 
kidneys. Ererichs has well named casts " messengers from the kidneys." The 
blood-casts and the red blood-corpuscles sticking to the cylinders point to the 
occurrence of renal haemorrhages ; the epithelial casts to a desquamation of the 
epithelium in the kidneys; the white blood-corpuscles to an emigration of the 
colorless cells from the vessels; the fatty granular cells to processes of fatty 
degeneration in the kidneys. 

We have already learned to recognize in a great measure in the preceding, as 
occasional deposits on the casts, the other morphological constituents found, be- 
side the casts, in the sediment of the urine in renal disease. Briefly recapitulated, 
they are as follows : 

1. Red blood-corpuscles. The presence of a large amount of blood in the urine 
(haematuria) is almost always to be recognized by its blood-red color. The blood 
may be made out with certainty by the microscope, or by Heller's blood-test. The 
latter is performed by heating the urine in a test-tube with sodic or potassic 
hydrate. The blood-corpuscles are thus dissolved, and the haematine formed 
from the blood-pigment is precipitated with the phosphates, giving to the pre- 
cipitate of the latter a very characteristic blood-red color. Van Deen's test is very 
distinct and easily performed. It requires a freshly prepared mixture of equal 
parts of old oil of turpentine and newly made tincture of guaiac. This mixture 
is poured upon the urine to be examined, and slightly shaken. At the place of 
contact of the two fluids there will immediately form a beautiful blue ring, if 
there is the slightest trace of blood in the urine. Finally, of course, the spectro- 
scope may serve for the detection of haematuria. Hemoglobinuria will be de- 
scribed in a special chapter later. 

2. White blood-corpuscles. Only when they are also attached to the casts can 
we assume with certainty that these come from the kidneys, and not from the 
lower portions of the urinary tract. 

3. Renal epithelium. 

4. Fat-drops and fatty granular cells. 

5. Uric-acid crystals, urates and calcic oxalate, bacteria, etc. 

For microscopic examination of the urinary sediment, we let the urine settle 
in a tall beaker; it is more convenient, and, if the urine contains few morpho- 
logical constituents, far more reliable to employ a centrifugal machine. 

3. The Dropsy of Renal Disease 
Although the changes in the urine must be alone decisive in the diagnosis 
of any renal disease, there are yet certain other symptoms which are also due 
immediately to the renal affection, and which may first direct our suspicions to 
the existence of a disease of the kidneys, and consequently lead to a careful exam- 



REMARKS UPON THE PATHOLOGY OF RENAL DISEASE 595 



ination of the urine. Among these symptoms the dropsy of renal disease is one of 
the commonest and most important. This may, indeed, quite frequently be en- 
tirely absent, both in acute and chronic nephritis, and in other diseases of the kid- 
neys ; but in many cases it is decidedly prominent in the whole clinical picture. 

If we ask what is the reason of the frequent occurrence of dropsy in renal dis- 
ease, the answer at first does not seem difficult. Since the main function of the 
kidneys is to excrete water from the body, and since, as we shall see later, in many 
cases the diseased kidney can no longer fulfill this task, or can fulfill it only to 
a slight degree, we are not, in fact, very much out of the way in considering the 
retention of water in the body as the main cause of the consequent oedema. Clin- 
ical observation seems in general to agree completely with this assumption. The 
oedema in renal disease seldom appears until the daily amount of urine has been 
below the normal for some time, while, on the other hand, in those cases where 
the amount of urine passed is normal, or even abnormally great, in spite of the 
existing renal disease, oedema is usually wholly absent. In individual cases, 
too, we very often see a decrease of the oedema associated with an increase in the 
amount of urine, and an increase of the oedema associated with a corresponding 
diminution in the excretion of urine. The pathological process accordingly seems 
to consist of an accumulation in the body of the water which can not be excreted 
from it, and which transudes from the vessels and thus gives rise to the develop- 
ment of oedema. 

On more careful consideration, however, there are some objections to this 
theory, which is apparently so simple. In the first place, it might be supposed 
that, when there is retention of water, the body must get rid of the surplus water 
by employing to a greater degree the other channels of elimination which are at 
its service — the skin and the intestines. Since we can never determine accurately 
the time when the water first begins to be retained in the body, the clinical experi- 
ence just mentioned may also be thus interpreted, that the lessened excretion of 
urine is not the cause of the oedema, but that, on the contrary, the appearance of 
oedema is rather the cause of the diminished elimination of water by the kidneys. 
The other clinical facts, also, are inconsistent with the view that the oedema de- 
pends upon the simple accumulation of water in the blood. In many forms of 
nephritis, and particularly in the nephritis of scarlet fever, we very often see 
extreme oedema appear suddenly, while, on the other hand, many severe varieties 
of nephritis — e. g., those associated with diphtheria, septic diseases, and pneu- 
monia, run their course with little or no oedema, although they are characterized 
by a marked diminution in the amount of urine. Moreover, cases have been 
repeatedly observed in which, as a result of obstruction of the ureters, or from 
pressure on these canals, there has been complete anuria for several days without 
a trace of oedema developing; and experimental investigations have given corre- 
sponding results. The bilateral ligation of the ureters in animals does not lead 
to the development of oedema even after several days. Cohnheim and Lichtheim 
introduced large amounts of a one-half to one-per-cent. solution of common salt 
into the vascular system of an animal, and despite this great artificial " hydraemic 
plethora," observed no oedema, even when the renal arteries were tied. Nor 
can oedema be provoked by slow and continuous infusion (Gartner, Francotte). 

Consequently, we must seek some other cause to explain the oedema of nephri- 
tis, and this is in all probability the peculiar change in the vascular walls, 
which renders them more permeable and permits the water accumulated in the 
blood to transude into the tissues. Just what this change in the vascular walls 
may be and what produces it we do not yet know; probably there are chemical 
agents which change the vascular walls, either the same substances which excite 
the nephritis, or matters secondarily formed, or certain products of metamor- 
phosis retained in the blood because of the inefficiency of the kidneys. That 



596 



DISEASES OF THE UKINAKY OBGAXS 



dropsy develops because of direct damage to the blood-vessels is rendered probable 
from the cases of so-called " acute essential dropsy," in which there develops a 
considerable general dropsy, just as in acute nephritis, often preceded by mild 
gastro-intestinal symptoms, and yet without a trace of albumen in the urine or 
any other demonstrable cause for this dropsy, which usually soon abates. 

Many clinical peculiarities of nephritic oedema harmonize with this concep- 
tion of its origin. In general, we may say that the oedema of nephritic patients 
appears first in the skin (" anasarca "), and has a striking tendency to show first 
in the face, in contrast with the oedema due to the passive congestion of heart 
disease, which usually begins in the ankles. The puffy and noticeably pale coun- 
tenance of the patient will often suggest the existence of kidney trouble at the 
first glance. In severe cases the dropsy often develops over the whole body in an 
extreme degree, involving the skin of the trunk, and particularly the dependent 
parts, the extremities, and scrotum, so that the patient is a pitiable object. In 
such cases there are also apt to be dropsical transudations into the internal cav- 
ities of the body, causing hydrothorax, ascites, and hydropericardium ; and these 
aggravate the patient's distress. It is, however, a striking fact that often there 
will be marked dropsical effusions (ascites, hydrothorax), and yet no marked 
oedema of the skin ; and hydrothorax is sometimes much greater on one side than 
on the other. All these facts indicate special local conditions — viz., the changes 
in the blood-vessels, which we have surmised. Still more is this the case with 
regard to the oedema of mucous membranes which sometimes occurs. There may 
be oedema of the conjunctiva, of the soft palate, of the ary-epiglottic ligaments 
(oedema of the glottis), and other parts. (Edema of this sort is apt to resemble 
a mild local inflammation, and in general it is impossible to deny a certain rela- 
tionship between " inflammatory " oedema and nephritic oedema. The nephritic 
oedema of the skin may in places have suggestions of an inflammatory nature, 
such as slight redness and tenderness. (Edema may affect the internal organs, and 
nephritic pulmonary oedema is of great practical importance. The question of 
the existence of cerebral oedema and of its possible importance will be discussed 
below (see uraemia). 

The preceding remarks relate only to genuine nephritic oedema. We shall see 
later that oedema may have an entirely different origin, particularly in cases of 
chronic nephritis — that is, if there is a cardiac hypertrophy and the powers of the 
heart become impaired, dropsy may at last develop. This oedema is of course a 
genuine congestive oedema, and exactly similar to that seen in failing compensa- 
tion in heart disease. 

In its chemical composition, the dropsical fluid corresponds to a very thin 
blood-serum. The amount of water is usually 97 to 98 per cent., the amount of 
salts one to one and a half per cent. The amount of albumen is usually very 
slight. Urea has been repeatedly found in the fluid. 

4. Ur.oiia 

If the diseased kidneys can no longer perform their secretory functions in a 
satisfactory way, not only does the elimination of water from the body thereby 
suffer, but the soluble constituents of the urine, the salts, the urea, and the other 
final products of tissue metamorphosis may also be retained in the blood and ac- 
cumulate there. Hence we often find the blood, in patients with renal disease, not 
only more watery than under normal conditions, so that the specific gravity of 
the serum may fall from 1030 to 1020, or even lower, but, in almost all cases where 
there is a diminished excretion of urine, it is also richer in urea, as many experi- 
ments have shown, and under corresponding conditions it is probably also fre- 
quently richer in the other constituents of the urine, or in substances correspond- 
ing to them but not completely metamorphosed. 



EEMAEKS UPON THE PATHOLOGY OF KENAL DISEASE 597 



This accumulation of the urinary constituents in the blood, and further, per- 
haps, in the tissues themselves, is the cause of a class of symptoms which are often 
seen in diseases of the kidneys, and which are termed uraemic symptoms or 
uraemia. 

Probably no one to-day doubts that uraemia must be regarded as essentially an 
intoxication of the body by the retained products of tissue metamorphosis. Nu- 
merous experimental investigations have proved that in animals extirpation of 
the kidneys, or ligation of the ureters, will produce a symptom-complex, charac- 
terized by vomiting, convulsions, and coma — almost completely analogous to. the 
uraemia of Bright's disease ; but if we inquire what constituents of the urine are 
the particular occasion of the uraemic phenomena, we can not as yet obtain any 
definite answer. For a long time it was believed that urea played a chief part in 
the development of uraemia, but the result of experiments upon animals does not 
support this view. / It is possible to inject enormous amounts of urea into the cir- 
culation or into the peritoneal cavity of animals without any symptoms of poison- 
ing. Voit did, indeed, show that the healthy kidneys remove from the blood the 
excessive amount of urea with extreme rapidity, and that accordingly uraemic 
symptoms do really appear if, while we are feeding an animal with large amounts 
of urea, we impede the excretion of the urea by a simultaneous withholding of 
water. Yet the amount of urea necessary for the success of this experiment is 
greater than can possibly exist in the ordinary uraemia of Bright's disease ; and, 
moreover, the withholding of water might also prevent the excretion of other 
matters; hence we must seek for other poisonous substances as factors in the 
production of uraemia. Many experiments seem to indicate that the potassium 
salts are especially poisonous, while some authors have laid the blame mainly on 
the extractive matters, such as creatinine. Bouchard has sought to prove that 
certain alkaloid substances (urotoxines), which are probably developed during the 
digestion of albumens and are always demonstrable in normal urine, occasion the 
phenomena of uraemia ; but to all these suppositions there are serious objections, 
so that really the substances which occasion uraemic intoxication are as yet un- 
identified. It might be possible that the poison corresponding to uraemia is not, 
in every case, the same. 

The mode of action of the toxic material is as unsettled as is its chemical 
nature. This much only is certain, that in uraemia the disturbances are almost 
exclusively cerebral, and in the main located in the cortex of the brain; but 
whether there is actually a direct injury of the nervous elements, or whether the 
immediate action is upon the blood-vessels, is uncertain. The occurrence of 
uraemic focal symptoms, to which we shall refer below, renders the former supposi- 
tion the more likely. Fleischer produced uraemia experimentally in animals, and 
in every case observed an extreme anaemia of the brain and spinal cord, so that he 
concludes that there is a spasm of the blood-vessels. 

Clinical experience also agrees perfectly with the theory that uraemia is caused 
by a retention of urinary constituents in the body. In most cases the uraemic 
symptoms appear only when the daily amount of urine has fallen to a very low 
figure, or when the secretion of urine has wholly ceased for several days. That 
in these cases not only the elimination of water, but also the elimination of 
an amount of urea corresponding to the food taken, and also the elimination of 
the other urinary constituents, is very much diminished, is shown by the experi- 
ments in regard to this point made by Fleischer and others. Furthermore, a 
great increase of the amount of urea in the blood in uraemic patients has been 
found in many if not in all cases. 

Of course there can be no question that some clinical facts can not be brought 
into exact harmony with what has been previously said. If cases are repeatedly 
reported in which no uraemic symptoms have appeared in spite of anuria lasting 



598 



DISEASES OE THE UKINARY ORGAN'S 



several days, it does not prove very much, since we can never make an exact esti- 
mate of the matter accumulated in the blood which ought to have been eliminated ; 
for the organism can certainly get rid of the final products of tissue metamor- 
phosis in other ways than through the kidneys — for instance, through the skin 
or the intestines — and we must also bear in mind that different individuals show 
a great diversity in tolerating the action of any poison in the body, particularly 
as regards the nervous system. It is harder to explain those cases which are some- 
times seen, in which uraemic symptoms suddenly appear in patients with renal dis- 
ease, although these symptoms are not preceded by any noticeable diminution of 
the secretion of urine. We may, however, assume that, despite the abundant ex- 
cretion of water and the normal amount of urine, there has been a slight retention 
of solid matters. Analogy with other kinds of poisoning makes the supposition 
very plausible that the long persistent retention of even extremely small portions 
of toxic matter may occasion an absolutely sudden explosion of the severest symp- 
toms. In chronic lead and mercurial poisoning the symptoms often appear with 
great abruptness, although the poisoning has taken place very slowly and grad- 
ually. In the same way we explain to ourselves the not very infrequent cases of 
the sudden development of severe uremic symptoms, as seen particularly in 
patients with contracted kidney (vide infra), in whom it may seem as if no single 
prodromal symptom had indicated the impending outburst of intoxication. Often, 
also, peculiar circumstances may favor the occurrence of uraemia — for example, 
the development of cardiac weakness, so that the blood tension is diminished and 
the excretion of urine impeded. In some cases again it is observed that the devel- 
opment of uraemia coincides with the absorption of previously existing oedema. 
This is explained by the supposition that the rapid absorption of the oedema in- 
troduces into the blood a comparatively large amount of the poisonous products 
of metabolism, which had not been excreted, but had been contained in the 
cedematous fluid. 

While we are firmly of the opinion that uraemia is to be regarded as a poison- 
ing of the body by the retained constituents of the urine, yet we should not fail 
to mention that attempts have been made to explain in other ways the uraemic 
phenomena. In particular, Traube has propounded the theory that the so-called 
uraemic symptoms are dependent upon an acutely developing cerebral oedema, and 
consequent cerebral anaemia. This theory can be regarded as, on the whole, unten- 
able. Still, it may contain a certain amount of truth, for we can not wholly 
deny that sometimes there may be actual anatomical lesions, such as inflamma- 
tory oedema of the brain, in the course of a nephritis, sufficient to occasion severe 
cerebral symptoms. During nephritis, secondary inflammation may appear in 
almost all the internal organs, and often suddenly; and this sort of nephritic 
inflammation is especially frequent in the retina, a structure composed of nervous 
elements, so that the possibility of similar disease in the brain is very great. If 
we consider that cases of uraemic hemiplegia and monoplegia have been repeat- 
edly observed, and that likewise cases have been described of uraemic J acksonian 
epilepsy, hemianopsia and aphasia, it will be seen that the supposition of an ac- 
tual local lesion as the explanation of such well-marked focal symptoms is very 
plausible. Yet we must also consider that in the last analysis the cause of such 
limited cedematous — or inflammatory-oedematous — changes in the brain is to be 
sought in the action of some retained products of metamorphosis. 

Einally, we may mention here the theory advanced by Frerichs in the year 
1851, which at first found much favor, but which at present is almost universally 
abandoned. According to this, the urea retained in the blood was not in itself 
the cause of the uraemic symptoms, but it was changed into carbonate of ammo- 
nium by the action of a ferment in the blood, and from this the severe nervous 
symptoms arose. This theory is untenable, because carbonate of ammonium is 



REMARKS UPON THE PATHOLOGY OF RENAL DISEASE 599 



scarcely ever found in the blood of uraemic patients. It is much more probably 
formed first in the stomach and intestinal canal of uraemic patients from the urea 
there excreted (vide infra), as Claude Bernard, Treitz, Voit, and others have 
shown. 

In regard to the clinical symptoms of uraemia in the individual case, they show 
all possible transitions from the mildest symptoms, which are only intimated, up 
to the severest nervous symptoms, which may be the immediate cause of death. 
The severe forms of uraemia may sometimes come on quite suddenly, while in 
other cases they may be preceded for a long- time by milder uraemic symptoms, 
which are then termed prodromata. The severest symptoms may not appear at 
all, and the milder symptoms may exist alone for a longer or shorter time. This 
latter condition is called chronic uraemia. 

The milder ursemic symptoms, which are observed either alone or as precursors 
or as sequelae of severe uraemia, consist of headache, somnolence, and mental 
stupor, of a peculiar uneasiness, or of a feeling of anxiety and constraint (some- 
times associated with hurried respiration), and very often of nausea, spasmodic 
eructations, and repeated vomiting; and, finally, not infrequently, of various 
symptoms of motor irritation, of slight twitchings or temporary tonic rigidity of 
the face or the extremities, etc. 

Among the characteristic symptoms of this milder form of uraemia, besides the 
vomiting, we would place the peculiar restlessness and praecordial distress of 
patients as especially important. Not infrequently, observers use the term 
uraemic asthma (vide infra). 

The most characteristic symptom of severe uraemia is the uraemic convulsion, 
or the so-called uraemic eclampsia. It corresponds almost exactly in its details 
to an epileptic attack; it usually begins with a short tonic stage, in which the 
whole body is generally in a position of extension in opisthotonos, and then follow 
vigorous clonic contractions in the face and extremities. The face becomes cya- 
notic, a bloody froth comes from the mouth, the pupils are usually dilated and 
almost without reaction, the respiration is accelerated (but at times it is intermit- 
tent from spasm of the respiratory muscles), the pulse is small and accelerated, 
and it can scarcely be felt in the radial artery, and the temperature is sometimes 
raised. In other cases the spasm begins with short jerky contractions in one ex- 
tremity, as in the arm, and then invades the trunk muscles, the face, and the legs. 
One half the body is often more affected in the attacks than the other. The 
spasms usually cease in a few minutes, and are followed by deep coma and stertor, 
which last for several hours or more. There is only rarely a single attack. The 
attacks are much oftener repeated after longer or shorter intervals, so that there 
may even be twenty or more in the twenty-four hours, during the whole of which 
time a complete loss of consciousness persists. Severe and fully developed epilep- 
tiform attacks often alternate with slighter convulsions. 

Some other uraemic symptoms, besides the convulsions, which have already 
been briefly mentioned, merit a somewhat fuller description. 

The uraemic amaurosis occasionally seen is especially interesting. It is usually 
left after recovery from the convulsions. Only rarely does it precede them or 
appear without them. It always develops quite rapidly, so that the first disturb- 
ance of vision soon passes into complete blindness. The reaction of the pupils to 
light is almost always retained, and the ophthalmoscope shows a perfectly normal 
retinal image. At what spot in the visual apparatus the lesion is situated is not 
yet known. Many investigators assume that there is an oedema of the sheath of 
the optic nerve; while others, including the author, think it more probable that 
there is disturbance of the cerebral visual centers, and particularly of the occip- 
ital cortex. 

Its prognosis is on the whole favorable, since the disturbance of vision usually 



600 



DISEASES OF THE URINARY ORGANS 



disappears completely in a day or two, though sometimes not until after a longer 
time. Anomalies are only rarely seen in the domain of the other nerves of special 
sense, the most frequent, comparatively, being a difficulty in hearing, or even 
complete deafness. 

Other motor disturbances, except twitchings and convulsions, are rare. Only 
in a few cases have hemiplegic or monoplegic paralyses, contractures, trembling, 
etc., been observed. Mental symptoms are more common. Delirium, and mani- 
acal or sometimes melancholic states, occasionally follow uraemic coma. 

Those ursemic symptoms have also a great interest which are to be regarded 
as a sort of self-help on the part of the organism, since they often lead to a vica- 
rious elimination of urea and presumably of the other products of tissue metamor- 
phosis. The first of these is uremic vomiting, which is a frequent and often an 
extremely obstinate symptom both in acute and chronic uraemia. In many cases 
it is of central origin, and is to be regarded as analogous to the vomiting so fre- 
quent in different forms of cerebral disease ; but it is often produced by the irri- 
tation which the gastric mucous membrane suffers from the urea eliminated, or 
rather from the carbonate of ammonium arising from it. The latter is always 
first formed from the urea in the stomach itself, and we find in the vomitus of 
ursemic patients either the still undecomposed urea or the carbonate of ammoni- 
um in considerable quantities. Sometimes there is quite a violent hiccough 
besides the vomiting. 

Ursemic diarrhoea has the same significance as uraemic vomiting. It is usually 
provoked by the carbonate of ammonium arising from the urea in the intestines. 
The latter often causes quite a severe catarrhal, and even at times a diphtheritic, 
inflammation of the intestinal mucous membrane. 

Another way in which the organism sometimes tries to get rid of the large 
amount of urea accumulated in it is by the sweat-glands. Schottin first described 
the remarkable discovery of a coating of urea on the skin in the uraemia of chol- 
era, an observation which since then has been repeatedly confirmed in other cases 
of uraemia. This coating is most frequently seen on the face, especially on the 
sides of the nose, to which little faintly lustrous scales are seen sticking after the 
evaporation of a clammy sweat. Chemical examination shows that these scales 
are urea. The excretion of urea is much more rare in other parts of the skin, 
but perhaps the occasional severe uraemic itching of the skin is due to an irri- 
tation of the cutaneous nerves by some of the constituents of the urine that are 
excreted. 

Other organs besides the skin and the digestive tract are but rarely to be con- 
sidered as a means of the vicarious elimination of urea, but Fleischer was once 
able to discover considerable amounts of urea in the saliva and sputum of a 
uraemic patient. 

In conclusion, we must describe the condition of the pulse, of the temperature, 
and of the respiration in uraemia. The pulse is often very slow before the appear- 
ance of severe symptoms, sometimes 48 or 40, but it is almost always tense and 
hard. In chronic uraemia, also, a moderate slowness of the pulse is not infre- 
quent. When uraemic convulsions appear, however, the pulse usually becomes 
small and very frequent, especially in cases that terminate unfavorably. The 
temperature but rarely remains unchanged in severe uraemia. If there are con- 
vulsions, it usually rises several degrees, in severe cases even to 106° or 108° (41°- 
42° C). We have seen these high temperatures, especially, as a terminal rise with 
an unfavorable issue, although there may sometimes be an improvement even in 
such cases. On the other hand, there are also great declines in temperature, down 
to 93° or 91° (34°-33° C), most frequently again as a terminal temperature of 
collapse, in cases which end in deep coma without marked symptoms of motor 
irritation. We might also mention the " uraemic chills " which we have seen sev- 



REMARKS UPON THE PATHOLOGY OF RENAL DISEASE 601 



eral times — that is, a chill coming on suddenly along- with other uraemic symp- 
toms,, with a great increase of temperature, and followed by a rapid fall in the 
temperature. The respiration in uraemic patients is sometimes very much accel- 
erated, and is especially deep — a symptom which recalls the peculiar breathing in 
diabetic coma (vide infra). Certain severe attacks of dyspnoea in patients with 
renal disease have been described as " uraemic dyspnoea " or " uraemic asthma " ; 
but it is not always easy to decide whether this is really a uraemic nervous symp- 
tom in these cases, since similar conditions of sudden dyspnoea may depend upon 
coincident heart disease and insufficiency of the left ventricle or upon inflamma- 
tory affections of the lungs. 

In regard to the duration of uraemic symptoms and to the different forms and 
ways in which the various ursemic symptoms may be combined in the clinical 
picture, we can give only a few general statements. The division of uraemia into 
an acute and a chronic form, already mentioned, is generally very useful practi- 
cally. In the acute form we usually have the severe uraemia symptoms, especially 
uraemic convulsions and uraemic coma. This condition usually lasts some days, 
while chronic uraemia, in which the milder cerebral symptoms — uraemic vomiting, 
difficulty in breathing, etc. — are most prominent, may last as many weeks. The 
severe acute form of uraemia may, as has been already stated, begin with almost 
absolute abruptness. Quite often, however, there are first mild uraemic symptoms, 
such as headache, vomiting, general restlessness, and an occasional slight twitch- 
ing of the muscles, and then suddenly uraemic convulsions or other uraemic 
symptoms. 

The termination of uraemia is always doubtful in every severe case, but it is by 
no means always unfavorable. Even after coma lasting for several days, with 
very severe and often-repeated convulsions, the uraemic symptoms may wholly 
disappear, while on the other hand, of course, uraemia is by no means a rare cause 
of death in the most diverse forms of acute and chronic renal disease. In judging 
of the individual case, the most stress is to be laid on the condition of the pulse, 
the respiration, and the temperature; we must also consider, of course, the char- 
acter of the urinary secretion, and especially the other morbid symptoms depend- 
ent upon the primary disease. 

5. The Changes in the Circulatory Apparatus in Kexal Disease 
Although it had not escaped Bright's observation that changes in the heart are 
also present in diseases of the kidney, this condition was first generally known 
when Traube, in 1856, in a treatise which has become famous, explained that a 
change in the heart was very common in certain renal affections, and thus gave 
the chief impulse to the numerous clinical and experimental investigations that 
have been made since then as to the connection between cardiac and renal disease. 
This connection, generally considered, may be accounted for in three ways : 
Eirst, the heart disease may without doubt be the primary disease, and only 
secondarily lead to a disease of the kidneys. In this way develop the kidney of 
passive congestion (vide infra, and page 331), acute nephritis secondary to acute 
primary or recurrent endocarditis, and the embolic processes in the kidney (vide 
infra). 

Secondly, heart disease and renal affections may also develop independently of 
each other, as a result of an injurious influence that affects both organs at the 
same time. Thus, for example, a general arterio-sclerosis leads to cardiac hyper- 
trophy or to myocarditis, and also to a granular kidney (vide infra), as a result 
of an implication of the renal vessels. Certain other injurious influences, such as 
toxic and constitutional influences, alcohol, syphilis, or improper living, may also 
cause a disease of the heart and the kidneys at the same time. Later on, if both 
affections have developed, their influence upon each other is often, of course, con- 



602 



DISEASES OF THE UKINARY OEGANS 



siderable — a circumstance which may render our judgment as to the condition 
decidedly difficult. 

In the third place — and this is the point with which we are here chiefly con- 
cerned — the renal affection may be the primary disease, and of itself the cause 
of a change in the heart, and especially of a secondary hypertrophy of the left 
ventricle. At present there can no longer be any doubt of the fact of this depend- 
ence. We also know now that the secondary development of cardiac hypertrophy 
is not confined to one form of chronic nephritis, the so-called contracted kidney, 
as was at first believed, but that it is almost as constant in all other forms of 
chronic, and also even in prolonged acute, nephritis. Opinions are at present still 
much divided as to the precise nature of this connection, and as to the causal 
factors. 

The theory which Traube himself advanced for the explanation of the cardiac 
hypertrophy in nephritis rested on the assumptions that, in the first place, less 
water is withdrawn from the blood in nephritis for the formation of the renal 
secretion, and that, in the second place, the flow of arterial blood into the venous 
system is hindered by the changes in the kidneys, particularly by the destruction 
of many of the smaller blood-vessels. Both circumstances must raise the pressure 
in the arterial system, and therefore gradually lead to cardiac hypertrophy. 
Traube's theory can not be maintained. The first claim especially is untenable, 
because in many cases of chronic contraction of the kidney with co-existing car- 
diac hypertrophy there is never a diminution of the elimination of water by the 
kidneys, and, besides, this can never of itself cause an increase of the arterial pres- 
sure. The second supposition, that the destruction or the narrowing of a large 
number of the small blood-vessels of the kidneys must produce a general rise in 
arterial tension, is disproved by the fact that even the complete ligation of both 
renal arteries does not raise the tension in the arterial system, because the blood 
at once passes off into other vessels which dilate. 

In place of the " mechanical theory," therefore, there have been of late many 
supporters of the " chemical theory " of cardiac hypertrophy, which was in a cer- 
tain sense propounded by Bright himself, and later by Johnson and others. Ac- 
cording to this view which, with some modifications, is held by the author, the 
retention of urinary constituents in the blood is the cause of the cardiac hyper- 
trophy because the retained material occasions a rise in arterial tension, and this 
increased tension, if it persists for a sufficiently long time, must occasion a hyper- 
trophy of the left ventricle. Clinical experience shows beyond a doubt that any 
severe case of acute nephritis occasions in a few days an increase in the arterial 
tension, which can usually be easily perceived in the pulse. This increased ten- 
sion, which certainly precedes the cardiac hypertrophy, is best explained by the 
supposition that the matters which ought to be but are not excreted occasion a 
contraction of the smaller arteries. It is also possible to conceive that there 
may be a direct irritation of the cardiac muscle. At any rate, the occurrence of 
a rise in arterial tension is of decided benefit to the body, as it promotes the ex- 
cretion of urine. If, in the course of a nephritis, the normal conditions return 
after a few days or weeks, the increased tension is relaxed arid the heart suffers 
no noticeable change ; but if the nephritis and consequent impairment in urinary 
secretion and increased arterial pressure persist for a considerable time, we often 
see, even after six or eight weeks, a hypertrophy of the left ventricle develop, 
under our own eyes, in a way that can be demonstrated most distinctly at the 
bedside. This is the necessary consequence of the increased effort which the heart 
is obliged to make in order to overcome the abnormal resistance in the systemic 
arteries. 

We have precisely the same conditions in the chronic forms of nephritis, ex- 
cept that they develop more slowly and insidiously. In these, also, the first fac- 



ACUTE NEPHRITIS 



603 



tor is the insufficiency of the kidneys, occasioned by the disease — that is, failure 
to excrete all the products of metabolism. To this the body responds immedi- 
ately by a rise in arterial tension, which is intended to serve, and does actually 
serve, as a compensation of the impairment; then, thirdly, hypertrophy of the 
left ventricle develops, and enables the heart for a long while to supply the de- 
mands put upon it. This hypertrophy is consequently the most important and 
indispensable compensatory arrangement by means of which the body is pro- 
tected from the onset of uraemic intoxication. Just as any patient with valvular 
heart disease would invariably fail much earlier if his heart did not become 
hypertrophied in portions corresponding to the lesion, so, also, in chronic nephri- 
tis, the unfavorable termination would occur much earlier if the body were not 
in a position to effect and maintain an increase in the arterial tension, and thus 
for a time, at least, ward off the threatening enemy. Viewed in this light, the 
chemical theory of cardiac hypertrophy not only gives us an insight into the 
clinical phenomenon as such, but also enables us to perceive its true significance. 

The question naturally arises here, just as when we were considering the 
theory of uraemia, what substances are the chief occasion of the rise in arterial 
tension. This question, however, can not at present be answered. We can merely 
say that the results of experiment indicate that urea probably does not play the 
most essential, and certainly not the sole, part in the matter. The question 
whether the hypertrophy of the left ventricle associated with nephritis is mainly 
simple (concentric), or whether it may not sometimes be accompanied by dilata- 
tion of the cardiac cavities (eccentric), we do not regard as of any special impor- 
tance. It should, however, be noted that while the hypertrophy always affects the 
left ventricle chiefly, and often it alone, yet not infrequently the right ventricle 
is also found to be hypertrophied. If we assume that there is a direct irritation 
of the myocardium (vide supra), this condition will not seem remarkable. Oth- 
erwise, the hypertrophy of the right ventricle might be regarded as a compensa- 
tory hypertrophy, supplementing failure of the left ventricle. 

The relation between certain diseases of the vessels and diseases of the kidneys 
will be spoken of in the chapter on contracted kidney. 



CHAPTER II 

ACUTE NEPHRITIS 

(Acute BrighPs Disease) 

etiology. — Acute nephritis, like most of the other forms of nephritis, is not 
a disease whose aetiology is uniform. The same anatomical change, which we 
term "nephritis," and which is attended by about the same morbid phenomena, 
may be excited by influences of very different kinds. Almost all these influences 
have one thing in common, namely, that, as we have stated in the preceding chap- 
ter, they reach the kidneys by way of the circulation and are here in part elimi- 
nated, and thus exert their specific injurious action upon the parenchyma of 
the kidneys ; but they differ considerably from one another in their precise chem- 
ical nature. Since the pathological change in the kidneys depends upon the 
amount of the noxious material, upon the intensity of its action and the duration 
of its influence, we see that the cases of nephritis that arise in this way must 
present a perfectly continuous series from the mildest to the severest, from those 
that pass off rapidly to those that last perhaps for years and years. The history 
of renal pathology teaches us in the plainest way that all attempts to divide the 



604 



DISEASES OF THE URINARY ORGANS 



forms of nephritis into different clinical and pathological " varieties " can not 
be strictly carried out. The more scientific experience increases, the more numer- 
ous must be the forms established, and still we only too frequently have to assume 
all sorts of " transitional forms " merely to bring the reality into harmony with 
the scheme. It therefore corresponds merely to our practical needs if we take 
certain types from this whole list and divide nephritis into various groups; for, 
from the nature of the case, there can be no question of a sharp separation of the 
various forms. 

We accordingly call those inflammatory renal affections acute nephritis which 
arise comparatively rapidly from any of the injurious influences soon to be enu- 
merated, and which terminate, after a few days or a few weeks, either fatally or 
with recovery; or occasionally, after a rapid onset of this sort, pass gradually into 
a chronic form. Acute nephritis, on the one hand, follows immediately, without 
any fixed boundary, the mildest morbid changes in the kidney, which are usually 
not termed actual nephritis, but simple " parenchymatous degeneration " ; while 
on the other hand it shows a continuous transition to those forms which last for 
several weeks or months, or longer, and hence are called subacute or subchronic 
nephritis. 

Let us now consider more minutely the conditions under which acute nephritis 
develops. In the first place, it occurs with very great frequency as a sequel or 
complication of all sorts of infectious diseases. We may assert that there is 
really no acute infectious disease in which a secondary acute nephritis may not 
occasionally appear. There are, however, many diseases in which this complica- 
tion is peculiarly frequent and characteristic. The exact causes of its develop- 
ment are as yet imperfectly known. Formerly, authorities were inclined to as- 
sume that the original germs had directly invaded the kidney itself, but probably 
this is true in only a few cases, if we except genuine metastatic pyonephritis. 
According to the views of the present day, it is much more likely that abnormal 
chemical substances, toxines, which develop in the body under the influence of the 
infection, reach the kidneys and excite disease in them. The amount and char- 
acter of these substances determine, of course, the severity of the renal disease. 
Since we have already dwelt upon the occurrence, the frequency, and certain 
peculiarities of secondary nephritis in the description of the different infectious 
diseases, a brief recapitulation of the facts, which have already been for the most 
part discussed, will suffice here. 

The infectious disease which most frequently gives rise to an acute nephritis 
is scarlet fever. As has been shown previously (see page 43), the renal affection 
appears but rarely at the beginning of the disease, and then in a very mild form, 
while the special severe scarlatinous nephritis usually attains its development 
only toward the end of the third week of the disease. In measles, secondary 
nephritis is very much rarer than in scarlet fever; in rotheln it is only of very 
exceptional occurrence. It is commoner again in small-pox, especially in the 
severe hemorrhagic forms. In varicella, renal affections are very rare, but they 
have been occasionally observed. They are always of but slight intensity. In 
typhoid fever a slight albuminuria is very common, but genuine acute nephritis 
is quite rare. There are some cases, however, where a nephritis appears very 
early, and where the other typhoid symptoms are so crowded into the background 
by it that we have decided difficulty in making the diagnosis of typhoid; this is 
called the " renal form of typhoid fever." In typhus and recurrent fevers severe 
cases of nephritis are not especially common, but they are seen more frequently 
than in typhoid fever. 

The nephritis that often comes on in cholera is of great practical importance. 
This is seen in the earlier stages, and is especially one of the most frequent 
causes of the so-called cholera typhoid (see page 89). Of course it may appear 



ACUTE NEPHRITIS 



605 



questionable whether the renal affection here is always of a genuine inflammatory 
nature, or develops only in consequence of the disturbance of circulation. 

Nephritis develops quite frequently in the course of diphtheria, especially in 
severe cases of this disease; but the renal affection only rarely reaches a high 
degree. We sometimes see, however, very severe forms of nephritis in all the so- 
called septic diseases (septic nephritis, see page 120), in acute ulcerative endocar- 
ditis and endocarditis verrucosa, and allied affections, such as puerperal fever, 
septic wounds, etc. 

Erysipelas also is very often associated with nephritis, and likewise croupous 
pneumonia; while, on the other hand, acute articular rheumatism is seldom ac- 
companied by albuminuria. It is not very exceptional for sore throat, particularly 
follicular tonsillitis, to occasion acute nephritis, and the same is true of acute 
intestinal diseases. It is of great practical importance to know that a severe 
secondary nephritis may follow primary diseases of this sort, even if the latter 
seem to be very mild. 

We ought also to speak of the acute nephritis sometimes seen in patients with 
pustular eruptions, such as impetigo, pustular eczema, severe scabies, etc. Prob- 
ably we have to do in most of these cases with a mild septic infection, which 
has found ingress through one of the many minute scratches or other lesions of 
the skin. We must also bear in mind the possibility (vide infra) of damage done 
by external applications which are absorbed by the skin. 

There are many chronic infectious diseases besides these acute ones, in the 
course of which acute nephritis may appear. We see this complication most fre- 
quently in the case of primary tuberculosis, but it seems to us highly probable 
that the nephritis in this instance is not directly connected with the tubercu- 
losis, but is the result 'of absorption of septic matters from the pulmonary cavities 
and similar places. Syphilis should also be mentioned in this connection. We 
have ourselves repeatedly seen mild and even severe acute nephritis develop in 
the secondary stage of syphilis. Einally, malaria might be mentioned, although 
the nephritis which occurs in this connection usually takes a chronic form. 

Besides the infectious forms of nephritis just described, there is a second great 
group, which may be classed under the general heading of toxic nephritis. In 
these cases we are dealing with the deleterious action of definite chemical sub- 
stances which enter the body from without and are excreted from it by the kid- 
neys. It is wholly impossible to enumerate all the substances which have this 
injurious effect; we will therefore confine ourselves to mentioning those of the 
greatest practical importance. Among the poisons proper we may mention the 
mineral acids, sulphuric, hydrochloric, and nitric acids, oxalic acid, phosphorus, 
arsenic, lead, mercury (corrosive sublimate), and chromate of potassium. Among 
remedies used internally, which may excite nephritis when given in too great 
doses, we may mention cantharides, squills, balsam of copaiba, turpentine, sali- 
cylic acid, and chlorate of potassium. This last causes hemoglobinuria as well 
as nephritis. It is also very important to know that many remedies applied exter- 
nally are absorbed by the skin, and that in this way they may reach the kidneys 
and excite severe changes there. Among these are cantharidal plaster, prepara- 
tions of tar, petroleum, styrax, naphthol, and pyrogallic acid. We must men- 
tion, in addition to these, the nephritis which may arise from the too abundant 
use of carbolic acid or iodoform on the surface of open wounds. Under some 
circumstances renal affections may even arise in individual cases from taking 
excessive amounts of certain foods and drinks, such as spices, alcohol, horse- 
radish, or very acid foods. 

The many cases of nephritis thus far discussed are directly referable to some 
definite cause, but in a comparatively small number of instances acute nephritis 
appears as an apparently primary disease in persons previously healthy. In many 



606 



DISEASES OE THE UBINAKY OBGAXS 



such, cases we are absolutely unable to make out any causative factor, while in oth- 
ers, again, we do find certain unfavorable influences affecting the patient, such as 
hard drinking or severe labor in the open air. It can not be doubted that expo- 
sure to severe cold and thorough wetting promote the development of acute ne- 
phritis. The author's experience has convinced him of this fact. Thus, the 
disease may occur when a man works in the snow or in cold water. We possess 
as yet, however, scarcely any knowledge of the conditions which bring about this 
result. Many investigators assume that cold interferes with the excretory func- 
tion of the skin ; others imagine that the blood is damaged as it circulates in the 
cutaneous vessels. We have repeatedly seen cases of apparently primary acute 
nephritis in great beer drinkers. We suppose that in such cases the effect of the 
long-continued chronic intoxication with alcohol is cumulative, and finally leads 
to the apparently spontaneous acute development of nephritis (acute alcoholic 
nephritis). Sometimes, however, even in such cases there seems to be some other 
factor, such as catching cold, which gives the final impulse to the development 
of the disease. A considerable number of cases of apparently primary acute 
nephritis must, however, be regarded in the last analysis as the results of a septic 
infection of some sort. If we question the patient closely, we learn in such cases 
that the appearance of the nephritic phenomena has often been preceded by 
symptoms of a mild sore throat which scarcely attracted the patient's attention, 
or an insignificant gastro-intestinal disturbance, etc. Such statements are in- 
dicative of the possible place of infection. Again, slight purulent affections of 
the skin, such as f urunculosis, phlegmon of a finger or toe, and eczema may some- 
times furnish a gate of entrance for infection. In considering all cases of appar- 
ently primary idiopathic and acute nephritis, it is very important to remember 
that not infrequently a chronic nephritis may exist for a long while, perhaps 
without any symptoms whatever, and suddenly flame up into an acute disease 
(acute recurrent nephritis of Wagner), and thus simulate a primary acute nephri- 
tis. We can not get at the correct interpretation of such cases without careful in- 
quiry into the previous history, and sometimes only after observing the subsequent 
course of the disease. 

In conclusion, we have an especial form of acute renal disease to mention in 
this connection — viz., the nephritis of pregnancy (nephritis gravidarum). This 
does not usually appear until the last months of pregnancy. It may attack 
women whose health was previously perfect, and it is much more frequent in 
primiparse than in multipart. The precise causes of the nephritis of pregnancy 
are very obscure. The earlier explanations, according to which the renal dis- 
turbance was occasioned by pressure of the pregnant uterus upon the renal arte- 
ries, the renal veins, or the ureters, are entirely unsatisfactory. Perhaps there 
are special toxic influences, the origin and nature of which are as yet entirely 
unknown. 

Pathological Anatomy. — The anatomical changes of acute nephritis show a 
continuous series from the mildest to the severest degrees, according to the in- 
tensity of the injurious action. The mildest changes, which, as we have said, are 
not called actual " inflammation," but usually simple parenchymatous degenera- 
tion, affect exclusively the parenchyma of the kidney — that is, the epithelium — 
while the interstitial tissue, the connective tissue, and the vessels remain per- 
fectly normal. This fact is of prime importance, since it implies that, in almost 
all the injurious influences acting on the kidneys, the specific renal parenchyma 
itself is diseased first and before any other. On macroscopic examination, the 
kidneys of "parenchymatous degeneration" may show scarcely any plainly per- 
ceptible changes, but it sometimes strikes the practiced eye that the kidneys are a 
little enlarged, that the cortex on section shows either a more reddish-gray, 
dimmed coloring (cloudy swelling), or a more grayish- white, yellowish hue (fatty 



ACUTE NEPHKITIS 



607 



degeneration). The microscopic examination gives more accurate information 
as to the degree and the extent of the disease. We distinguish different condi- 
tions according to the form of change in the epithelium, of which the three fol- 
lowing are most important: 1. Cloudy Swelling: It is most easily made out in 
the epithelium of the cortical tubules, but it may also be seen in the epithelium 
of the glomeruli. The cells swell, their contents become uniformly granular and 
cloudy, the nuclei swell, and finally disappear. Such changes are often found in 
acute infectious diseases, such as typhoid, small-pox, and diphtheria. 2. Fatty 
Degeneration: This may proceed from the cloudy swelling, or may develop inde- 
pendently. Many fat-drops appear both in the cells of the uriniferous tubules 
and also in the epithelium of the glomeruli, and they may finally lead to the dis- 
integration of the cells. Simple fatty degeneration of the kidneys is sometimes 
found in acute infectious diseases, after certain poisons, such as phosphorus, and 
finally in anaemic conditions. 3. Necrosis of the Renal Epithelium: The nuclei 
of the cells disappear, and the cells are changed to clear homogeneous flakes, 
while in some cases they are greatly swollen (" dropsical degeneration " of Nau- 
werck-Ziegler). Genuine epithelial necrosis is found in the kidneys, chiefly after 
the action of toxic substances — cantharides, the chromic and chloric salts, etc. 
— but sometimes also in infectious diseases. Combinations of simple necrosis 
with granular cloudiness and fatty degeneration are not infrequent. Both the 
last-named states may undergo resolution if they have not reached a high degree. 
Otherwise all the degenerations mentioned lead to the destruction and disinte- 
gration of the cells; nevertheless, a complete restoration is possible, from the 
regeneration of new epithelial cells from epithelium that is still present. 

We term those changes in the kidneys genuine acute nephritis, in which not 
only the renal parenchyma proper, the epithelium, but also the interstitial tissue, 
especially the vessels, is affected ; so that we can make out the exudative changes 
characteristic of all inflammatory processes — the escape of fluid and cells from 
the vessels. In these cases the different histological processes may be combined 
in the most varied ways, so that the anatomical picture presents quite great vari- 
ations, although it is almost always seen on analysis to display the same pro- 
cesses. 

If we begin with the histological lesions in acute nephritis, in order to learn to 
recognize at once the essential changes, we have first precisely the same processes 
of degeneration in the epithelium which have been already described, but they are 
usually present here in a more marked degree. In some cases the simple ne- 
crotic processes predominate; in others, the fatty degeneration. We often find 
degenerated cells, and not infrequently a more or less marked desquamation of 
epithelium. We see also the special inflammatory changes. We find a fluid 
inflammatory exudation, rich in fibrine, and therefore soon coagulating in the in- 
terstitial connective tissue, which is dilated and swollen by it — inflammatory 
oedema. The same exudation is also found in the uriniferous tubules, and, by the 
proper methods, by alcohol or by boiling the fresh kidney, the albuminous effusion 
can be made out both in the capsules of the glomeruli and in the uriniferous 
tubules. The interpretation of the exudation is, of course, made very difficult, or 
often wholly impossible, by the presence of albuminous urine in the uriniferous 
tubules. The second characteristic of inflammation, the " cellular exudation " — 
that is, the emigration of white blood-corpuscles — is also present. In the inter- 
stitial tissue we find accumulations of round cells, usually distributed in foci, 
and white blood-corpuscles in greater or less numbers also enter the interior of 
the uriniferous tubules. We often find many hyaline casts in the lumen of the 
straight tubules or of Henle's loops, whose origin is, in all probability, connected 
with the albuminous exudation and the emigrated white blood-corpuscles (see 
page 593). The vessels themselves are often hyperaemic and dilated, but in some 



608 



DISEASES OF THE UKINAKY OEGAISTS 



cases they are compressed by the interstitial inflammatory oedema. It is of spe- 
cial significance that in very many cases there are haemorrhages, either into the 
interstitial tissue or into the interior of the uriniferous tubules, or even into 
Malpighi's capsules. 

Special care has been recently devoted to the study of the minute changes in 
the glomeruli, although at present there is a conflict in the views regarding them. 
Klebs called attention to the fact that in scarlatinal nephritis the lesions may be 
almost exclusively confined to the glomeruli (glomerulo -nephritis). Sometimes 
kidneys of this sort seem almost normal to the naked eye, although during the 
life of the patient there have been the severest symptoms, such as anuria and 
uraemia. Eriedlander, Ribbert, Langhans, and others have pursued the study of 
the histological changes in the glomeruli. In part there are degeneration, hyper- 
plasia, and desquamation of the glomerular epithelium; in part changes in the 
walls of the blood-vessels themselves. With regard to the secretion of urine, and, 
in particular, the development of albuminuria, these changes in the glomeruli are 
certainly of the greatest importance, and it is not improbable that in many cases 
of acute nephritis the disease begins chiefly in the glomeruli; but, on the other 
hand, it is not proper to suppress too completely the other changes in the renal 
parenchyma as compared with the glomerulo-nephritis. 

In regard to the extent of all these changes which have been described, it 
should be noted that not infrequently certain portions of the kidney are more 
severely diseased than others, so that sometimes the nephritis tends to develop 
in separate foci. In general, however, acute nephritis is diffuse. 

If the histological processes have been made clear, the understanding of the 
macroscopic appeararce of the inflamed kidney is very simple. We can under- 
stand that either this or that " form " of acute nephritis must be present accord- 
ing to the predominance of this or that histological process. If an abundant 
interstitial exudation is present, the kidney is much enlarged; if this exudation 
is slight, the kidney varies but little, or not at all, from its normal size, not- 
withstanding any other severe changes. In the first case it usually feels soft, 
from inflammatory oedema; in the second case, it is comparatively firm. If 
there is a marked hyperaemia of the kidney, it appears much reddened; if the 
kidney is anaemic, it is paler ; and if an extensive fatty degeneration is also pres- 
ent, it is yellowish-white or yellow. If haemorrhages are present, they can easily 
be recognized with the naked eye on the outer surface beneath the capsule as dark- 
red points that can not be wiped away. We speak then of an " acute hemor- 
rhagic nephritis." On section, the medullary substance is more or less dilated, 
often projecting somewhat above the general level of the cut surface, its normal 
striated appearance is almost always obliterated, and its color shows the same 
variations as the outer surface of the kidney. ~Not infrequently the diseased 
Malpighian corpuscles can be recognized by the naked eye as grayish-red or whit- 
ish points. Since, as we have said, the nephritic changes often show not a uniform 
and diffuse, but a nodular arrangement, we can understand that the kidneys some- 
times have quite a mottled appearance, since hyperaemic or haemorrhagic red spots 
alternate with the lighter anaemic and the yellow fatty-degenerated parts. 

There are, accordingly, cases of nephritis which show almost nothing abnor- 
mal to the naked eye, while, on the other hand, there are haemorrhagic and non- 
haemorrhagic forms, appearing pale, yellow, red, or variegated, none of which 
can in the essential features be separated from one another, but which are com- 
bined with one another in all conceivable ways. The forms of nephritis that 
differ in aetiology have, to a certain degree, definite and characteristic anatomical 
types, but strict rules can not be laid down in regard to this. 

Clinical History. — The most essential symptom of acute nephritis is the ab- 
normal character of the urine. In most of the milder, and even in many of the 



ACUTE NEPHRITIS 



009 



severer cases of nephritis, the change in the urine is the sole objective clinical 
symptom which renders the diagnosis possible- The physician must, therefore, 
make it his practice to submit the urine to repeated examinations in every case of 
disease where there is any possibility of the presence of a nephritis. 

The simple parenchymatous degeneration of the kidneys, cloudy swelling, 
fatty degeneration, etc., may probably sometimes exist without being followed 
by any discoverable change in the urine; but they often lead to a slight albu- 
minuria, which is easily explained from the change in the epithelium of the 
glomeruli. If, then, the urine contains a slight amount of albumen (which usu- 
ally soon passes off) in the course of any febrile infectious disease or other affec- 
tion (the so-called febrile albuminuria, etc.), we are justified in assuming some 
of these mild conditions of degeneration in the kidneys. Usually the urine shows 
no other peculiarities, but sometimes we find in the sediment a few hyaline casts, 
a few white blood-corpuscles, etc. As we have repeatedly stated, these conditions 
pass into nephritis proper without any sharp limitations. 

Character of the Urine in Acute Nephritis. — In almost every case of severe 
nephritis the amount of urine for the twenty-four hours is more or less dimin- 
ished. This is caused directly either by the lessened elimination of water by the 
kidneys, or by the plugging of many uriniferous tubules by casts, desquamated 
epithelium, etc. The amount evacuated daily is often only fifteen or twenty 
ounces (400-700 cubic centimetres), but it sometimes falls to a much lower figure, 
two or three ounces (100-50 cubic centimetres), and there may finally be even com- 
plete anuria. In general, though not without exceptions, the diminution of the 
amount of urine runs parallel to the severity of the anatomical changes in the 
kidney. Improvement in the disease is very often first seen in an increase of the 
amount of urine. If there was a previous oedema, and this is absorbed, the daily 
amount of urine often rises during convalescence to a very considerable quantity, 
eighty to a hundred ounces (2,500-3,000 cubic centimetres). Even in cases in 
which there had been no decided oedema, we have often seen during recovery from 
acute nephritis very abundant diuresis. In so far as this symptom did not relate 
to the excretion of water that had been retained in the system, it might perhaps 
be referable to an abnormal permeability of the glomeruli, similar to the condi- 
tion sometimes seen after a severe attack of typhoid fever. 

The specific gravity of the urine is at first usually increased, since the urine is 
poor in water, but comparatively rich in solid constituents, especially in albumen 
(vide infra). Of course there are great differences here, and a urine secreted in 
an abnormally small amount may show a specific gravity of only 1010 or 1015, 
while, on the other hand, urines with a specific gravity of 1020 to 1030, or even 
more, have been observed. If during convalescence a very abundant, watery urine 
is passed, it of course usually has a low specific gravity, about 1005 to 1008. 

In many cases, but of course not in all, we may suspect the abnormal character 
of the urine from its appearance. This depends chiefly upon an admixture of 
abnormal morphological constituents. If these are present in large numbers, as is 
usually the case, the freshly passed urine is cloudy, and deposits a more or less 
abundant floccular sediment. The appearance of the urine is most altered if 
blood be mixed with it (hsemorrhagic urine). According to the amount of blood, 
the urine is a light or dark red, or even a dark black-red, and often has a greenish 
reflection when the light falls on it. 

The microscopic examination of the sediment gives more accurate information 
upon the different morphological constituents. We can not, of course, enumerate 
all the possibilities that may exist (see page 592 et seq.). In general, it may be 
said that in most of the severe cases of acute nephritis the urine contains numer- 
ous casts of the hyaline and other varieties. As has been already mentioned, the 
epithelial casts and the firm, waxy casts are especially common in the severer 
39 



610 



DISEASES OF THE URINARY ORGANS 



forms of acute nephritis. The hyaline casts have usually adherent to them red 
and white blood-corpuscles, as well as epithelium, fat-drops, and detritus. These 
morphological constituents are also found free in greater or less amount. The 
sediment is apt to contain also numerous beautiful crystals of uric acid. 

Individual cases are often characterized by a striking predominance of some 
one constituent — epithelium, white blood-corpuscles, or red blood-corpuscles — 
but no special rules in regard to this can be given. We have spoken previously 
(page 594) of the special conclusions we can draw from the different objects 
found in the sediment. We can accordingly distinguish an acute hemorrhagic, 
or non-hsemorrhagic, an acute desquamative, and a fatty degenerative nephritis, 
but we must always bear in mind that all these forms pass into one another with- 
out sharp boundaries. 

The chemical examination of the urine gives, as the most important and con- 
stant result, usually a considerable amount of albumen. Since the reaction of the 
urine is almost invariably acid, the albumen is immediately precipitated on heat- 
ing the urine, and sinks to the bottom of the test-tube, where it usually takes up 
about one half or three fourths of the volume of urine used for the heat-test. 
More accurate quantitative determinations of albumen give most frequently in 
acute nephritis an amount of albumen of from three tenths to one per cent.; 
higher percentages are rare. The daily total amount of albumen eliminated 
amounts to about one or two drachms (grammes 5-8), or sometimes more, but the 
daily loss of albumen from the body hardly ever exceeds the amount of five 
drachms (grammes 20). The variation in the amount of albumen eliminated 
in different cases is quite noticeable. 

The examination of the other solid constituents, which is not generally em- 
ployed in practice, usually gives a diminished secretion of urea, phosphoric acid, 
etc., corresponding to the diminution in the whole amount of urine. 

The other Symptoms of Acute Nephritis. — Local symptoms in the kidneys 
themselves are only rarely present. There is, of course, a certain tenderness in 
the region of the kidneys, which, however, is too ambiguous to have very great 
symptomatic importance. It is more often the case that the abnormally concen- 
trated urine causes frequent micturition, associated with a disagreeable burning 
sensation — a sort of vesical tenesmus. 

The subsequent symptoms of acute nephritis, which appear in the rest of the 
body, and among which dropsy takes the first place, are far more important than 
the local symptoms. (Edema may be entirely wanting in acute nephritis, particu- 
larly in cases of secondary nephritis after pneumonia, erysipelas, diphtheria, and 
usually in cases of septic nephritis. On the other hand, oedema is especially char- 
acteristic of many cases of acute nephritis, including cases due to scarlet fever, to 
catching cold, to alcoholic excess, and to pregnancy, as well as the so-called pri- 
mary nephritis and the nephritis which follows cutaneous diseases, such as 
scabies or pustulous eczema. This oedema is not infrequently the most promi- 
nent clinical symptom. We must always be prepared for its appearance, espe- 
cially when the amount of urine shows a considerable and persistent dimi- 
nution. 

The oedema is usually discovered first in the face, which has a bloated, and 
often a pale and somewhat shiny appearance. The eyelids are usually most 
swollen at first. Besides the face, the ankles, the legs, the scrotum, and the depend- 
ent parts of the trunk may be the chief seat of the oedema, the severity and extent 
of which may of course vary greatly in different cases. If a high degree of gen- 
eral dropsy develops, this is a source of great distress to the patient. The move- 
ments of the body are much restrained, and all changes of position are difficult, 
associated with great exertion, and painful. In the severest degrees of dropsy 
small fissures may form here and there in the excessively tense skin, from which 



ACUTE NEPHEITIS 



611 



the dropsical fluid oozes. Such little wounds are sometimes the starting-point for 
disagreeable erysipelatous inflammations, etc. 

If great oedema of the skin is present, we usually find at the same time a more 
or less marked dropsy of the serous cavities. It is often *hard, however, to make 
out ascites or hydrothorax on physical examination, owing to the oedema of the 
skin that is present. The symptoms mentioned acquire their chief clinical signifi- 
cance from the difficulty of respiration necessarily associated with them, since the 
diaphragm is pressed upward by ascites, and the lungs are compressed by hydro- 
thorax. If a hydrothorax is more marked on the left, or especially if hydroperi- 
cardium sets in, the activity of the heart is materially impaired. 

A marked oedema of the mucous membranes develops but rarely; in a few 
cases we have seen oedema of the conjunctivas, oedema of the soft palate, and 
oedema of the glottis. Of the oedemas of internal organs, oedema of the brain has 
already been mentioned as a possible cause of severe nervous urasmic symptoms. 
(Edema of the lungs, which often comes on toward the end of the disease, when 
it terminates unfavorably, is usually not to be regarded as a part of the general 
oedema, but as a result of the final cardiac weakness. 

In regard to the other symptoms in the different organs, the symptoms on the 
part of the circulatory apparatus must first be mentioned. The pulse is often 
abnormally tense, hard, and full (see page 600). In the beginning of the disease 
it is often somewhat slow; later it is usually accelerated. A beginning cardiac 
hypertrophy can often be made out post mortem, and sometimes clinically, in 
cases which have lasted a rather long time, four to six weeks. It seems 
to develop most rapidly in children who were previously well and strong. We 
pay especial regard to the condition of the apex-beat, and to the accentuation of 
the aortic second sound. The occasional nose-bleeds are probably connected with 
the increased arterial tension. Pericarditis is seen as a rare complication — a 
complication which is connected with the general fact that in all forms of nephri- 
tis the different internal organs, especially the serous membranes, have a tendency 
to inflammation. Whether this circumstance is connected with the retention of 
urinary constituents, as has been repeatedly surmised, can not at present be de- 
cided with certainty. 

Of the symptoms in the respiratory apparatus, we have mentioned above the 
dyspnoea consequent upon the dropsical symptoms. In severe cases the lungs 
themselves are often drawn into sympathy, as shown by the development of a dif- 
fuse bronchitis or a peculiar form of pneumonia. The latter stands midway 
between a catarrhal and a croupous inflammation. It exhibits, to a certain degree, 
a form of stiff inflammatory oedema, and occurs in just the same way in the 
chronic forms of nephritis as in acute nephritis. When it involves both lungs to a 
great extent, it may be the immediate cause of death. The development of gen- 
eral pulmonary oedema is usually a sign of beginning weakness of the left ven- 
tricle, as we have said above, although here, too, inflammatory factors may have 
some influence. 

Vomiting is the most important symptom in the digestive apparatus. If it 
appears in a marked degree, it may almost always be considered as a uraemic 
symptom, and then is often the precursor of severe nervous symptoms. The appe- 
tite is almost always diminished in acute nephritis; the bowels are usually consti- 
pated, but there may be quite severe diarrhoea (see page 600). We may mention 
peritonitis, which is sometimes purulent, as a very rare complication (vide supra). 

The temperature is markedly influenced by acute nephritis only in those cases 
where the disease develops in previously healthy persons, or at least in those free 
from fever. Then we see quite frequently a moderate fever, with an irregular 
rise of temperature of about 100° to 102° (38°-39° C). It is quite rare that an 
apparently primary acute nephritis begins suddenly with a chill and high fever, 



612 



DISEASES OE THE URINARY ORGANS 



104° (40° C). The condition of the temperature on the onset of uraemic symp- 
toms has already been described (page 600). 

The state of the general nutrition suffers in quite a noticeable degree in most 
of the severe cases of acute nephritis. The emaciation is often concealed by the 
oedema; but the anaemia is the more prominent, and often lends to the bloated 
face a peculiar aspect. 

Uraemic symptoms may come on at any time in the course of acute nephritis. 
We are often prepared for the onset of uraemia by a previous marked decrease in 
the secretion of urine, or by the veil-known prodromal symptoms, but in other 
cases it begins very suddenly with severe symptoms of eclampsia. In regard to 
all further details we may refer to what was said on page 5 l J6 et seq. 

The Course and Different Forms of Acute Nephritis. — The whole clinical 
picture of acute nephritis depends very materially upon the form of its develop- 
ment. If an acute nephritis comes on in the course of a severe infectious general- 
disease, as in the course of a septic affection, of ulcerative endocarditis, or of 
severe typhoid, the changes in the urine are often the sole indication of the occur- 
rence of the complication. The type of the severe febrile general disease is in no 
way materially modified by the added renal affection; oedema and uraemic symp- 
toms do not usually appear, often because the primary disease soon ends in death. 

Also when nephritis comes on in previously healthy persons or in chronic 
invalids, the tuberculous, etc., in many cases the changes in the urine are the 
chief symptom, while the other general and secondary symptoms are scarcely evi- 
dent at all, or at least only in a very slight degree. Such mild cases are associated 
only with more or less general dullness and loss of appetite. (Edema is entirely 
absent, or present only to a very slight degree. Of course such cases demand 
great caution, since even in them we may have a sudden outbreak of severe 
uraemic symptoms. 

The fully developed type of severe acute nephritis is seen especially in scar- 
latinous nephritis (q. v.), which comes on in children who are fully convalescent 
or apparently wholly well ; it is also seen in many cases of apparently idiopathic 
nephritis (vide supra), or nephritis coming on after exposure to cold, etc. In these 
cases there is often the development of a general dropsy, secondary pulmonary 
affections, uraemic symptoms, the symptoms mentioned in the circulatory appa- 
ratus, etc. In these cases, too, the examination of the urine affords the only cer- 
tain means of judging accurately of the condition, but the other morbid symptoms 
which appear early — oedema, anaemia, and vomiting — may direct our suspicions 
to the developing renal affection. 

Scarcely any general statements can be made as to the course and the dura- 
tion of acute nephritis, since the variations in this respect are too great. To 
describe here in particular all the different forms of nephritis according to the 
astrological conditions in question would lead us too far. We will therefore refer 
to the description of the different primary diseases, in which the characteristic 
marks of any renal complication are always stated. A few remarks must be 
added about some of the simple forms of acute nephritis. 

The so-called primary idiopathic nephritis usually appears rather suddenly 
without any demonstrable cause, or it may follow a marked chill (" nephritis due 
to catching cold")- The first symptoms of the disease are sometimes insignifi- 
cant, but at other times they are quite severe — chills, fever, renal pain. etc. Some- 
times other "rheumatic symptoms," such as angina or articular pains, are also 
present. Often the first thing which attracts the attention of the patient is the 
occurrence of oedema, the puffiness of the face, or slight shortness of breath due to 
hydrothorax. Sometimes the first symptom is vomiting. The further course of 
the illness may be mild or severe. In the former case the oedema that has ap- 
peared is but slight, the changes in the urine (albuminuria, haematuria, etc.), do 



ACUTE NEPHRITIS 



613 



not attain a very high degree, and after a few weeks- complete recovery ensue3. 
In other cases, however, the type of a severe, acute, and very often hemorrhagic 
nephritis develops, with great general dropsy, uraemia, etc., which in three or 
four weeks, or sooner, may lead to death; but improvement may follow in spite 
of the severest symptoms. Then the amount of urine gradually increases, and the 
abnormal constituents of the urine, the oedema, and the other morbid symptoms, 
gradually disappear. Of course, it is often a long time before complete recovery 
ensues, since, even when the patient feels perfectly well subjectively, the urine 
may still sometimes contain some albumen, a few casts, or a few red blood-corpus- 
cles. In such cases one must think of the possibility of a transition of acute 
into chronic nephritis. !Not infrequently there is apparently complete recovery, 
but several weeks or months later there appears suddenly, perhaps after some spe- 
cial cause, such as catching cold, or over-exertion, or some febrile disease, a fresh 
attack of acute nephritis (" acute recurrent nephritis," vide supra). 

The nephritis of pregnancy usually begins gradually. Frequent micturition 
and oedema of the lower extremities make their appearance, and beside these there 
are often nausea and even vomiting. If we examine the urine, we usually find 
it quite rich in albumen, but comparatively poor in morphological elements. The 
slight sediment consists of hyaline casts, a few white blood-corpuscles, and some 
epithelium. Only rarely does the urine assume a hemorrhagic character. 

The condition described almost always lasts to the end of pregnancy. In the 
cases that proceed favorably a very rapid recovery often follows after the birth 
of the child; but the onset of eclampsia gravidarum is to be dreaded as a not 
infrequent and a dangerous complication. This is to be regarded as entirely anal- 
ogous to uraemia. It begins after mild prodromal symptoms, or even quite sud- 
denly, with violent general convulsions, during which the child is usually born. 
A more or less persistent coma follows the convulsions. The convulsions may be 
very frequently repeated. Death ensues in about one third of the cases ; the other 
cases usually recover, only rarely passing into chronic nephritis. A slight albu- 
minuria may, however, persist for months after delivery. The prognosis is still 
more unfavorable for the child than for the mother, inasmuch as the child dies in 
nearly one half of the cases. 

Moreover, it should be noted that eclampsia sometimes occurs without any 
preceding albuminuria, and perhaps of itself leads to a mild albuminuria because 
of the circulatory disturbances incident to the convulsive seizures. 

The anatomical changes in the nephritis of pregnancy are hardly ever very 
striking to the eye. The kidneys are usually pale and but little enlarged. Under 
the microscope we usually find a slight interstitial oedema and degenerative 
changes in the epithelium. Only rarely are more marked nephritic appearances 
present. 

Acute alcoholic nephritis is a term which we apply to that form of the disease 
which we have repeatedly observed in excessive beer drinkers — for instance, in 
brewers. The appearance of the disease seems to be favored by coincident excit- 
ing causes, such as catching cold, but beyond this it is to be regarded as the sud- 
den development of a renal disease, resulting from the toxic influences of alcohol 
habitually ingested. There is a rapid and great development of general dropsy. 
The amount of urine is moderately diminished. The urine contains much albu- 
men, but usually remains rather clear and contains no blood. As a rule, the 
patients are obese, and their discomfort is great. A favorable termination is pos- 
sible under suitable treatment, but yet there is always danger of a transition into 
chronic nephritis. 

Diagnosis. — Acute nephritis can be overlooked only when the examination of 
the urine is neglected or when it is impracticable. The latter sometimes happens, 
for example, when the patient does not come under observation until after the 



614 



DISEASES OF THE URINARY ORGANS 



onset of severe uraemic symptoms. Otherwise, however, the changes in the urine 
always furnish evidence enough to recognize the existence of the affection of the 
kidneys. We can, of course, decide that the nephritis is acute only by considera- 
tion of the history, the serological conditions, and the whole course of the dis- 
ease. We must also bear in mind the possibility that there may be an acute ex- 
acerbation in a chronic nephritis that has already existed for a long time, and has 
been perhaps without symptoms — acute recurrent nephritis, usually hsemorrhagic. 

Prognosis. — The prognosis of acute nephritis depends in many cases not only 
upon the renal affection, but also upon the underlying primary disease. We can 
not here describe in detail the numerous conditions that must be considered, but 
they are to be found in the appropriate chapters. 

Many cases of primary nephritis from toxic action, or exposure to cold, and 
also many cases of secondary nephritis after scarlet fever, in pneumonia, typhoid 
fever, or syphilis, during pregnancy, etc., recover perfectly in a short time or 
after several weeks, according to the severity of the individual case. On the 
other hand, however, it must be said that every case of nephritis must be viewed 
with great caution, partly because it may be the starting-point of a subsequent 
chronic renal disease, and partly because dangerous sequelae may sometimes de- 
velop in cases that at first are apparently mild. The dangers of acute nephritis 
are chiefly : First, the appearance of severe general dropsy, especially in the inter- 
nal cavities of the body. Of the forms of dropsy hydrothorax is the most danger- 
ous, as it may produce suffocation by compression of the lungs. Second, uraemia, 
especially in its severe convulsive forms, with high temperature and finally car- 
diac paralysis. Third, the inflammation of internal organs, among which second- 
ary pneumonia, in particular, is a frequent cause of death, while secondary peri- 
carditis and peritonitis, as we have said, are seen in but very few cases. We musi 
bear in mind, however, that in individuals otherwise healthy the severe sequelae 
just mentioned may also be recovered from. The most extreme dropsy may be 
re-absorbed, and we sometimes see recovery, especially in children, after the 
worst uraemic symptoms. 

Treatment. — With regard to prophylaxis, the reader should be reminded that 
in all diseases which experience has shown to be prone to lead to secondary ne- 
phritis — for instance, scarlet fever — the kidneys should be guarded as much as 
possible, from the start, by suitable diet (milk) ; by promoting the secretion of the 
kidneys ("flushing the kidneys"), by administering an abundance of liquids, 
such as mineral waters, milk, and lemonade ; and by stimulating the cardiac activ- 
ity by warm clothing, warm baths, and rubbing with alcohol. 

If nephritis has already developed we can scarcely hope to influence directly 
the inflammatory process. The remedies recommended for this purpose are tan- 
nin, uva ursi, fuchsine, and methyl blue, but to an unprejudiced observer they 
seem absolutely useless. 

We expect as little result at present from " external antiphlogosis " as from the 
internal remedies mentioned — that is, from local blood-letting, applications of ice 
to the region of the kidneys, etc. Only in the rare cases where severe pain in the 
region of the kidneys comes on at the beginning of nephriiis, in an otherwise 
robust individual, are we at present justified in trying leeches or a few dry cups. 
The warm baths, to be described more fully below, have perhaps an indirect 
favorable action on the process in the kidneys, since they produce a hyperaemia 
of the skin, and thus lessen the flow of blood to the kidneys. 

Although we must accordingly admit that there is scarcely any remedy at our 
service which has a direct therapeutic influence upon the diseased kidneys, the 
treatment of nephritis may nevertheless produce very .significant results, since 
both a number of hygienic measures and the fulfillment of certain symptomatic 
indications are of the greatest importance. 



ACUTE NEPHRITIS 



615 



Among the general hygienic measures we must mention first strict confine- 
ment to bed. In the severe cases its necessity is self-evident; but, even in the 
milder cases, which run their course without any severe subjective symptoms, 
constant rest in bed is necessary throughout. In this way we not only avoid the 
unfavorable action of cold upon the external skin, but the activity of the skin, 
which must act vicariously for the kidneys, is also excited by the uniform warmth 
of the bed; while any useless muscular exertion, which would tax the heart's ca- 
pacity for work, is also avoided by staying in bed. In general it is advisable to 
cover the patient quite warmly, so as to keep him in a constant slight perspiration. 

The regulation of the diet is very important. All those foods and drinks which 
may irritate the kidneys are to be strictly avoided, especially spices, very sour 
substances, strong tea and coffee, or alcoholic drinks. Milk has for a long time 
proved itself to be by far the most suitable and best food. It has won for itself 
the reputation of a remedy in renal disease, and the best results have often been 
seen from a methodical " milk-cure " — that is, from feeding the patient almost 
exclusively with milk. The great aversion of some patients toward milk, how- 
ever, is sometimes an obstacle to its use. We may often be aided, then, by mak- 
ing the milk more acceptable to the patient by the addition of a little coffee, salt, 
a little cognac, or soda-water. Among other foods to be recommended are but- 
termilk, milk-gruel with rice or groats, and flour-gruel. We should be very cau- 
tious about giving meat as long as there are severe symptoms. 

Less harmful are light broths made from pigeons, fowls, or veal, with eggs. In 
every case of acute nephritis, even when there is dropsy, we regard the abundant 
ingestion of liquids as advantageous. For beverages, besides milk we may give 
Seltzer, Wildinger, or Fachinger water, tea, and lemonade. The last is particu- 
larly to be recommended. Alcoholic beverages must be entirely withheld, or, at the 
most, we may allow a little claret. The stronger wines are given only when the 
heart becomes weak, and even then their usefulness is dubious. 

The chief object in the symptomatic treatment consists in preventing the in- 
jurious results of the defective elimination of the water and the solid constituents 
of the urine by the kidneys, or in remedying these results if they have already 
occurred. This purpose can be attained only by exciting, as far as possible, the 
activity of other organs which in this respect may act vicariously for the kidneys. 
The skin deserves the first attention here, through which, by means of the sweat- 
glands, large amounts of water, and also, to a certain extent, the solid constituents 
of the urine, which have been retained, may be eliminated. The diaphoretic treat- 
ment of renal diseases has, therefore, been generally in vogue for a long time. If 
the patient's general condition permits, we always begin with it as early as possi- 
ble, even before there have been any signs of oedema, ursemic symptoms, etc. For- 
merly we employed, like most other physicians, hot baths from 95° to 105° (36°- 
40° C). The patient stays about half an hour or an hour in the bath, is then 
rapidly dried somewhat, wrapped up in bed in a previously warmed sheet, and 
well covered up to the neck with blankets. In order to make the procedure 
somewhat easier for the patient, it is a good plan to cover the forehead with 
a cold compress, always to wipe the sweat carefully from the face, and fre- 
quently to give a little swallow of fresh cold water. The production of sweat 
is, of course, better excited during the pack if the patient takes some hot drink, 
hot milk with soda-water, or hot elder-tea. It sometimes seems to aid diaphoresis 
if an internal diaphoretic be given at the same time, the best being five to ten 
grains of Dover's powder (gramme 0.3-0.5), or a teaspoonful or two (grammes 
5-10) of liquor ammonii acetatis [U. S. P.] (spiritus Mindereri) in a cup of 
elder-tea. We have also found a good rubbing of the whole body with dilute 
warm French brandy of service before the pack. The pack may last two or three 
hours. Of late years, particularly in severe cases with marked dropsy, we have 



616 



DISEASES OF THE UKIXARY OEGAXS 



almost entirely abandoned baths and in their stead employed with the best re- 
sults the hot, wet pack, or dry heat (vide infra). For the pack, the patient is 
completely wrapped up in a hot, wet sheet; on both sides are arranged several 
jugs filled with hot water, and likewise enveloped in moist cloths; then the pa- 
tient is covered with several dry blankets and is given two or three cups of some 
hot drink. The duration of a pack of this sort is about two or three hours. In- 
stead of moist heat, dry heat may be applied with the purpose of sweating the 
patient. There are complicated arrangements, such as sweat-boxes and a patent 
sweat-bed, but these can seldom be employed outside of hospitals, and we have for 
a considerable time adopted with good results the arrangement made by Quincke. 
A tin pipe is bent at an angle and fastened upon a board, and its upper end is 
introduced under the bed-clothes, which should be, if possible, somewhat raised 
up, while under its lower open end a lighted alcohol lamp is placed upon the floor ; 
the warm air rises and is conducted beneath the bed-clothes, where the heat 
becomes so great that the upper end of the pipe must always be wrapped in a cloth 
wet in cold water. 

In this way we succeed in many cases in causing a considerable sweat, so that 
the patient loses several pounds in weight at each pack, and an existing dropsy 
may sometimes be made to disappear completely in a comparatively short time. 
On the other hand, however, we can not deny that it is very hard sometimes to 
make patients sweat, even when there is oedema of the skin, and also that many 
patients do not bear hot baths and packs at all. The latter is especially true if 
the patient has dyspnoea, and if signs of cardiac weakness have already set in. 
In such cases we must be very cautious about sweating the patient, and we should 
employ merely warm baths ; or if we put the patient in a pack, it should be for 
a brief time. 

Of internal diaphoretics there is one remedy which is particularly useful in 
renal disease — viz., the hydrochlorate of pilocarpine, prepared from jaborandi. 
This is best employed subcutaneously, one sixth to one third of a grain at one 
dose (gramme 0.01-0.02), but the drug may also be given internally in pills in the 
same dose. Its effect consists in the production of a rather profuse perspiration, 
and likewise a marked increase in the salivary secretion, which latter is often 
a great annoyance to the patient. For this reason, and because it sometimes 
induces cardiac weakness, pilocarpine is, on the whole, scarcely to be recom- 
mended. We ourselves employ it only occasionally when the hot baths are not 
used or when they do not have a satisfactory effect. 

Next to the skin, the intestinal mucous membrane is the organ from which we 
may soonest expect to produce a vicarious elimination of water, and also of urea. 
It is sometimes, therefore, of distinct service to prescribe drastic cathartics in 
nephritis with a diminished secretion of urine, especially if there is a tendency 
to constipation besides the dropsy, dyspnoea, etc. The drastic cathartics chiefly 
used are infusion of senna, extract of colocynth, gamboge in two-grain powders 
(gramme 0.1), tamarinds, Epsom salts, etc. 

Finally, it may be asked whether we should not excite the secretory function 
of the kidneys themselves by the exhibition of diuretics. Certainly the employ- 
ment of vigorous diuretics is opposed by the consideration that we might still 
further irritate and consequently damage the renal epithelium. The milder 
diuretics, particularly the acetates of potash and of sodium, in doses of about one 
to two and a half drachms (grammes 5-10) in the course of twenty-four hours, 
and diuretine, one to one and a half drachms (grammes 4-6) a day, are usually 
well borne and are often efficient. The use of calomel in renal disease has been 
repeatedly commended, but we would warn against its employment because very 
disagreeable symptoms of mercurial poisoning, such as stomatitis, are apt to 
occur. 



ACUTE NEPHRITIS 



617 



The therapeutic measures so far spoken of are intended to prevent as far as 
possible the retention of urinary constituents in the body. They are also very 
much employed when the signs of this retention have already appeared. The 
dropsy especially is best treated by methodical sweating, with the aid, eventually, 
of drastic and diuretic remedies. If there is persistent and extreme dropsy we 
may determine to remove the dropsical fluid by direct mechanical means from the 
subcutaneous cellular tissue. Letter than the so-called capillary trocars and 
similar apparatus (such as aspiration through a funnel placed like a wet cup 
upon the incised skin) are simple scarifications of the skin made longitudinally 
in the dependent parts (scrotum and posterior surface of the thigh and calf). 
From these the dropsical fluid is allowed to escape into pads made of peat, 
[gauze], or similar substances. Absolute antisepsis and asepsis are demanded, 
lor there is a great tendency to erysipelatous infla mm ation. 

When uraemia is threatening, and often even when it has broken out, we may 
try to produce an elimination of the injurious products of tissue metamorphosis 
from tne body in the well-known ways above described, by sweating or drastic 
purgatives. Beside this, the ursemic symptoms, however, often demand a special 
symptomatic treatment. If very violent and frequent ursemic convulsions appear, 
we consider it advisable to try to suppress the attacks by chloroforming the pa- 
tient. At any rate, it seems to us to be better to use chloroform in uraemia than 
to give narcotics internally, because with this we can watch the action of the rem- 
edy better, especially with regard to the pulse and respiration. Chloroform is 
also generally used by the obstetricians as the main remedy in the eclampsia of 
pregnancy. If the attacks are not very frequent, but if there is marked somno- 
lence or coma, tepid baths with cold shower-baths are often employed with dis- 
tinct advantage. Cool baths are also serviceable when there is a great increase 
of the temperature. If we are treating a robust individual with a full pulse, and 
during severe uraemia there is a decided redness or cyanosis of the face, venesec- 
tion may be indicated. This sometimes has a striking and instant effect, as has 
lately been confirmed by various observers. Great attention is to be paid to the 
condition of the heart. As soon as the pulse becomes small and weak, energetic 
stimulants, such as strophanthus or subcutaneous injections of camphor, must be 
used. If the signs of cardiac weakness appear before the beginning of severe 
uraemic symptoms, infusion of digitalis must be used, two or three parts to three 
hundred of water. Through its action in raising the blood-pressure — it being ad- 
visable under some circumstances to combine with it acetate of potassium — free 
diuresis sometimes comes on, and with it a disappearance of the danger from 
uraemia ; but meanwhile we must watch for symptoms of the toxic action of digi- 
talis. The tinctura nervina Bestuscherni [nearly equivalent to the tincture of the 
chloride of iron, U. S. P.] may also be sometimes used to advantage in uraemia. 
We are not apt to interfere with uraemic vomiting or uraemic diarrhoea, because 
these symptoms, as we have said, are to be regarded as a form of self-help by the 
organism. Only when such symptoms are very distressing do we give cracked ice, 
morphine, opium, cocaine, chloroform, etc. If the vomitus contains ammonia, it 
is a good plan to give ten or fifteen drops of dilute hydrochloric acid in water sev- 
eral times a day. An abundance of liquids is always to be prescribed upon the 
appearance of uraemic symptoms, because in this way it is probable that the poi- 
sonous blood is diluted and also the excretion of the toxines promoted. 

[A method of treatment of ursemic convulsions, whether post partum or con- 
nected in no way with parturition, which gives excellent and prompt results, is the 
administration of pilocarpine hypodermically — grain i, and repeat in twenty 
minutes — followed by the hot-air bath, to maintain the action of the skin after 
it has once been started. Pilocarpine sometimes acts as a decided cardiac depress- 
ant, so one must be ready to administer stimulants — brandy or ether — under the 



618 



DISEASES OF THE UKIXAKY OKGANS 



skin if, as is apt to be the case, there is doubt as to the readiness with which they 
will be absorbed from the stomach or rectum.] 

In severe cases, the patient's dyspnoea often demands prompt relief. If the 
dyspnoea be caused, or at least increased, by hydrothorax, and we do not succeed 
in removing the hydrothorax in any other way, it is necessary to evacuate it by 
puncture. In acute nephritis, indeed, we may hope by this means sometimes to 
preserve the patient's life until improvement sets in. Great ascites must also be 
relieved by tapping. Against " renal pneumonia " our remedies are powerless. 
Tepid baths, shower-baths, and wet packs sometimes procure relief. In " uraemic 
asthma," morphine injections may act beneficially. If pulmonary oedema ensues, 
the heart again is chiefly to be considered. We may try, besides the remedies 
already mentioned, large mustard plasters, baths, and acetate of lead. 

We accordingly see that many remedies are at our service in the treatment of 
nephritis, the choice of which in the individual case must be committed to the 
personal judgment of the physician. In the main, we should always begin with 
the necessary hygienic measures, and, if possible, with a methodical diaphoretic 
treatment, and govern ourselves otherwise by symptomatic indications. After 
recovery has set in, great caution is still necessary for a long time. The patient 
must guard against physical over-exertion, errors in diet, and exposure to cold. 
Preparations of iron are to be prescribed when there is a secondary anaemia. 

In regard to the influence of the onset of an acute nephritis on the treatment 
of the primary disease, we may mention that cold baths are in general not to 
be freely used, as in typhoid fever with nephritis, but still they may be tried if 
they are otherwise urgently desirable. We would also suggest that certain 
internal remedies, especially calomel and salicylic acid, must be used only with 
great caution when there is nephritis. In the eclampsia of lying-in women the 
induction of premature labor is only rarely indicated, since the child is usually 
born during the paroxysms without interference. 



CHAPTEK III 

THE SUBCHRONIC AND CHRONIC FORMS OF NEPHRITIS, WITH THE 
EXCEPTION OF THE GENUINE CONTRACTED KIDNEY 

{Chronic Diffuse Nephritis, Chronic Parenchymatous Nephritis, Chronic Hemorrhagic Nephritis, 
Large White Kidney, Secondary Contracted Kidney) 

^Etiology. — While the acute nephritis described in the preceding chapter runs 
its course in several days or weeks, and only rarely extends over some months, 
we will now speak of inflammatory degenerative affections of the kidneys which 
last at least several months, and often go on for a year or two. The term " sub- 
acute " or " subchronic " is chosen for the cases that last a comparatively short 
time. As we must once more repeat, there is no sharp limit in this respect. 

In regard to the aetiology of these forms of nephritis, they do arise from an 
acute nephritis, but this is quite rare. Formerly such an origin was erroneously 
regarded as the rule, and this is the reason why the changes in the kidney in these 
cases were described as the "second stage of Bright's disease" (Frerichs). The 
English clinical observers Wilks and Johnson, whom Bartels followed in Ger- 
many, first pointed out the fact that in most cases the disease shows a chronic 
character from the start, and that we can only exceptionally, as after scarlet 
fever, recognize an acute " first stage." The name " chronic parenchymatous ne- 
phritis," since frequently used, is chosen entirely from practical reasons, inasmuch 



SUBCHRONIC AND CHRONIC FORMS OF NEPHRITIS 619 



as it briefly states the distinction from the genuine contracted kidney; but it is 
incorrect in principle, as will be shown from the description of the anatomical 
conditions later. It is more correct, therefore, to employ the term "chronic diffuse 
nephritis," because we have, in fact, to deal with what is essentially a chronic uni- 
versal or diffuse disease of the kidneys, as contrasted with the " contracted kid- 
ney" in which there are always bits of normal tissue interspersed between the 
numerous separate foci of disease. 

If we look for the aetiological conditions in cases that have a chronic course 
from the beginning, we can often discover nothing definite at all. The disease 
seems to have developed " of itself " in previously healthy persons. Most probably 
we have here some toxic or infectious agency that acts on the kidneys, whose 
detection, however, is at present impossible. In malarial regions the malarial 
poison may often lead to chronic nephritis. It is also attributed to syphilis and 
tuberculosis, but the cases met with are usually combinations of these diseases 
with amyloid kidney (vide infra). Frequent exposure to wet and cold, damp 
dwellings, etc., seem sometimes to be of more material significance. That hard 
drinkers, particularly beer drinkers, are especially liable to nephritis seems to the 
author indubitable, because of his personal observations (vide supra) ; but it is, of 
course, difficult to form a definite opinion on all these points. 

Persons in early middle life are most frequently affected by the disease, and 
men more often than women. In children and old people the disease is quite rare. 

Pathological Anatomy. — There is no essential distinction between the ana- 
tomical lesions of the kidney in acute and in chronic nephritis. The changes that 
are seen in both are essentially the same, only they develop and extend more 
slowly in the chronic forms; and they also, during their longer duration, lead to 
certain sequelae in the kidney, which can not develop at all in acute nephritis, 
owing in part to the lack of time. Even in chronic nephritis the individual cases 
differ from one another in many respects. First this and then that histological 
process is especially prominent, and thus lends certain peculiarities to the macro- 
scopic appearance of the kidneys. Certain sequelae — such as contractions — have 
also developed but little in many cases that soon end fatally, but they develop 
far more in other cases of longer duration. Hence it happens that we can quite 
well regard certain anatomical forms that are more frequently observed as types, 
although we must never lose from sight the important fact that there is a patho- 
logical unity in all these forms and types. Then we shall not lose the clew to the 
understanding of the morbid process if the individual case does not always har- 
monize with the scheme of the text-books. 

We distinguish the three following chief anatomical types of subchronic and 
chronic nephritis: 

1. Chronic Hemorrhagic Nephritis in the form of the Large Red or Varie- 
gated Kidney. — The kidney is at least of normal size, and often a little or a good 
deal enlarged. It feels firmer than normal; its capsule is often adherent to the 
surface in some places. The surface looks either uniformly a more gray red or 
more mottled, while dark-red spots alternate with lighter gray or even yellow 
spots. The red spots on the surface can not be wholly wiped off, and thus they 
prove to be haemorrhages. The gray or yellow parts correspond to the anaemic or 
fatty-degenerated portions. On section, the cortical substance is usually broader, 
its normal boundary is obliterated, and its color is a uniform gray red, or mottled 
and striated. 

Under the microscope we find in part the same changes as in acute nephritis — 
parenchymatous and fatty degeneration of the epithelium, casts or haemorrhages 
in the uriniferous tubules, inflammatory oedema or granular infiltration of the in- 
terstitial tissue, the capsules of the glomeruli sometimes thickened, the epithelium 
of the glomeruli sometimes proliferated or desquamated, etc. The special char- 



620 



DISEASES OF THE UEINAKY OKGANS 



acteristic of this chronic form, in contrast with acute nephritis, is that in many 
places a complete destruction of the uriniferous tubules has occurred, and that 
a genuine interstitial connective tissue, more or less rich in cells, has taken 
their place. In this lies the anatomical evidence of the longer duration of the dis- 
ease, since the two processes — both the complete atrophy of the epithelium, and 
especially the secondary proliferation of connective tissue — of course need a cer- 
tain time for their development. The atrophy and the consequent proliferation of 
connective tissue usually predominate in some parts, while in others nothing but 
fresher inflammatory and degenerative changes are perceived. 

2. The Inflammatory Eatty Kidney, or the Large White Kidney (yellow 
would be more exact). — In this form of chronic nephritis the kidney is usually 
enlarged, or at least of normal size. Its outer surface is smooth and of a yellow 
or an alternating yellow and gray-yellow color throughout. The broader cortical 
substance shows a yellow and usually somewhat mottled appearance, while the 
pyramids almost always appear considerably reddened. Haemorrhages are also 
almost always present in this form, usually, of course, in smaller numbers than 
in the variegated kidney, but they are sometimes quite abundant, as in the hem- 
orrhagic fatty kidney. 

The microscope shows the great affinity between this form of nephritis and the 
preceding. We have almost precisely the same changes, including always a par- 
tial destruction of renal tissue with a subsequent increase of interstitial con- 
nective tissue. The macroscopic appearance of the kidney is due to the fact that 
it is anaemic, and that the fatty degeneration preponderates in the epithelium. 
It is worthy of note that in these kidneys marked changes in the glomeruli are 
usually present. 

3. The Secondary Contracted Kidney. — While in the two forms of nephritis 
thus far described the outer surface of the kidney is still smooth, and the kidney, 
on the whole, is somewhat enlarged, we have to do here with kidneys of about 
normal size, on whose surface there are granulations, which as yet are slight, but 
which still are already plain. This granulation signifies nothing more than that 
the destruction of the renal tissue has here advanced farther, and that the newly 
formed connective tissue has in part undergone cicatricial contraction. These 
kidneys, therefore, represent a later stage of the two forms first named. They 
usually come under observation when the nephritis has lasted about a year and a 
half or two years, or even somewhat longer. The first beginnings of granulation 
may, of course, show themselves earlier, while, on the other hand, when the 
process lasts a longer time, a completely contracted kidney may develop. 

The color of these kidneys is usually reddish or mottled, the red spots corre- 
sponding to the sunken atrophic parts, and the gray or yellowish spots to the ele- 
vated parts. Yellow kidneys, however, may also show at times decided granu- 
lations. Microscopically, we find already marked atrophy of the renal paren- 
chyma, with a corresponding increase of the interstitial connective tissue. 

Formerly these kidneys were called the " transition between the second and 
third stages of Bright's disease." As follows from the above, they are to be 
regarded only as a more advanced form of chronic nephritis. Since the kidneys, 
in spite of their granulation, have on the whole a normal size, we can infer 
from this, and from the clinical course, that they were previously enlarged. 
Therefore the name of " secondary contracted kidney " is quite suitable, in oppo- 
sition to the genuine contracted kidney, which represents a much more chronic 
form of renal atrophy. In the latter the contraction takes place in an extremely 
chronic manner in a kidney which was previously normal, while in the " secondary 
contracted kidney" the cicatricial process develops in a kidney which was pre- 
viously the subject of diffuse disease. 

Of other pathological lesions, apart from the changes in the kidney, we will 



SUBCHROXIC AXD CHKOXIC FOBMS OF NEPHRITIS 621 



mention here only the hypertrophy of the left ventricle, which is found (vide 
infra) in all the above-mentioned forms of nephritis. The chronic parenchym- 
atous nephritis without cardiac hypertrophy, assumed by Bartels in his time, 
does not exist. Such cases were probably instances of unrecognized amyloid dis- 
ease. Exceptionally it may happen that when a patient with chronic nephritis is 
very much debilitated and enfeebled, the cardiac hypertrophy is not developed. 

Clinical History. — Only in the comparatively rare cases when the renal affec- 
tion begins acutely, do the symptoms of chronic nephritis follow immediately on 
the first acute stage. In most cases, however, the disease develops slowly and 
gradually from the start, as we have said, so that it is usually impossible to deter- 
mine accurately the moment when the disease begins. Still we may assume that 
the onset is decidedly more rapid in chronic diffuse nephritis than in genuine 
contracted kidney. 

The first signs of the disease consist of certain general symptoms, pallor, 
dullness, loss of appetite, nausea and headache, and later of oedema. The latter 
is often the first symptom which sends the patient to the physician, since in 
the beginning he is apt to pay little attention to the symptoms first named. The 
oedema usually appears first in the ankles and legs, more rarely at an early period 
in the face. It often disappears at first after a night's rest, but always develops 
afresh during the day, gradually increasing in intensity. The patient himself 
now sometimes notices a change in the urine, either an abnormal color or cloudi- 
ness or a diminished amount. The accurate examination of the urine by the 
physician first establishes the diagnosis. 

In regard to the more special symptomatology of chronic nephritis, we meet 
exactly the same symptoms as have been described in the preceding chapter on 
acute nephritis. The characteristic distinction is based merely upon the whole 
course of the affection and the order of development of the different symptoms, 
and not upon the symptoms themselves. 

The urine almost always is diminished. Of course the figures vary con- 
siderably both in different cases and at different times in the same case. A 
small amount of urine, ten to twenty-five ounces (300-700 cubic centimetres) a 
day, is almost always an unfavorable sign, while a free diuresis signifies an ab- 
sorption of the dropsy and an improvement of the condition. There is also a 
persistent increase in the amount of urine when the chronic nephritis passes into 
a secondary contracted kidney. Under such circumstances the daily amount of 
urine may rise to 1,500 or 2,000 cubic centimetres or more. 

The specific gravity of the urine is often increased to about 1015 to 1025, cor- 
responding to the amount of albumen and of other solid constituents. It is of 
course correspondingly lower when there is a more abundant elimination of water 
by the kidneys. 

The amount of albumen in the urine is quite marked in all severe cases, being 
one third to three fourths of its volume. It amounts to about 1.5-3 per cent, by 
weight, so that the patient's daily loss of albumen may reach half an ounce to an 
ounce (grammes 15-30). 

The examination of the sediment, which is usually abundant, is of the great- 
est importance for the accurate determination of the form of the anatomical 
changes in the kidneys. Above all, the question arises as to the presence or ab- 
sence of blood in the urine. If abundant, hematuria may be recognized by the 
naked eye from the color of the urine. The detection of smaller amounts of blood 
can be made only by the aid of the microscope. It goes without saying that the 
amount of blood in the urine varies considerably in the different cases, and in 
the same case the urine often contains much more blood during certain periods 
in the course of the disease than at other times. The portions of urine passed at 
different times taken separately often show quite marked variation in this respect ; 



622 



DISEASES OF THE URINARY ORGANS 



the day's urine usually contains more blood than the night's. Erom the detec- 
tion of renal hemorrhages, of course in connection with other symptoms, 
we can always make with certainty the diagnosis of a " chronic hemorrhagic " 
nephritis. 

In most cases casts are quite abundant in the sediment of the urine, but natu- 
rally their amount and variety undergo quite great variations in different cases 
and at different times in the same case. They are the direct sign of the presence 
of an inflammatory exudative process in the kidneys, although the deposits on the 
casts are more important for the diagnosis of the special form of renal disease 
than are the casts themselves. Those formed constituents of the sediment are 
most characteristic in this respect which point directly to the processes of fatty 
degeneration in the kidneys : the fatty granules and fatty granular cells, free or 
attached to the casts. The number of these elements is especially great in the 
chronic inflammatory fatty kidney, the " large white kidney." The usually clear, 
non-hemorrhagic urine may in some cases have even a fatty lustrous surface. 
Renal epithelium is, on the whole, more rarely present in the sediment in chronic 
nephritis than in acute, but it occurs in some cases. 

Of the other symptoms, the one that usually most strikes the eye is dropsy. It 
usually come on, as we have said, in the beginning of the disease, and slowly or 
rapidly reaches a great extent and intensity. A medium or even a high degree of 
general dropsy may often persist almost unchanged for months. In other cases 
it shows either spontaneous variations or variations influenced by treatment ; it 
decreases for a time only to increase anew. The severer and more comparatively 
acute the case, the greater in general is the dropsy. In the more chronic cases, in 
secondary contracted kidney, its intensity may be slight for a time or even perma- 
nently. The dropsy may even be absent in some cases, as we learn especially 
from the observations reported by Wagner under the name of " chronic hemor- 
rhagic Bright's disease without oedema " (vide infra). In regard to the different 
localizations of the dropsy, and to dropsy of the internal cavities, hydrothorax, 
ascites, and hydropericardium, and their results, the same holds true as in acute 
nephritis. 

Of the internal organs, the condition of the heart lays claim to the most inter- 
est. In all cases of chronic nephritis, in which we do not have to do with espe- 
cially weak and run-down patients, who can not save the necessary nutritive 
material for the formation of a cardiac hypertrophy, we find a pronounced and 
often a very marked hypertrophy of the left ventricle, either with or without a 
co-existing dilatation of its cavity. The detection of cardiac hypertrophy during 
the patient's life is sometimes difficult, especially when there is general dropsy, but 
the diagnosis can usually be correctly made with proper attention to the abnor- 
mally tense radial pulse, the accentuated, valvular aortic second sound, and the 
displacement outward of the apex-beat, or at least its increased strength. We 
often find in the cadaver, and can sometimes make out during life, a hypertrophy 
of the right ventricle (vide supra, page 603). 

A second important sequel of chronic nephritis consists of the changes in the 
retina — albuminuric retinitis. Although very rare in acu,te nephritis, these 
changes are present in the majority of the cases of this class. Sometimes the pa- 
tient's subjective visual disturbance (dimness of vision, defects in the field of 
vision) points to a disease of the retina, but the existence of disease can be estab- 
lished with certainty only by ophthalmoscopic examination. In these cases we 
find two kinds of changes, in varying numbers and combinations : first, retinal 
hemorrhages ; and, second, white spots and streaks, especially in the vicinity of 
the optic nerves. The origin of the spots, which may appear and disappear again, 
is not yet entirely clear. At any rate, they are circumscribed fatty degenerations 
of the special retinal elements. The degree of amblyopia depends, of course, 



SUBCHROXIC AND CHRONIC FORMS OF NEPHRITIS 623 



chiefly upon the localization of the changes, whether in the macula lutea, or other 
parts. 

We need say little in regard to the other symptoms, since they agree essen- 
tially with those of acute nephritis. The general anaemia is very pronounced in 
many cases, but it is less marked in the very chronic forms. The cerebral symp- 
toms, especially the headache and the mild vertigo, may depend in part upon the 
cerebral anaemia; otherwise, they are due to uraemia (vide infra). Cerebral 
haemorrhages have been observed in a very few cases. Haemorrhages on the 
inner surface of the dura mater are more frequent, but they are usually without 
clinical significance. The mouth, larynx, and pharynx usually show nothing 
particular, except accidentally complicating inflammations. We must, however, 
remember the occasional occurrence of a very distressing or even dangerous 
oedema of the soft palate, or of the arytaeno-epiglottic ligaments — oedema of the 
glottis. Forms of bronchitis and pneumonia occur, similar to those seen in acute 
nephritis. Bronchitis and chronic oedema of the lungs also make their appear- 
ance in the more advanced stages of the disease, as a result of cardiac insuffi- 
ciency. Finally, we must remember the hindrance to respiration from hydro- 
thorax, and also from uraemic dyspnoea. The changes in the heart have already 
been spoken of. Endocarditis or pericarditis may occur, but they are very rare. 

As to digestive disturbances, loss of appetite is a very common symptom. Very 
persistent vomiting is usually to be regarded as a chronic uraemic symptom. The 
bowels, as a rule, are constipated, but there may also be severe diarrhoea, as in 
acute nephritis. In severe cases, especially in the last stages of the disease, ulcer- 
ative and dysenteric processes have repeatedly been observed in the large intestine 
and the ileum. Peritonitis may occur, but it is at all events extremely rare. The 
liver and spleen usually show no peculiarities. 

Uraemic symptoms, both of the milder chronic variety and also in their severest 
acute form, may come on at any time, although they do not by any means attain 
their full development in all cases, and are somewhat rarer than in genuine con- 
tracted kidney. 

The temperature remains normal, as a rule, as long as it is not influenced by 
complicating inflammations, or by the appearance of uraemia. 

Course, Duration, and Termination of Chronic Nephritis. — In general, the 
whole course of chronic nephritis presents quite a great uniformity. The different 
symptoms may show certain variations within long periods, but the patient often 
presents almost the same appearance day after day for months. The duration of 
the disease varies greatly, from three to six months, in the subacute cases, to 
two or three years, or even more, in the very chronic cases. The cases of long 
duration are almost all cases of secondary contracted kidney. They some- 
times show in their clinical relations the transition from the enlarged to the 
granular kidney, since the picture in many of its details is more like that in the 
genuine contracted kidney: the oedema decreases, disappears completely, or, at 
least, continues in a lesser degree ; the amount of urine becomes more abundant, 
and the specific gravity and the amount of albumen become correspondingly less. 
The condition thus lasts for a long time until it grows worse again, through 
uraemia, or disturbance of the compensation in the heart. 

The final termination of chronic nephritis is in most cases unfavorable. In 
the severe forms death ensues in from three months to a year, either in conse- 
quence of general dropsy or from uraemia, from complicating inflammations, etc. 
The conditions when the nephritis goes on to secondary contraction are com- 
paratively more favorable, inasmuch as the patient may then find himself in a tol- 
erable state, for a time at least. Complete recoveries doubtless occur in chronic 
nephritis, but they are rare. The longer the disease lasts beyond the first six 
months the less likely is recovery. The development of secondary contraction 



62± 



DISEASES OF THE URIXARY ORGAXS 



may simulate recovery or, at any rate, the subjective condition of the patient may 
be almost perfect. Even after signal improvement, however, relapses are always 
to be feared. There are even genuine acute attacks in the course of chronic 
nephritis. 

Different Forms of Chronic Diffuse Nephritis. — Diagnosis. — By means of 
careful examination of the urine in all suspicious cases — for example, those pre- 
senting oedema, anaemia, and similar symptoms — we may in general be certain of 
making a correct diagnosis of chronic nephritis, but all experienced observers will 
acknowledge that the diagnosis of the particular form of chronic nephritis is diffi- 
cult and uncertain, even when the examination of the case is most painstaking. 
Still, the following schematic resume may at least furnish some indications : 

Chronic Hemorrhagic Nephritis (large variegated or mottled kidney). — Dura- 
tion from six to eighteen months. Urine haemorrhagic ; usually quite rich in red 
blood-corpuscles and casts. (Edema. Cardiac hypertrophy. Retinal changes. 
Quite frequently uraemia. 

Inflammatory Fatty Kidney (large white kidney). — Duration also six to eight- 
een months, but usually somewhat shorter than in the preceding form. Urine not 
at all, or only slightly, haemorrhagic. Erequentlv many white blood-corpuscles, 
and especially signs of fatty degeneration in the kidneys, fatty granular cells, fat- 
drops in the urine, etc. Large amount of albumen in the urine. Marked oedema. 
Cardiac hypertrophy. Very often retinal changes. Death by uraemia frequent. 

Secondary Contracted Kidney. — Longer duration of the disease, from a year 
and a half to three years. At first the svmptoms of the preceding forms ; later, 
urine more abundant, less oedema, etc. Death from an increase of the dropsical 
symptoms dne to cardiac insufficiency, uraemia, etc. 

Chronic Hemorrhagic Nephritis without (Edema. — This form has been already 
mentioned (page 622), but it should receive somewhat further consideration. Up 
to this time it has been too little regarded, although we ourselves have observed 
not a few cases of this variety of chronic nephritis. The disease has a rather 
chronic course. Eor a long time the patient is but slightly inconvenienced, par- 
ticularly if he has good care. The urine is usually quite abundant, and contains 
very little albumen, but has always, or almost always, small amounts of blood 
mixed with it, and this continues for many months or even longer. Erom time to 
time there will appear a more or less considerable haematuria, so that the urine 
has an abundant dark, brownish-red sediment. This is especially likely to occur if 
the mode of life has been indiscreet, but it may also happen without exciting 
cause. The urinary sediment is composed of red blood-corpuscles, some of which 
are entire and some already disintegrated, together with a moderate number of 
hvaline casts. The latter usually have red blood-globules or granules of hasmatoi- 
dine and detritus adherent to them. The amount of urine temporarily diminishes, 
but it soon increases again. Little, if any, increase in the size of the heart can be 
demonstrated; oedema is entirely absent, nor have we yet observed retinitis in 
association with this form of nephritis. Uraemia does occur, but it is rare. The 
course of the disease is very tedious, as we have said. Whether recoverv may take 
place is uncertain. Usually apparent recovery is followed by, the sudden appear- 
ance of a fresh haemorrhage. It is probable that in most cases the final result is a 
secondary contracted kidney. 

With regard to the aetiology of this form of chronic nephritis, it is our opinion 
that in most cases there is a chronic septic infection or intoxication; at anv rate, 
it is noticeable that such patients not very infrequently give a history of some 
suppurative process. 

Treatment. — The treatment of chronic nephritis corresponds in all its details 
so closely to that of acute nephritis that we can refer almost entirely to the pre- 
ceding chapter. 



CONTKACTED KIDNEY 



625 



The main thing here also is regimen and symptomatic treatment. The patient 
must always keep himself warm, wear flannels, <^r stay in bed. The diet must be 
unirritating. At first, for a time, we may try giving milk alone; it is always 
advantageous to give an abundance of liquids, except that alcoholic beverages 
should be avoided so far as possible. It is well to pay careful attention to the 
skin — bathing, or sponging with warm water and alcohol. Under some circum- 
stances climatic treatment, in Italy, Egypt, etc., are indicated in the more chronic 
forms. 

The treatment of dropsy follows entirely the methods previously described, and 
so does the treatment of any ursemic symptoms. If there is persistent haematuria, 
ergotine may be tried, but it seldom seems to do any good. 

In the more chronic cases with great anaemia, preparations of iron, such as 
iodide of iron, are often to be used, and also frequently stomachics, cathartics, etc. 
The condition of the heart always deserves careful attention (digitalis!). The 
retinitis rarely demands special treatment. 



CHAP TEE IV 

CONTRACTED KIDNEY 

{Genuine Contracted Kidney. Granular Atrophy of the Kidney. Granular Kidney. Chronic Inter- 
stitial Nephritis) 

Definition and ^Etiology. — The genuine contracted kidney is the result of an 
extremely chronic and very slowly but constantly progressive atrophy of the 
renal tissue. The term " chronic nephritis " is also used for contracted kidney, 
but the special inflammatory processes are very subordinate here, for the anatom- 
ical change consists essentially in nothing but a simple degenerative atrophy of 
the renal parenchyma, and in a corresponding gradual increase of the interstitial 
connective tissue. From a general pathological point of view the process is to be 
regarded as wholly analogous to the corresponding changes in the liver in cirrhosis 
of that organ, in the spinal cord in the chronic degenerations of the different sys- 
tems of fibers, etc. In all these cases we have a primary destruction of the special 
tissue-elements as a result of some deleterious action, and, following a general 
pathological law (Weigert), a partial replacement of the parts destroyed by a 
newly formed cicatricial connective tissue. 

In the "genuine" contracted kidney the atrophy of the renal parenchyma 
begins in a previously healthy kidney. Cell after cell of epithelium, islet after 
islet of tissue, are slowly attacked, while other parts still remain intact. It was 
therefore an error of the older pathologists to regard the contracted kidney as the 
" third stage of Bright's disease," as if every granular kidney were first found in 
the stage of acute inflammation, and then passed into the stage of chronic enlarge- 
ment, and lastly into that of contraction. This theory, of course, suits certain 
cases in part, for chronic nephritis at least may often finally pass into contraction, 
but these " secondary contracted kidneys " {vide supra) can clinically, and almost 
always anatomically, be differentiated from the genuine contracted kidneys. The 
contracted kidney may arise from an acute nephritis in some cases, and careful 
investigation indicates that such cases are not very rare; but then the process 
hardly ever passes through the three stages mentioned above, for the acute ne- 
phritis apparently recovers. A slight remnant of it is left — a little fire, as it 
were, smouldering under the ashes; its work of destruction advances, wholly in 
secret, and perhaps only after many years do the symptoms of a pronounced renal 
contraction appear. 
40 



626 



DISEASES OE THE UKTXAHY ORGAXS 



If we inquire into the causes which, produce the atrophy of the renal tissue in 
the ordinary cases of contracted kidney, which are chronic from the first, we are 
very often unable to make out any special etiology. Of course, one of the first 
things to consider in this disease is chemical or toxic agents, whether these are 
introduced directly as such into the body, or whether they are manufactured in 
the body because of abnormalities in metabolism, or as a result of infectious pro- 
cesses. 

Experience teaches us that there are three chemical substances to be mentioned 
which may favor the development of contracted kidney: alcohol, lead, and uric 
acid. Chronic alcoholism is often to be regarded as the most probable cause of 
renal contraction, especially in people who have " lived well " otherwise, and have 
become corpulent. In these cases contracted kidney is to be viewed as a sort of 
atrophy, due to wearing out, or to strain. It is difficult to decide how much influ- 
ence should be ascribed to the alcohol itself and how much to the excessive inges- 
tion of food. The specific effect of alcohol is almost indubitable in those cases in 
which contracted kidney and hepatic cirrhosis are both present, a combination 
repeatedly observed. 

We are, therefore, strongly inclined to assume that the chief cause of inter- 
stitial nephritis is an improper mode of life, but yet it can not be denied that the 
disease is also frequently observed in individuals whose lives are not open to 
criticism. There are cases of genuine contracted kidney in youthful patients, 
twenty-five to thirty-five years old, and of both sexes, for which not the slight- 
est cause can be discovered. One might suppose, under such circumstances, that 
there are kidneys which are peculiarly vulnerable and which can not permanently 
meet even the ordinary demands of life. The connection between contracted 
kidney and chronic lead-poisoning, in type-setters, painters, etc., is also incon- 
testable. It is a remarkable circumstance, and one not yet fully explained, that 
in these cases we very often see at the same time genuine gout (arthritis 
uratica saturnina). Gout, however, alone, without any co-existing chronic lead- 
poisoning, often leads to the development of contracted kidney, " gouty kidney," 
in which we probably have to do with the noxious action of an abnormal amount 
of uric acid on the renal parenchyma; but it always seems to be especially unfa- 
vorable to have an accumulation of several injurious factors — for instance, lead- 
poisoning associated with chronic alcoholism. 

Infectious influences are, probably, first to be considered in those cases where 
the contracted kidney can be referred to a former acute infectious nephritis, as 
after scarlet fever. We may also mention here the appearance of contracted 
kidney sometimes observed after severe acute articular rheumatism. We may 
perhaps imagine a similar connection in the cases where contracted kidney is 
found combined with chronic endocarditis (valvular heart disease), or with 
chronic arthritis not of gouty origin. Of the chronic infectious diseases, which 
sometimes have a connection with the origin of contracted kidney, we may men- 
tion malaria and syphilis. The latter ought especially to be considered more 
than it is at present, because we may have either an immediate action of syphilitic 
toxines, or a renal atrophy as the result of a specific disease of the renal arteries. 

We must here devote a little time to a consideration of the connection between 
renal contraction and primary disease of the vessels, which has been much dis- 
cussed. It is true that we often find general arterio-sclerosis, and also atheroma, 
especially in the renal arteries, in the bodies of persons who have died from con- 
tracted kidney, but this frequent coincidence can not be remarkable in such cases, 
because contracted kidney is seen chiefly in elderly persons, and those in whom 
atheroma of the arteries is also a very common symptom. The theory advanced 
by the English authors, Gull and Sutton and others, that the vascular disease, 
" arterio-capillary fibrosis," always represents the primary process, to which the 



CONTKACTED KIDNEY 



027 



renal atrophy is only secondary, is, however, utterly untenable. We often find the 
most pronounced contraction of the kidneys without any vascular changes suffi- 
cient to explain the atrophy; and where the latter can be found in the small renal 
arteries, we usually have not a primary but a secondary process — namely, the well- 
known obliterating arteritis, which is seen in almost all chronic inflammations 
and degenerative atrophies of various organs. 

Of course, it can not be denied that primary disease of the arteries in the kid- 
ney may check the flow of blood to certain portions of the tissue, and thus occasion 
secondary atrophy in limited areas (arterio-sclerotic contracted kidney), just as, 
for example, interstitial myocarditis results from primary arterio-sclerosis of the 
coronary arteries. This is particularly true of the so-called senile kidney — that 
is, the granulated kidney of old persons, due to atheromatous changes in the blood- 
vessels, and perhaps also certain other cases of nephritis subsequent to syphilis, 
and especially the rare cases of unilateral contracted kidney, which have been 
seen chiefly in association with syphilis. 

With relation to the age and sex of patients with contracted kidney, it has 
already been repeatedly stated that the disease occurs mainly in later life. The 
explanation of this fact lies in the peculiar circumstances which occasion the 
renal process. Eor the same reason, also, the male sex is much oftener attacked 
than the female ; yet the causes which lead to contracted kidney are so numerous 
that it is easy to understand why the disease is not infrequently seen even in 
younger individuals and in women. Contracted kidney does occur in children, 
though rarely. In all cases in youthful persons we must make careful inquiry as 
to any previous attack of acute nephritis, subsequent perhaps to scarlet fever, 
diphtheria, or measles. 

The relations of contracted kidney to amyloid disease of the kidney (so-called 
amyloid-contracted kidney), and to chronic disease of the urinary passages, par- 
ticularly of the pelvis of the kidney, will be discussed later in the appropriate 
chapters. 

Pathological Anatomy. — In the genuine contraction of the kidney, both kid- 
neys are always diminished in about the same degree. Their size is sometimes 
reduced to one half or even one third of the normal, so that it is almost difficult to 
find the little kidney in the very abundant and thick fatty capsule that is often 
present. The kidneys feel firm and dense, and show on their surface a very plain, 
coarse or fine, uniform or irregular, granulation. On pulling off the somewhat 
thickened fibrous capsule, these granulations become more prominent, and the cap- 
sule usually adheres quite firmly to the depressed portions. The raised portions 
are almost always darker and redder — that is, richer in blood — than the lighter 
and grayer depressions. Whether the whole kidney appears more red or more 
white depends only upon the amount of blood in the organ, and there is no reason 
for separating the " small red " from the " small white " contracted kidney. 

On section of the contracted kidney, we find the cortex very thin, and pale 
atrophic streaks alternating with the darker portions. The pyramids are also 
rather small, and, as a rule, are darker than the cortex. In the pelvis of the kid- 
ney, which is often somewhat dilated, there are sometimes a number of uric-acid 
concretions. Striated uric-acid infarctions in the pyramids are a very character- 
istic mark of the gouty contracted kidney. The microscope shows an advanced 
destruction of the renal parenchyma, which is replaced by a cicatricial connective 
tissue in which the nuclei are still numerous or else have already become scanty. 
We can always make out signs of degeneration and atrophy of the epithelium, and 
the formation of casts in the uriniferous tubules which still remain, but which are 
already diseased. Atrophy, thickening of the capsule, etc., are found in many of 
the glomeruli. The uriniferous tubules that are still preserved in some places are 
often in part dilated. We can not here go more fully into the manifold histo- 



628 



DISEASES OE THE UKIXAEY OEGAXS 



logical details, especially the formation of cysts, the changes in the vessels (vide 
supra), the deposition of lime-salts, etc. Haemorrhages are only very rarely 
present. 

Thus the contracted kidney may be regarded as the form of chronic nephritis 
with by far the longest course (lasting from three to five years, and even much 
longer), and also the form with the widest extent. Its essential nature can in no 
way be contrasted with " chronic parenchymatous nephritis " as a " chronic inter- 
stitial nephritis " ; for we always find interstitial processes in the former, which 
hare reached a far higher degree in the contracted kidney only because the slow 
atrophy of tissue is compatible with a much longer duration of life, and hence can 
attain a much greater extent. 

The anatomical changes in the other organs of the body beside the kidneys 
will be spoken of in connection with the symptomatology of contracted kidney. 

Clinical Symptoms. — Except in the comparatively rare cases where we can 
refer the origin of a contracted kidney to a previous acute or chronic nephritis, 
the clinical symptoms of contracted kidney develop as gradually and insidiously 
as the anatomical process itself. There is no doubt but that a contraction of the 
kidney may exist for years, without calling the patient's attention to his disease by 
a single serious subjective symptom. This is evident from the chance discov- 
eries on autopsy of a contraction of the kidney in people who have lost their 
lives in some other way, but especially from the cases where the severest symp- 
toms, such as uraemia, cerebral haemorrhage, etc., which often lead immediately to 
death, suddenly come on in persons previously regarded as perfectly healthy, 
while the autopsy shows a quite far advanced contraction of the kidney as the 
special cause of these symptoms. The less prominent the subjective symptoms of 
renal contraction are in the earlier stages of the disease, the more we should con- 
sider the objective changes, which in fact usually permit the diagnosis of the dis- 
ease quite early on careful examination of the patient. 

The condition of the urine is most important in this respect. As soon as 
changes have taken place in the epithelium in different parts of the kidneys, the 
results previously spoken of must make themselves manifest in the secretion of 
the urine, although still in a slight degree, and the diseased portions will secrete a 
urine diminished in amount and in solid constituents, but containing albumen. 
Since, however, many normal uriniferous tubules and glomeruli are still present, 
and since the whcle process, as we have seen, develops only very slowly, the body 
gains time for the development of one of those apt compensatory arrangements 
which we recognize in so many pathological processes, and which we must regard 
in a teleological sense. This compensatory process consists of an increase in the 
arterial pressure, coming on as gradually as the renal contraction itself, and con- 
stantly increasing, and of a hypertrophy of the left ventricle dependent upon it. 
The blood therefore courses through the many normal glomeruli of the contracting 
kidney under an increased pressure, and the consequence is that in these portions 
the secretion of the urine, especially of the water, is much more abundant. It is 
possible, also, that the incipient disease of the glomerular walls which tends to 
increase their permeability contributes to the polyuria. At any rate, it is a fact 
that in cases of contracted kidney there is usually an abnormally large amount of 
pale, watery urine of low specific gravity, containing merely a trace of albu- 
men (originating from the diseased portions of the organ). The daily amount 
of urine is often seventy to a hundred and twenty ounces (2,000-3,500 cubic cen- 
timetres) or more; the urine looks light-yellow and clear, contains scarcely any 
morphological constituents, has a specific gravity of 1010 to 1005 or even lower, 
and gives, on heating, only a slight precipitate of albumen, the amount excreted 
in the twenty-four hours being about half a drachm to a drachm (two to five 
grammes). On careful microscopic examination of the urine, we usually succeed 



CONTKACTED KIDNEY 



629 



in finding a few hyaline casts, which only exceptionally may be more abundant. 
The urine also frequently contains some white, and more rarely a few red blood- 
corpuscles. In rare but definitely attested cases it may happen that for a time, 
or even during the main part of the disease, the urine contains no albumen at all, 
or only a trace of it. This is probably explained by the fact that the diseased 
glomeruli have wholly ceased secreting, and that therefore the urine is secreted 
only by the healthy portions of the kidney. As to the character of the urine in 
arteriosclerotic contracted kidney, vide supra. 

It is apparent of how great significance this abundant secretion of water, as a 
result of the abnormally high blood-pressure, must be for the whole morbid pro- 
cess; for, in spite of the renal disease, there is now absolutely no retention of 
water in the body, and we therefore understand why there is often no oedema in 
contracted kidney, even after a course of years. The secretion of the solid con- 
stituents of the urine is not quite in such a favorable condition as the secretion of 
water. It is self-evident that the percentage of the former decreases with the 
increased amount of urine, but the whole amount of urea, uric acid, phosphoric 
acid, etc., eliminated is also at times somewhat less than normal in relation to the 
food. This diminution, however, is not very great, as long as the work of the 
heart is sufficient, and at certain times, especially in the earlier periods of the dis- 
ease, a normal amount may be secreted. We accordingly see that the symptoms 
dependent upon an accumulation of the urinary constituents in the blood do not 
appear at all for a long time. Thus it happens that the patient may still feel per- 
fectly well up to a time when the objective examination of the urine indicates 
marked pathological changes. Many patients, of course, notice the polyuria, but 
often no special attention is paid to it, and it is attributed to drinking a good 
deal of fluid. The patient gets accustomed to it, even if, as often happens, he 
has to pass his urine much more frequently than formerly, and even during the 
night. 

We need not go into detail here in regard to the special causes of cardiac 
hypertrophy (compare page 602). It was with regard to contracted kidney that 
Traube advanced his mechanical theory of cardiac hypertrophy, which, however, 
rested upon the considerations previously mentioned, and therefore was properly 
replaced by the chemical theory, which was also very applicable to this form of 
renal disease. In its clinical relations it is an important fact that the cardiac 
hypertrophy causes no subjective symptoms at all, as long as the heart can suffice 
for the work put upon it without strain, a condition which is perfectly analogous 
to that of any fully compensated valvular disease. We can usually recognize the 
condition correctly only by a careful physical examination of the heart and the 
vascular apparatus, although in contracted kidney the percussion and palpation of 
the heart are often rendered difficult by a co-existing pulmonary emphysema. 
We can often perceive, however, the displacement and the increased strength of 
the apex-beat, the extension of the cardiac dullness to the left, and almost invari- 
ably the abnormal tension of the radial pulse, and the accentuation of the aortic 
second sound. In the later stages of the disease a hypertrophy of the right ventri- 
cle is often added to that of the left (compare page 603). Complete, or almost 
complete, absence of the cardiac hypertrophy is observed, as we have said, only 
in weak and cachectic patients. 

As long, therefore, as the high arterial pressure kept up by the cardiac hyper- 
trophy regulates the renal secretion in the way above described, the condition of 
the patient as a rule shows no special abnormality. At most it happens that cer- 
tain cerebral symptoms now appear, especially attacks of headache and occasional 
vertigo, which, unless they are ursemic, are probably to be referred to active cere- 
bral hyperemia. Frequent nose-bleed also sometimes results from the abnor- 
mally high blood-pressure. 



630 



DISEASES OF THE UKINAKY OKGANS 



The clinical picture is completely transformed, however, upon the appearance 
of the first signs of incipient cardiac insufficiency — that is, the moment that the 
hypertrophy of the left ventricle ceases to be sufficient to overcome the obstacles 
to the secretion of urine occasioned by the deficiency in the renal parenchyma. 
The disturbance is evident either when the left ventricle itself grows weak, or 
when the gradual advance of the diseased process has reached such a point that 
even the most vigorous efforts of the heart are no longer sufficient to bring about 
compensation. In the latter case the symptoms which appear are to be regarded 
as ursemic, in the broadest sense of that word. The pulse is frequent, but it still 
remains unusually full and hard. On the other hand, in case there is a diminu- 
tion in the cardiac energy the pulse becomes more compressible, smaller, more 
frequent, and sometimes, toward the termination of the disease, irregular. The 
heart-sounds remain pure, but the first sound often becomes indistinct. When 
there is a decided disturbance of compensation we hear a well-marked bruit de 
galop. In all these cases the symptoms result from the disturbance to the circula- 
tion, and from the consequent retention of urinary constituents. 

Ordinarily, the subjective symptoms of contracted kidney begin very gradually, 
then disappear for a time, then appear again, and grow worse slowly but stead- 
ily. Apart from the feeling of general languor and weariness, it is usually 
the dyspnoea which first calls attention to the disease. The patient grows short 
of breath, is much disturbed by even slight physical exertion, and is perhaps 
subject to attacks of palpitation. "Not infrequently the dyspnoea occurs, in the 
later stages of the disease, in distinct paroxysms which suggest asthma. This 
nephritic asthma has long been recognized. It does not have the same origin 
in every case ; often it is undoubtedly the result of the attacks of cardiac weak- 
ness, and is then a merely cardiac asthma and corresponds in its individual 
symptoms to angina pectoris (see page 355). In other cases the asthma seems to 
be connected with the retention of the products of metabolism (nrsemic asthma, 
vide supra). The clinical picture is most peculiar in those cases in which the 
dyspnoea is associated with the signs of acute pulmonary oedema, and is attended 
with the expectoration of a large amount of foamy, serous sputum, which is often 
tinged with blood. These conditions, which may pass off and reappear at stated 
intervals, are mainly those to which the name of humid asthma was formerly 
given. It may seem questionable whether we should regard the pulmonary oedema 
in such cases as a purely congestive transudation due to cardiac weakness, or 
as an oedema occasioned by nephritis and in a certain degree inflammatory. In 
the last stage of the disease there is often constant dyspnoea, and this may be the 
chief complaint of the patient. It is in such cases often referable to various 
causes acting simultaneously — for instance, pulmonary congestion, diffuse bron- 
chitis, pneumonia (vide infra), and hydrothorax. 

Another result of beginning cardiac failure in the later course of the disease 
may be oedema of various portions of the body. This is certainly in many cases 
to be regarded as a purely congestive oedema, particularly when associated with 
contracted kidney; but, on the other hand, we can not always exclude conditions 
which occasion nephritic oedema (vide supra). It has, indeed, been repeatedly 
observed that dropsy may be entirely absent in contracted kidney; but this is the 
case only when death ensues from some intercurrent attack before the pronounced 
cardiac insufficiency. Otherwise oedema is by no means rare in contracted kidney. 
It usually appears first in the ankles, the eyelids, or the prepuce, disappears again 
when the patient remains at rest, and, after a longer or a shorter pause, comes 
on anew, until finally, in the last period of the disease, a high degree of gen- 
eral dropsy may develop. 

Among the disturbances of the internal organs we must mention first the 
cerebral symptoms. While at first, as we have said, these have more of an active 



CONTRACTED KIDNEY 



631 



kyperaeniic character, the frequent and very violent, headaches that come on 
later in part are of a uraemic nature and in part depend upon the passive hyper- 
emia, or the arterial anaemia of the brain, The pain sometimes shoots into the 
back of the neck, and sometimes is localized chiefly in one half of the head; it is 
often associated with symptoms of vertigo, with a gloomy or morose mood, 
with troubled sleep, etc. The stasis is usually also apparent in the abdominal 
organs. Chronic dyspeptic disturbances appear, the appetite fails, the bowels 
become irregular, and we can even make out a moderate enlargement of the liver. 
The influence which the altered activity of the heart exerts upon the function of 
the kidneys themselves is, however, particularly important. From what has been 
previously said of the dependence of the secretion of urine upon the arterial pres- 
sure, it follows directly that any compensatory activity of the still normal renal 
territory must at once experience a reduction, as soon as the blood-pressure falls. 
Corresponding to this we see, in fact, that the secretion of urine also usually 
suffers a decline at the same time with the other symptoms of stasis. The 
amount of urine is less abundant: it drops to forty or fifty ounces (1,500-1,000 
cubic centimetres), and even lower; the specific gravity rises, rarely to a high 
figure, but still up to 1010 or 1012, or over. The urine often retains its light 
color for quite a long time, but it may finally more and more resemble the 
genuine urine of stasis. The point, however, which is especially to be consid- 
ered, is the simultaneous and increasing retention of the solid constituents of 
the urine in the blood, and the consequent possibility of the onset of uremic 
symptoms. 

It must be stated that, in contracted kidney, the immediate exciting causes of 
uraemia are not always clear. Thus, it is a well-known and very important fact, 
clinically, that very severe and often fatal uraemic convulsions may sometimes 
attack the patient quite suddenly, apparently when in the best of health. Cases 
have been repeatedly seen, by other observers and by ourselves, where the daily 
amount of urine has shown no discoverable diminution in the days preceding the 
uraemia. Probably the explanation of this is that for a long time very minute 
amounts of toxic material are daily retained in the blood, and that these of them- 
selves occasion no noticeable disturbance until suddenly the severe symptoms of 
uraemia develop as a cumulative result of long-continued, though slight, injurious 
influences. These cases of suddenly developing uraemia always remind us of the 
similar phenomena in chronic poisoning from lead or mercury. In these cases, 
also, after a long-continued absorption of trifling amounts of poison, the symp- 
toms of intoxication may finally appear abruptly. In other cases of uraemia 
associated with contracted kidney, the condition of the heart is of great impor- 
tance. The uraemic symptoms develop in different ways, according to the slowness 
. or rapidity with which the cardiac insufficiency causes diminution in the urinary 
secretion. If the amount of urine is slowly diminished, we observe the symptoms 
of chronic uraemia (page 596), consisting of headache, vomiting, diarrhoea, severe 
pruritus of the skin, etc., but these symptoms are, of course, often combined with 
the immediate symptoms of stasis, and are not always to be easily and distinctly 
separated from them. Such a condition of chronic uraemia, in patients with con- 
tracted kidney, often presents a very mournful picture, since the unrestrainable 
and constantly recurring vomiting, the headache, and the general mental anxiety 
may last for weeks. The severe acute uraemia either is preceded by chronic 
uraemic symptoms, or comes on at once in the severest form, with general and 
often-recurring convulsions, and coma. The uraemia may pass off again, even in 
contracted kidney, but quite frequently it is the immediate cause of death (vide 
infra). 

Beside the symptoms so far described, we must now mention a set of anatom- 
ical complications which may appear in the course of contraction of the kidney. 



632 



DISEASES OF THE URINARY ORGANS 



Erom its diagnostic and clinical importance the albuminuric retinitis, already 
known to us from the preceding- chapter, takes the first place. It may come on 
at any time in the course of the disease; but it often develops so early that the 
patient, up to this time, knows nothing at all of his other disease. He merely 
consults an oculist, who often first recognizes, from the ophthalmoscopic image 
(see page 622), the special seat of the primary disease. Even in the cases where 
no subjective visual disturbance is present, the retinal examination sometimes 
discloses retinitis. In general, the contracted kidney is that form of renal dis- 
ease in which retinal changes are decidedly most frequent. 

Another rarer but clinically important complication consists of the haemor- 
rhages in internal organs, whose cause is to be found either in the increased arte- 
rial pressure, or in an abnormal weakness of the walls of the vessels — arterio- 
sclerosis in older persons, defective nutrition of the vascular walls in young and 
anaemic patients. Haemorrhages into the brain are comparatively the most fre- 
quent. They cause both mild and severe apoplectic attacks, which pass off com- 
pletely or leave a hemiplegia behind, and sometimes they are the direct cause of 
death. Beside the haemorrhages into the brain itself, there may also be haemor- 
rhages on the inner surface of the dura mater — haematoma. Nose-bleed is also of 
significance ; in many patients it is frequent and very stubborn ; we have ourselves 
seen two cases where the fatal termination was caused directly by an unrestrain- 
able nose-bleed. Haemorrhages into the other organs are more rare, but they 
have been observed in the skin, the stomach, the intestines, and the lungs. In 
a few cases, indeed, a sort of haemorrhagic diathesis seems to develop. We must 
remind the reader again, in this connection, of the general truth that in renal 
disease all the internal organs display a somewhat increased tendency to sec- 
ondary inflammation; thus the mucous membranes often present an accom- 
panying catarrhal inflammation, such as chronic bronchitis, gastritis, gastric 
catarrh, and intestinal catarrh. These catarrhal troubles are in part to be re- 
garded as due to congestion, but in part they certainly result from the retention 
of the products of metabolism. In serous membranes we often observe pleurisy, 
pericarditis, etc. The surface of the body sometimes displays a tendency to 
obstinate eczema. Of the inflammations of internal organs, pneumonia is the 
most frequent and important. Some cases are croupous or lobar, and some are 
of that diffuse lobular variety which is peculiar to all sorts of nephritis. We have 
already mentioned that the kidney itself may suffer from inflammatory exacerba- 
tions, in addition to the chronic disease. 

Quite great variations appear in regard to the general nutrition. In most 
cases where the disease develops quite gradually in persons in middle or advanced 
life, the general nutrition for a long time shows no striking anomaly. The patient 
is often very well nourished, and even corpulent, at the period when the first 
cardiac symptoms begin. To the more practiced and attentive eye, of course, he 
shows a certain appearance of suffering, which later becomes more pronounced. 
He becomes emaciated, and has a sallow and often cyanotic complexion. Marked 
anaemia usually develops only in younger individuals, who then show the pallor 
characteristic of so many patients with renal disease. 1 

We desire to append a few remarks with regard to arterio-sclerotic contracted 
kidney. This may pursue precisely the characteristic course of the ordinary 
disease, but in many cases its symptoms are very obscure. If we examine care- 
fully, from day to day, the urine of old persons who present other signs of gen- 
eral arterio-sclerosis, we shall be likely to find at many times a small trace of 
albumen, and at other times none at all. In such cases we may be almost cer- 
tain that there is an arterio-sclerotic contracted kidney. Still, the renal symp- 
toms are usually of minor importance in the clinical picture of senile marasmus, 
senile emphysema, senile dementia, or the other changes of old age. 



CONTRACTED KIDNEY 



633 



General Course, Duration, and Termination. — The most important peculiar- 
ities in the course of renal contraction have already been spoken of above. We 
have stated that the disease may be latent for a long" time ; that the severest symp- 
toms — such as uraemia or apoplexy — sometimes come on suddenly and unexpected- 
ly; that in other cases the disturbances of compensation in the heart, dyspnoea, 
palpitation, or slight oedema, are the first symptoms; that, under some circum- 
stances, certain complicating 1 conditions, such as retinitis, or frequent nose-bleed, 
first direct suspicion to a renal disease, and suggest an examination of the urine; 
while, finally, in a last class of cases, only general disturbances, loss of appetite, 
pallor, general physical weakness, and similar symptoms induce the patient to 
consult a physician. It is usually hard to decide how long the disease has lasted 
before a diagnosis is made. We must especially inquire into the existence of 
polyuria, which patients may not notice, however, even if it exists. 

The further course may vary according to the onset of complications, the 
external conditions under which the patient lives, etc. In general, as we must 
repeatedly emphasize, much depends upon the heart's capacity for work and its 
staying qualities. If death does not ensue sooner from some intercurrent dis- 
ease, the last stage of the disease almost always presents itself under the picture 
of cardiac insufficiency with predominant symptoms of dyspnoea and general 
dropsy. 

As has been said, we usually can not determine with any accuracy the dura- 
tion of the disease. It may, at any rate, last many years, probably even ten years 
or more, although there may be many variations in its course. It is not impos- 
sible that, during* the earlier period of the disease, there may be a cessation in 
the process of renal atrophy, but it is hard to decide with certainty. At all events, 
the disease must generally be termed absolutely incurable, although life may not 
only be preserved for a long time, but the patient may even exist without much 
discomfort. We need not refer especially here to the different intercurrent at- 
tacks, the possibility of which must always be kept in mind in regard to prognosis. 

Diagnosis. — The diagnosis of contracted kidney can be made with certainty 
only by examining the urine. We must, therefore, dwell again on the necessity 
of making this examination in all suspicious cases, because only in this way can 
we avoid overlooking the condition. The suspicion of a developing- renal contrac- 
tion should demand an examination of the urine, especially in all cases where the 
patient complains of frequent headache, of congestive conditions, of palpitation 
and dyspnoea, asthmatic attacks, disturbances of vision, general dullness, and dvs- 
peptic symptoms, without finding- any other reason for these symptoms. The poly- 
uria, the clear urine of low specific gravity, containing a slight amount of albu- 
men, in connection with the signs in the circulatory apparatus, the tense pulse, 
and the hypertrophy of the left ventricle, permit us to recognize the disease cor- 
rectly in most cases. If retinal changes are present, they may sometimes be of 
much aid in confirming the diagnosis. The serological conditions — lead, gout, 
alcoholism, etc. — of course also merit attention. 

The diagnosis presents great difficulty in the quite rare cases where albumin- 
uria is absent. In these cases we are sometimes able to reach the correct interpre- 
tation of the morbid condition only by repeated examinations of the urine. Other- 
wise we can scarcely avoid mistaking it for chronic affections of the heart, such 
as myocarditis or idiopathic hypertrophy. 

The diagnosis is also very difficult if the patient does not come under observa- 
tion until the stage of fully developed disturbance of compensation. The charac- 
teristic features of the urine of contracted kidney are then absent, the urine is 
scantier, darker, richer in albumen, and it is often scarcely possible to decide 
whether we have a primary renal affection with secondary cardiac hypertrophy 
or a primary heart disease with a secondary congested kidney. If general arterio- 



634 



DISEASES OE THE UKIKAEY ORGANS 



sclerosis or marked pulmonary emphysema is present at the same time, the judg- 
ment as to the condition is still more difficult. In such cases a correct diagnosis 
is possible only by very carefully balancing all the different symptoms, and con- 
sidering the whole course of the disease. 

Finally, the diagnosis of contracted kidney is very difficult in cases where the 
first examination of the patient is made during a sudden attack of uraemia or 
after an apoplectic seizure. Here the albuminuria is the symptom which points 
most to the existence of a renal disease, although, in spite of this symptom, the 
judgment as to the condition, and its differentiation from other acute cerebral 
affections, often presents great difficulties. 

We must devote a few words to those not very infrequent cases in which a 
small amount of albumen is found, often quite by chance, in the urine of youthful 
individuals who are apparently in perfect health ; thereupon the question is pro- 
pounded, which is often of extreme practical importance, whether we are dealing 
with a so-called physiological or intermittent albuminuria (vide supra, page 589), 
or with an actual renal disease — viz., an unsuspected contracted kidney. The 
diagnosis is never easy. In the first place, it is necessary to make careful obser- 
vations for a considerable period, at the same time varying the conditions as to 
nourishment (nitrogenous diet, milk diet, use of beer), and activity (complete 
physical rest, persistent exercise) ; then we must carefully investigate all the pos- 
sible serological circumstances, such as previous disease and mode of life; and 
finally, take into consideration the associated phenomena — for instance, of the 
circulatory apparatus. Erom a practical point of view it is advisable to be most 
cautious in all these cases, and, at any rate, to give such advice as to regimen 
with the aim of preventing damage to the kidneys, as if there were an actual 
renal disease. 

Treatment. — As soon as the diagnosis of renal contraction is established, the 
whole hygienic condition of the patient must be regulated so as to prevent the 
advance of the affection in every possible way. In this respect two indications 
are to be fulfilled, to guard against any irritation which may have an injurious 
action on the kidneys, and to relieve the work of the heart as much as possible, in 
order to keep off cardiac insufficiency as long as we can. The diet must be care- 
fully regulated, and must be of scant measure or abundant and strengthening, 
according to the patient's physical constitution. In these cases, too, milk is a 
food of great value. The use of meat is, in general, to be limited, while easily 
digestible dishes made from cereals and eggs, and vegetables and fruits, are to 
be recommended. Alcoholic beverages should be allowed in only limited amounts, 
their place being supplied by mineral waters (Eachinger, Wildunger, Wernarzer), 
and water with lemon-juice or the juice of other fruits. Great care of the skin 
is an important matter. We should recommend the regular employment of 
warm baths or salt baths, and daily sponging of the whole body with brandy or 
warm vinegar. All physical over-exertion is to be avoided, although moder- 
ate methodical exercise is to be recommended for corpulent patients. We should 
always provide for regular evacuation of the bowels by appropriate remedies, 
dietetic prescriptions, fruits, bitter mineral waters, etc. The general condition 
is often materially improved by proper air and recreation, and in this way resort 
to a bath may be of service, chosen according- to the individual conditions, such 
as Briickenau, Marienbad, Carlsbad, Kissingen, ISTauheim, Ems, or Baden-Baden. 
In appropriate cases, a winter residence in the south is advisable. 

If disturbances of compensation appear, we must be still more strict in our 
dietary, and must enjoin the utmost physical rest, at the same time employing 
other treatment according to the symptoms which may be present. Above all, we 
must endeavor to impart new vigor to the heart by means of digitalis, though 
unfortunately such efforts often prove unavailing. The minutiae of treatment in 



AMYLOID KIDNEY 



635 



this connection are almost precisely the same as in chronic heart disease (q. v.), 
and in other renal diseases. The treatment of the dyspncea and chronic uraemia, 
which develop in the last stages of the disease, is apt to be most unsatisfactory; 
but we can, sometimes at least, remove the symptoms by various external appli- 
cations upon the chest and the head (ice-bags or hot compresses), by various 
drugs to combat the nervous symptoms, bromide of potassium, antipyrine, nitro- 
glycerine, and by the combination of cardiac stimulants, such as digitalis and 
strophanthus, with diuretics, such as caffeine and diuretine. In the worst 
cases narcotics are indispensable, particularly subcutaneous injections of mor- 
phine. As yet we are unable to exert a direct beneficial influence by drugs upon 
the interstitial process in the kidneys. The only ones recommended for this pur- 
pose and worth a trial are the preparations of iodine — viz., iodide of potassium, or 
iodide of sodium, in daily amounts of three to eight grains (gramme 0.2-0.5), 
and, in ansemie patients, iodide of iron. We do not need to go minutely into the 
treatment of the numerous complications which occur. 

The prophylaxis of renal contraction is evident; we should avoid so far as 
we can the known ^etiological conditions. 



CHAPTEE Y 
AMYLOID KIDNEY 

Etiology. — The amyloid kidney is invariably associated with the more or 
less extensive amyloid degeneration of other organs in the body. In its clinical 
relations, however, it claims the most interest of all amyloid diseases, since it 
has by far the greatest significance for the whole clinical picture of amyloid 
degeneration. 

As is well known, we understand by amyloid degeneration a peculiar change 
which, under certain pathological conditions, is observed in the connective tissue, 
and especially in the smaller vessels. The walls of the vessels are thickened, they 
have a lustrous, homogeneous appearance, and they show peculiar reactions on 
treatment with certain coloring agents. These reactions are due to the presence 
of an albuminoid substance — amyloid — which either is deposited in the tissue 
from the blood, or, as is much more probable, is developed in that spot from 
the albuminoid substances there present. In marked amyloid degeneration the 
diseased organs often show macroscopically an altered, "bacon-like" appearance, 
and assume a characteristic red-brown color on treating the affected parts with 
Lugol's solution of iodine, changing to violet on the addition of sulphuric acid. 
The microscopic examination alone affords more accurate conclusions as to the 
presence and distribution of the degeneration. Eor this purpose we usually stain 
the tissues with methyl-violet or gentian-violet. The amyloid portions thus 
take on a very characteristic and clearly defined red color. In this way we can 
discover that the amyloid degeneration begins everywhere in the walls of the 
small vessels, that the interparenchymatous connective tissue may also be affected 
later, but that the parenchymatous cells proper, liver cells, renal epithelium, etc., 
almost always remain perfectly free. The latter often show atrophic and fatty 
degenerative changes (vide infra), but little if any amyloid degeneration. 

JSTothing is known as to the special causes which effect this peculiar metamor- 
phosis of the albumen of the connective substance into amyloid. We know only 
that there are a number of primary diseases in which experience has shown that 
amyloid degeneration quite frequently develops as a secondary condition in the 



626 



DISEASES OE THE UEIMEY ORGANS 



different organs. These conditions have, for the most part, the common charac- 
teristic of being- associated with general cachexia and debility, and of being con- 
nected with some localized chronic morbid process in some part of the body, from 
which abnormal chemical matters may be constantly carried into the blood. We 
suppose that the normal albuminous material is transformed into amyloid by 
means of such influences. With regard to the relations which may exist between 
the so-called hyaline degeneration of Recklinghausen, and amyloid disease, the 
investigations are not yet complete. 

The conditions in which amyloid degeneration in general, and consequently 
amyloid disease of the kidney also, are chiefly observed, are the following, ar- 
ranged in about the order of their frequency: 

1. Chronic pulmonary tuberculosis, particularly the ordinary ulcerative phthi- 
sis. Tubercular ulcers of the intestines, with or without co-existing marked pul- 
monary tuberculosis, may also lead to amyloid disease. 

2. Long-continued chronic suppuration in the bones or soft parts, especially 
chronic fungous processes with fistulse into the bones or joints, empyema with 
fistulas, vertebral caries, etc. 

3. Constitutional syphilis, chiefly the cases with ulcerative and usually ter- 
tiary processes in the bones and mucous membranes. 

4. Other ulcerative processes, or processes associated with chronic suppura- 
tion: saccular bronchiectases, chronic intestinal ulcers (for example, of dysen- 
teric origin), purulent pyelo-cystitis, vesico-vaginal fistulas, ulcerated new 
growths, such as cancer, etc. 

5. In rare cases amyloid has also been observed in other chronic diseases, as in 
malaria, gout, and other chronic articular affections. In the medical clinique 
at Leipsic we once saw a case of marked amyloid kidney in a girl of twenty-one 
with aortic insufficiency. 

6. Finally, in a small class of cases, of which we have ourselves seen some 
examples, so discoverable cause at all may be found at the autopsy for quite 
extensive amyloid degeneration. In such cases, therefore, there seems to be 
a primary intoxication with resultant amyloid disease. 

Pathological Anatomy. — With regard to the anatomical lesions of amyloid 
disease in other organs, we shall refer to handbooks on pathological anatomy. As 
to amyloid liver, see page 580. Here we shall discuss merely the pathological 
anatomy of amyloid kidney. 

In very slight and limited amyloid degeneration of the kidneys, the latter 
present a perfectly normal appearance to the naked eye. Careful microscopic 
examination alone shows amyloid degeneration of the walls of different vessels in 
the cortex, and especially in the medullary substance. 

The commonest and most characteristic form of amyloid kidney is the so-called 
large white amyloid kidney (waxy kidney, lardaceous kidney). The kidney is 
usually enlarged, and the surface is smooth and of a grayish-white or yellowish 
color, and usually somewhat mottled. On section, the cortex is wide and also of 
a yellowish-white color, and the glomeruli may often be recognized with the naked 
eye as dull, lustrous, translucent points. Haemorrhages are scarcely ever seen. 
The medullary substance may be also pale, or darker. In many cases the cortex 
may itself have a darker reddish or mottled appearance, which is due merely to 
the greater amount of blood in the organ. The pale-yellow color is due either to 
the anaemia or to the fatty degeneration, while the amyloid spots show a more 
translucent character with a bacon-like luster. 

If we examine the kidney microscopically, we find first the amyloid degenera- 
tion, which, in varying extent and combination, affects most frequently the glo- 
meruli and also the capillaries of the cortex, the vasa recta, and sometimes the 
membrana? proprise of the uriniferous tubules. In pure amyloid kidney the rest 



AMYLOID KIDNEY 



637 



of the renal tissue is normal, but in many cases we find changes in the epithe- 
lium — fatty degeneration, desquamation and disintegration — and also not infre- 
quently interstitial cellular infiltration. We see, therefore, that amyloid degen- 
eration of the kidney is not infrequently associated with degenerative changes of 
an inflammatory nature. Thus we observe, not infrequently, the combination of 
chronic diffuse nephritis (large white kidney) with amyloid. 

If the process has lasted for a long time, it leads, as in ordinary nephritis, to a 
complete atrophy of tissue in some parts, with a corresponding increase of con- 
nective tissue. Then the renal tissue sinks in at the affected spots, and there is a 
decided unevenness to the surface of the kidney. There is even a completely 
developed red or white contracted kidney, in which we find abundant amyloid, and 
which is, therefore, termed amyloid contracted kidney. In this form the paren- 
chymatous and interstitial changes correspond precisely to those in ordinary con- 
tracted kidney, only the amyloid degeneration is added to them. 

At present differences of opinion prevail as to the precise connection between 
amyloid and the inflammatory degenerative processes in the kidney. In our opin- 
ion there is, in most cases, an actual combination of both conditions, they being 
co-effects of simultaneously acting causes. We have seen that in tuberculosis 
chronic suppuration and genuine nephritis develop, as well as amyloid disease, so 
it can not be surprising that sometimes with these diseases both sequelae, nephritis 
and amyloid, should develop side by side, and that we should, consequently, find 
in the kidney not only the changes associated with an inflammatory, large, white 
kidney, a secondary contraction, or a genuine contracted kidney, but also a more 
or less extensive amyloid degeneration. On the other hand, it, of course, can not 
be questioned that the disturbance of circulation, which must arise in conse- 
quence of a marked amyloid of the vessels, is of influence on the nutrition of the 
renal tissue, and that, therefore, many changes in it, especially fatty degenera- 
tion of the epithelium, are, under some circumstances, the direct result of the 
amyloid disease. 

Clinical History. — If we consider the great diversity which the distribution 
of the amyloid in the kidneys shows, and its manifold combinations with inflam- 
matory processes, it is clear from the outset that we can not set up a uniform 
picture of the symptoms of amyloid disease in general. To this we must add that 
the symptoms of amyloid disease, which is almost always a secondary condition, 
are also modified in various ways by the primary disease. 

We must first state that many cases, where the amyloid in the kidneys is of 
comparatively slight extent, can not be recognized by any clinical symptom. The 
albuminuria in particular may be entirely absent, as has been repeatedly proved 
(Rosenstein, Litten, and others). That in such cases the vasa recta and not the 
glomerui are chiefly affected by the amyloid degeneration has been affirmed but 
not proved. 

Except in these instances, however, the urine secreted from the amyloid kid- 
neys shows marked changes, which, of course, present considerable variations ac- 
cording to the form of the individual case. The amount of urine is most fre- 
quently about normal, or somewhat diminished — in some cases much diminished 
■ — but in others it is decidedly increased, so that the patient may pass eighty to a 
hundred and twenty ounces (2,500-3,500 cubic centimetres) in the twenty-four 
hours. We quite frequently see considerable variations in the amount of the 
urine in the same patient at different times. All these differences are easily ex- 
plained if we remember how many circumstances may affect the amount of urine 
— the presence or absence of inflammatory changes in the kidney, the presence or 
absence of cardiac hypertrophy, co-existing perspiration, diarrhoea, oedema, 
fever, etc. 

The color of the urine is almost always light yellow. Only exceptionally, in 



638 



DISEASES OE THE URINARY ORGANS 



amyloid nephritis, does it contain an abundant sediment; usually it is entirely, 
or almost entirely, clear. The very considerable amount of albumen in the urine, 
which is often one or two per cent., is also characteristic of amyloid kidney. 
In many cases, indeed, particularly in the combination of amyloid with contracted 
kidney, the amount of albumen is smaller, although usually decidedly more abun- 
dant than in pure interstitial nephritis. Senator has pointed out that the com- 
parative amount of the globuline which is contained in the urine besides the 
serum albumen is often particularly large in amyloid kidney. The specific gravity 
of the urine varies very much according to the amount of water and albumen in 
it. It may be increased (1015-1020) or diminished (1010-1005). 

If we examine the urine under -the microscope, we usually find only a few 
hyaline casts, and also most frequently a small number of white blood-corpuscles. 
In general, it is very characteristic of amyloid kidney that there is an abundance 
of albumen, contrasting with the scanty or scarcely appreciable microscopic sedi- 
ment. In the combination of amyloid with more marked nephritic changes the 
sediment is more abundant, so that the urine is cloudy. The microscope then 
shows more numerous hyaline or moderately fatty casts, more abundant white 
blood-corpuscles, sometimes a little renal epithelium, and in quite rare cases even 
red blood-corpuscles. Amyloid reaction is said to occur in the casts, but it is very 
rare, and therefore of no value in diagnosis. 

The other morbid symptoms which are observed in amyloid kidney depend 
either upon the change in the kidneys themselves, or upon co-existing amyloid 
degeneration in other organs; or, lastly, upon the primary disease. The symp- 
toms of the latter are, of course, extremely varied, but in many cases they may be 
entirely subordinate. 

In regard to the directly resulting symptoms of amyloid kidney, their occur- 
rence is of interest, especially in comparison with the analogous conditions in 
acute nephritis. Dropsy of a moderate, or even a severe degree, is often present in 
amyloid kidney, but it may also be entirely absent. We must remember that an 
oedema independent of a renal affection may be produced by marantic venous 
thrombosis. Uraeinic symptoms are distinctly rare in amyloid kidney, but they 
are sometimes observed, especially in their milder forms, such as vomiting. It is 
a very important point that a hypertrophy of the left ventricle is absent in most 
cases of amyloid kidney. This is explained partly by the fact that the disease usu- 
ally affects feeble, cachectic individuals who have no superfluous material for the 
manufacture of cardiac hypertrophy, and partly by the fact that in pure amyloid 
kidney there is no appreciable retention of urinary constituents in the blood. This 
latter fact explains, also, the infrequency of uraemic symptoms (vide supra). If, 
however, the amyloid degeneration is combined with genuine nephritic changes, 
the condition of things is altered. In amyloid contracted kidney we have repeat- 
edly observed hypertrophy of the left ventricle. 

Albuminuric retinitis hardly ever appears in pure amyloid kidney. In the 
amyloid contracted kidney it has sometimes been observed, however, in cases 
where there has probably been originally a pure contracted kidney, with amyloid 
coming on later. The secondary inflammations in the internal organs, such as 
renal pneumonia, and the haemorrhages, such as cerebral haemorrhage, are also rare. 

The patient's general condition is dependent in part upon the renal disease, 
and in part upon amyloid degeneration in other organs, but mainly upon the 
primary disease. The patient with amyloid kidney is usually, therefore, cachectic, 
and shows in high degree a pallid, anaemic color of the skin. If, also, general 
dropsy develops, we have an external appearance very characteristic of amyloid 
disease ; still, in some few cases of syphilis, bronchiectasis, and unilateral pulmo- 
nary contracture, the general nutrition remains tolerably good for a consider- 
able time. 



AMYLOID KIDNEY 



639 



The symptoms which point to a co-existing amyloid degeneration in other 
organs beside the kidneys are of great diagnostic significance. The symptoms in 
the liver (enlargement, abnormal firmness, and a hard, sharp lower edge to the 
organ), the spleen (enlargement and hardness), and intestines (obstinate diar- 
rhoea not yielding to any remedy) are clinically important in this respect. The 
interpretation of the diarrhoea is, of course, usually difficult, since it may often 
depend upon tubercular intestinal ulcers as well as upon amyloid of the intes- 
tines. 

We can scarcely make general statements in regard to the whole course and 
the duration of amyloid kidney, since the form of the primary disease is to be es- 
pecially considered in these cases. In regard to the time that it takes for an 
amyloid degeneration to develop in an existing primary disease, the degeneration 
is certainly present sometimes after a few months. Of course, it is hardly ever 
possible to determine its onset accurately, since the first beginnings of amyloid 
degeneration in the kidneys do not usually permit themselves to be recognized at 
once by the appearance of albuminuria (vide supra). The duration of amyloid 
kidney varies very much according to the severity of the case; it may last only 
a few weeks or months before death, while other cases have certainly lasted for a 
year, especially in amyloid contracted kidney. 

The prognosis of amyloid kidney is in most cases utterly unfavorable, which is 
due mainly to the incurability of the primary disease; but trustworthy observers 
have repeatedly proved that, when the primary disease is curable, as with syphilis 
and many chronic suppurations, an already developed amyloid kidney may excep- 
tionally be completely restored. 

The diagnosis of amyloid kidney can be made with considerable certainty 
when the evident signs of a renal affection are added to those of a disease which 
we know by experience to promote the development of amyloid degeneration. 
Whether in such cases we have a pure amyloid or a pure nephritis, or a combina- 
tion of the two, can be decided with some certainty only from the condition of the 
urine : a clear urine, containing but few morphological elements, but rich in albu- 
men, points to pure amyloid, while a large number of casts and red and white 
blood-corpuscles in the urine points to the presence of inflammatory changes in 
the kidney. The diagnosis of amyloid contracted kidney is justified when the 
symptoms of contracted kidney (abundance of pale urine, secondary cardiac 
hypertrophy) are seen in association with such morbid conditions as are likely 
to occasion amyloid disease. Of great importance, as we have already pointed out, 
is the comparatively large amount of albumen and the consequently somewhat 
higher specific gravity of the urine. Of many cases of amyloid kidney it is very 
characteristic, and so of diagnostic value, that there is a rapid and frequent 
variation in the amount of urine and the percentage of albumen (Wagner). 

A very material support for the diagnosis of amyloid kidney, and therefore one 
which should always be looked for, is the discovery of amyloid in other organs. 
We have briefly mentioned above the most important symptoms in the liver, the 
spleen, and the intestines referable to this point. 

Treatment. — Only the treatment of the primary disease can, of course, be con- 
sidered, both as a prophylactic and also as a causal indication. In many surgical 
cases, and also in the cases of amyloid in syphilis, there is a possibility of this (as 
by iodide of potassium) ; but otherwise we try to improve the primary disease as 
far as we can. 

In other respects the treatment is purely hygienic and symptomatic. We must 
try to strengthen the patient as much as possible by good food and the exhibition 
of preparations of iron and quinine. The use of iodide of iron or small doses of 
iodide of sodium is to be recommended. In a symptomatic point of view the 
same remedies are used as in other renal diseases. 



640 



DISEASES OF THE URINARY ORGANS 



We insert here a synopsis of the condition of the urine and of the left ven- 
tricle in the most important varieties of renal disease. 



1. Acute nephritis. 



2. Chronic diffuse ne- 
phritis. 



3. Contracted kidney 

4. Amyloid kidney . . , 



5. Amyloid contracted 
kidney 



Passive congestion . 



Amount of urine. 



Diminished. 



Normal or 
somewhat 
diminished. 

Increased. 

Variable, 
normal, or 
increased. 

Increased. 

Diminished. 



Specific gravity. 



High. 

High. 

Low. 
Variable. 

Rather low. 
High. 



Amount of albumen 



Considerable. 



Slight. 

Considerable. 

Moderate. 

Absent o i 
scanty. 



Morphological constituents. 



Numerous casts ; blood- 
corpuscles ; epitheli- 
um. 

Numerous casts ; blood- 
corpuscles ; epitheli- 
um; compound granu- 
lar cells. 

Few casts ; small num- 
ber of blood-corpuscles. 

Few casts. 



Few casts ; blood-cor- 
puscles. 



CHAPTER VI 
PURULENT NEPHRITIS AND PERINEPHRITIS 

1. Purulent Nephritis 

JEtiology*. — Although in the forms of nephritis so far described the occurrence 
of large numbers of nuclei in the interstitial tissue has been repeatedly mentioned, 
none of them ever come to genuine suppuration — that is, to a purulent liquefac- 
tion of tissue, a true abscess-formation. The origin of a purulent nephritis is, 
rather, always associated with the entrance of perfectly definite morbid irritants 
into the kidneys. These are invariably organized and their special peculiarity is 
to excite a purulent inflammation. 

There are two chief ways through which the morbid irritants may reach the 
kidneys — the arterial blood-current and the urinary passages. The first-men- 
tioned means of entrance is to be considered in all the cases of purulent nephritis 
which come on as one symptom of pysemic processes and certain forms of ulcera- 
tive endocarditis (see pages 116 and 307 on the point). Far more rarely purulent 
nephritis develops in this way as a complication in other diseases, such as dysen- 
tery. Purulent nephritis also occurs in actinomycosis (Israel). 

The excitants of inflammation take the second path in those cases where a 
purulent nephritis follows an inflammation of the lower urinary passages, the 
pelvis of the kidney, the bladder, etc. Here the bacteria, which almost always 
enter directly into the urinary passages (the urethra and bladder) from without, 
pass gradually upward from the bladder through the ureter to the pelvis of the 
kidney ; from this they enter the apertures of the collecting tubes and the urinif- 
erous tubules of the kidney, everywhere exciting a purulent inflammation. We 
therefore term these forms of purulent nephritis — with regard to their origin — 
purulent pyelo-nephritis. 

We must remark in conclusion that a purulent nephritis and perinephritis 
{vide infra) may arise in direct wounds of the kidney from infection of the 
wound. 

Pathology. — Purulent nephritis shows quite characteristic peculiarities and 
differences according to its mode of origin. (We omit traumatic abscesses here.) 



PURULENT NEPHRITIS AND PERINEPHRITIS 641 



The renal abscesses in pyaemia and analogous diseases are usually focal suppu- 
rations, which only exceptionally attain a great extent, but which are usually to 
be recognized with the naked eye as numerous little yellowish dots or lines, scat- 
tered over the whole kidney, about half a millimetre or a millimetre in diameter. 
On microscopic examination, these nodules prove to be genuine little abscesses, in 
whose territory the renal tissue proper is completely destroyed. In the middle 
of them we often find the originating colony of micrococci, the " micrococci 
embolus," seated in a central vessel. The conditions are still plainer if we exam- 
ine an earlier stage of the process. We find vessels (the loops of the glomeruli, 
or the encircling capillaries), which are completely plugged with micrococci, and 
in whose vicinity the renal tissue is still perfectly normal. We further see analo- 
gous spots where the renal tissue is already necrosed in the vicinity of the colony 
of micrococci, and is infiltrated with emigrated cells. These nodules show, finally, 
a continuous transition to the completed abscess, which is often surrounded by a 
hypersemic or even a hemorrhagic areola. 

In purulent pyelo-nephritis the renal abscesses appear somewhat different. 
The abscesses also have a characteristic striated appearance, corresponding to the 
distribution of the inflammation along the straight tubules. They often extend 
from the point of the renal papilla through the cortex to the surface of the organ, 
so that from the outside we see the abscesses, showing through as yellowish 
points. The broader abscesses arise from the confluence of neighboring strige. 
The microscope shows that the purulent inflammation arises from the vessels of 
the interstitial tissue, in whose territory the uriniferous tubules are of course 
destroyed. The clusters of micrococci form the most interesting feature. These 
settle originally in the uriniferous tubules and are the special cause of the necrosis 
of epithelium and the inflammation. Pyelo-nephritis, indeed, was one of the first 
diseases for which a bacterial origin was discovered (Klebs). 

Clinical Symptoms. — We can speak very briefly here in regard to the clinical 
symptoms of purulent nephritis, since they can never be sharply separated from 
the symptoms of the primary disease. The pyemic renal abscesses, and the ab- 
scesses in ulcerative endocarditis, hardly ever cause special clinical symptoms, so 
that their presence is first recognized on the autopsy-table. Since the abscesses 
do not as a rule communicate with the uriniferous tubules, there is usually no 
great amount of pus in the urine. 

The clinical symptoms of pyelo-nephritis also depend less upon the nephritic 
abscesses than upon the previous and accompanying pyelitis and cystitis. We 
will therefore return to renal abscesses in the description of these diseases. 

2. Perinephritic (Paranephritic) Abscess 
Perinephritic abscess is the name given to suppurations in the vicinity of the 
kidney, especially in its fatty capsule or in the peri-renal connective tissue. Apart 
from any traumatic origin for such abscesses, they develop most frequently as a 
result of purulent nephritis or purulent pyelitis. The escape of pus, which in- 
volves the surrounding tissue in the inflammation, may come from the ureter or 
pelvis of the kidney, or from the kidney. The special form of primary disease dif- 
fers very much ; it may be either simple purulent pyelitis, or pyelitis from renal 
calculi, or sometimes tubercular processes and new growths that finally suppurate, 
such as cancer, or echinococci. The peri-renal suppuration may also take its start 
from the other organs in the neighborhood. Thus cases have been seen in which 
the perinephritis followed a perityphlitic abscess, a hepatic abscess, or a psoas ab- 
scess after vertebral disease. Perinephritic suppuration may also be due to actino- 
mycosis. It is a very important fact, however, that paranephritic abscesses may 
develop as a primary disease in persons in apparently perfect health, particularly 
in middle-aged men, and this without any discoverable cause. It is usually abso- 
41 



642 



DISEASES OF THE URINARY ORGANS 



lutely impossible to determine how and by what path the inflammatory germs 
reach the peri-renal connective tissue, unless possibly they migrate from the 
intestine. These cases of abscess are very important from a clinical standpoint, 
because the symptoms are at first difficult of interpretation. There is fever, usu- 
ally of a decidedly intermitting pyaemic type, and there are also dull, indefinite 
pains in the loins or abdomen, constipation, and constitutional symptoms. The 
cause of all these symptoms is gradually made apparent by the development of 
distinct local changes. 

In almost all cases of perinephritic abscess the accumulation of pus finally 
becomes so great that a swelling appears, usually in the lumbar region, and this 
grows more and more prominent; at first it is scarcely noticeable; but later the 
skin becomes oedematous there, it constantly protrudes more and more, it assumes 
an inflammatory hypersemic redness, until finally a definite fluctuation shows the 
advance of the abscess up to the skin. In other cases the inflammatory swelling 
extends forward into the iliac fossa; then there is also abnormal resistance and 
dullness above Poupart's ligament. The swelling may also extend upward toward 
the diaphragm, so that the diaphragm is crowded upward, giving rise to marked 
dyspnoea. The relations of the swelling to the descending colon are sometimes the 
same as in new growths of the kidney (compare Chapter VIII). 

Besides the swelling, there is almost invariably a very great pain in the 
affected region, either spontaneous or on pressure. If the swelling presses on 
the large nerve-trunks in the vicinity, it produces severe shooting pains in the 
leg of the same side, and sometimes a numb feeling and paresis. The leg is 
then often kept in a position similar to that in coxitis. 

The fever is persistent, and usually of an intermittent character and associ- 
ated with rigors. It and the pain make the patient thin and feeble, even to an 
extreme degree. The urine does not contain pus unless the abscess has some con- 
nection with the urinary passages. 

Recovery may occur if the pus finds some way out of the body. Apart from 
operative interference, the most favorable termination is the spontaneous dis- 
charge of the pus into the intestine (colon), or into the urinary tract (pelvis of 
the kidney, bladder). The course of the disease is much more tedious if the pus 
finds its way through the skin. If renal abscesses discharge outwardly, they most 
frequently point in the loins, less often like a psoas abscess, below Poupart's liga- 
ment. They may also discharge into the pleural or peritoneal cavities, with a 
consequent empyema or quickly fatal peritonitis. In other cases, if prompt surgi- 
cal aid is impossible, death occurs from exhaustion. 

The diagnosis is made chiefly from the swelling, pain, and fever, and a con- 
sideration of the astiological factors. We can settle any doubts in most cases by 
exploratory puncture. The condition may be confounded with hydronephrosis, 
psoas abscess, and solid tumors of the kidney. 

The only treatment, apart from the fulfillment of any symptomatic indica- 
tions, is surgical, and consists in opening and draining the abscess. The result 
depends chiefly upon the patient's general condition, and the character of the 
primary disease. The details are to be found in the text-books of surgery. 



DISTUKBAKCES OF CIECULATION IN THE KIDNEYS 613 



CHAPTEE VII 
DISTURBANCES OF CIRCULATION IN THE KIDNEYS 

1. The Congested Kidney. — Although local impediments to the flow of venous 
blood from the kidneys, such as thrombosis of the renal veins, hardly ever attain 
a clinical significance, the participation of the kidneys in a general venous stasis, 
as is seen chiefly in heart disease (compare page 331), pulmonary emphysema, 
etc., is of great diagnostic importance, since we possess in the condition of the 
urine quite an accurate measure of the intensity as well as of the increase and 
decrease of the stasis. 

The congested kidney is easily recognized anatomically. The organ is often 
somewhat enlarged, it feels firmer than normal, and shows, both on its surface 
and on section, a dark, bluish-red color — " cyanotic induration." The medullary 
substance is usually darker than the cortex. Under the microscope we see con- 
siderable dilatation and a tense fullness of the veins and capillaries. The paren- 
chyma is normal, but in more advanced cases it may show a beginning fatty 
degeneration of the epithelium, which is a result of the defective arterial blood- 
supply. At first the interstitial tissue is little changed, but if the congestion per- 
sists for a long while there may be a gradual destruction of the renal parenchyma, 
to a certain degree, with the formation of an abundance of contractile interstitial 
tissue (congested and contracted kidney). 

The clinical symptoms of congested kidney concern only the changes in the 
urine. The amount of urine diminishes, corresponding to the diminution of the 
arterial pressure and the diminished rapidity of the blood-current. Only twenty- 
five to twenty ounces (800-500 cubic centimetres), or less, ten to six ounces (300- 
200 cubic centimetres), are secreted daily. The urine is also more concentrated 
and darker than normal, and often has an abundant sediment of urates. If nutri- 
tive disturbances have begun in the epithelium of the glomeruli as a result of 
stasis, the urine is also albuminous, but the amount of albumen in pure congested 
kidney is always slight — about one tenth to one sixth of the volume. The urine 
often contains, besides, a few hyaline casts, and a few white and red blood-corpus- 
cles, the latter pointing to little congestive haemorrhages. 

If the changes mentioned come on as one symptom of a general venous stasis, 
and are, accordingly, associated with cyanosis and dropsy, the diagnosis of con- 
gested kidney can be made with certainty. If we succeed in restoring the cir- 
culation by appropriate remedies, such as digitalis, the urine at once becomes more 
abundant and clearer and its albumen disappears. Otherwise the characteristics 
of the urine of passive congestion last until the patient's death. 

2. Embolic Infarction in the Kidneys. — Since the renal infarction, although 
it has great pathological interest, is hardly ever of clinical significance, we will 
limit ourselves here to a brief description of the most essential points. 

If one of the smaller renal arteries is plugged by an embolus in heart disease, 
the affected portion of the organ cut off from the circulation must perish, since 
all the renal arteries are terminal arteries. The epithelium undergoes the well- 
known changes of coagulation necrosis, disappearance of the nuclei of the cells, 
and disintegration, and the tissue becomes entirely or in part a haemorrhagic 
infarction (compare page 331). In this way arise the characteristic wedge- 
shaped, red, hemorrhagic infarctions in the kidney, or far more frequently the 
yellowish-gray, anaemic infarctions (often surrounded by a haemorrhagic areola), 
the base of which is at the surface of the kidney; the base may reach a width of 
half a centimetre to a centimetre or more, while the apex extends a varying dis- 
tance into the cortex, or even into the medullary substance. Later on the grad- 



6M 



DISEASES OF THE URINARY ORGANS 



ually disintegrated tissue of the infarction is absorbed, round cells emigrate from 
without into the region destroyed, and a shrunken connective-tissue cicatrix grad- 
ually develops in place of the former infarction. Many kidneys may have such a 
granular surface from numerous infarction cicatrices that they may be appro- 
priately termed " embolic contracted kidneys." 

The anatomical processes just briefly described cause in most cases no special 
clinical symptoms at all. Sometimes, however, a slight amount of blood in the 
urine seems to depend on the development of a hemorrhagic infarction in the 
kidneys, so that when a cause for embolic processes, such as heart disease, is pres- 
ent, we may entertain the suspicion of the development of a renal infarction dur- 
ing life. In rare cases the development of a rather large infarction of the kidneys 
is associated with a sudden and violent pain in that region, with marked subse- 
quent hematuria or, as we observed in one case, hsemoglobinuria. 

The embolic processes in the kidney never demand special treatment. 



CHAPTER VIII 
NEW GROWTHS IN THE KIDNEYS 

Of the primary forms of tumor occurring in the kidney, two especially claim 
our interest : cancer of the kidney and congenital sarcoma. The latter is of great 
importance in regard to the general theory of tumors, since it points definitely to 
the development of the new growth from scattered portions of embryonic tissue. 
Striped muscular fibers have been repeatedly found in tumors consisting otherwise 
of round or spindle cells, from which the name of rhabdomyoma or myosarcoma 
striocellulare has been chosen for these tumors. Since there are no muscular 
fibers in the kidney itself, their occurrence, in the tumors points undeniably to dis- 
turbances of embryonic development. This theory obtains a further interesting 
confirmation from our own observation of the development of left-sided, and, 
probably, congenital renal sarcoma in two brothers. Both children died wh°n 
between two and three years of age, and the autopsy gave almost precisely the 
same lesions in both : numerous metastases in the liver and lungs, beside a new 
growth almost as large as a child's head in place of the left kidney. 

Renal cancer is also remarkably frequent, comparatively speaking, in children 
under four years of age, and about equally common in the two sexes. Of 
course, we find renal cancer in persons of more advanced years; in some cases 
of this sort renal calculi seem to occasion the development of carcinoma. This is 
like the relation between gall-stones and cancer of the biliary passages. Usually 
only one kidney is affected, chiefly the left, as it seems, but the new growth has 
sometimes been found in both kidneys. In its character, renal cancer belongs 
either to the denser or to the softer, medullary form. It may permeate the whole 
kidney and change it to a large tumor, weighing fifteen or twenty pounds (five or 
ten kilogrammes). Softening and haemorrhage very often take place within the 
tumor. The proliferation has been repeatedly observed to extend to the neighbor- 
ing parts, especially the pelvis of the kidney, and metastases also form in other 
organs, as in the Ivmph-glands, liver, or lungs. It should also be mentioned that 
several times renal cancer and cancer of the testicle have been combined. 

The clinical symptoms of renal tumor are entirely absent, or of a very indefi- 
nite nature, in the first period of the disease. Dull pain in the renal region is 
repeatedly given as the first symptom, but, of course, this is hardly ever of definite 
significance. The diagnosis almost always first takes a definite direction by the 



NEW GROWTHS IN THE KIDNEYS 



6±5 



appearance of a palpable tumor. This develops in the. lumbar and lower lateral 
abdominal region, constantly extending from this point upward and inward. As 
stated above, both carcinoma and sarcoma of the kidney may cause enormous 
tumors, especially in children, which may make the whole abdomen protrude to a 
marked degree. The tumor feels firm and sometimes smooth, sometimes uneven ; 
it does not usually move with respiration, but this rule has exceptions, particularly 
in the case of tumors of the right kidney. In tumors of the left kidney some 
diagnostic importance attaches to the relation of the new growth to the descend- 
ing colon, inasmuch as the latter is pushed forward by the growth of the tumor 
and comes to lie between it and the anterior abdominal wall. It is quite often 
possible to demonstrate that portion of the intestine which traverses the tumor 
by means of percussion, and sometimes even by means of palpation. For this pur- 
pose the colon may be examined alternately when empty and when artificially dis- 
tended with water, or, still better, with air. In the case of tumors of the right 
kidney, there may be corresponding relations to the ascending colon, but this is 
less frequent. Almost all larger tumors of the kidney occasion displacement of 
the diaphragm f.pward, and of neighboring organs laterally. Another factor in 
diagnosis is the ballottement renal described by Guyon: when a gentle thrust is 
made in the renal region the tumor is felt to strike softly upon the anterior ab- 
dominal wall. 

There may be scarcely any pain for a long while, but in some cases there is 
violent and persistent pain. Often the pressure of the tumor upon neighboring 
nerve-trunks — for instance, the sciatic — occasions obstinate neuralgia, sometimes 
associated with paresis. 

In many cases of renal tumor the urine shows no abnormal conditions at all, 
since its secretion is performed vicariously by the other healthy kidney. In 
carcinoma of the kidney it sometimes presents, however, one sign valuable for 
diagnosis — namely, an admixture of blood. This haematuria often comes on very 
early, even before there is any tumor to be felt. It is repeated either frequently 
or only rarely in different cases, and sometimes it is entirely absent. The haem- 
orrhage is associated with colicky pains only when large clots have to pass through 
the urinary passages. Sometimes, but very rarely, small particles and shreds of 
tissue from the disintegrated new growth may be found in the urine. 

The general symptoms are often very late at first, especially in children; but 
finally a general condition of marasmus almost always develops. A constant and 
great frequency of the pulse is often striking. We must also mention the peculiar 
symptom several times observed in girls with congenital renal tumors — viz., an 
abnormally early development of the pubic and axillary hair, and sometimes 
a peculiar pigmentation of the skin (Kiihn). 

The diagnosis of renal tumors is, in many cases, quite evident, but in others 
very difficult. The position of the new growth, its limited mobility, its relations 
to the colon, and, above all, our knowledge as to the occurrence of renal tumors 
in children, often suggest the correct interpretation of the case. In older persons 
renal haemorrhages which can not be otherwise explained must direct our sus- 
picions to the possibility of a cancer of the kidney. Often, however, the disease 
has been confounded with tumors of the retro-peritoneal glands and of the ovaries, 
with large psoas abscess, tumor of the liver, and splenic tumor. 

The prognosis is, of course, unfavorable. The disease sometimes lasts only a 
few months, sometimes a year or two, rarely longer. 

The treatment must in most cases be purely symptomatic. The only expecta- 
tion of success lies in the operative removal of the new growth, the details of 
which are to be found in recent monographs on renal surgery. 



646 



DISEASES OF THE URINAKY ORGANS 



CHAPTER IX 

PARASITES OF THE KIDNEYS AND OF THE URINARY PASSAGES- 

CHYLURIA 

1. Echinococcus of the Kidney * — Echinococcus cysts have been repeatedly 
found in the kidney, although much more rarely than in the liver. Usually only 
one kidney is affected, and the parasite is generally situated in the renal substance 
itself, only exceptionally between it and the capsule of the kidney. The size of 
the echinococcus cysts may be very considerable, the diameter reaching to twenty 
centimetres or more. 

Clinical symptoms usually first appear when the tumor can be felt through the 
abdominal walls. Subjective symptoms may even then be entirely wanting. Pain 
on pressure develops gradually later. The tumor usually has an approximately 
globular shape. Its relations to the neighboring organs, especially to the colon, 
are the same as we have learned to recognize in the preceding chapter, in the 
description of cancer of the kidney. The so-called hydatid thrill which is said to 
be characteristic, and which is obtained by giving the tumor a little push with the 
flat of the hand, can be distinctly felt in only the rarest instances. 

It is a comparatively frequent occurrence for the echinococcus cyst to burst into 
the pelvis of the kidney. Then single echinococcus cysts, or at least bits of mem- 
brane, hooks, etc., are passed with the urine, usually with severe colicky pains, 
which are exactly like the renal colic from the passage of a calculus. Such at- 
tacks may be often repeated, and may form a very severe type of disease by ob- 
structing the urinary passages — the bladder and urethra. In such cases the symp- 
toms of a secondary pyelitis and cystitis are often added. 

Perforations in other directions are much rarer. The rupture of a renal echi- 
nococcus into the lungs has sometimes been observed, the patient coughing up 
echinococcus cysts. 

Sometimes, especially after injuries, the sac of the echinococcus becomes in- 
flamed, suppurates, and leads to a general pysemic condition. 

The diagnosis of renal echinococcus is possible only when a tumor can be made 
out belonging to the kidney, and when portions of echinococcus are passed with 
the urine, or through an exploratory puncture. It has already been stated that 
one should be cautious about employing this procedure (see page 577). The cysts 
are most frequently confounded with hydronephrosis (vide infra), and, in women, 
with ovarian tumors. 

The prognosis is not wholly unfavorable. Permanent recovery has been re- 
peatedly observed, especially after the rupture, or single or repeated evacuations, 
of the sac of the echinococcus; but, of course, echinococcus of the kidney may 
also be attended with numerous dangers, such as suppuration of the sac. The 
course of the disease is always very tedious. 

A radical treatment is possible only by surgical means. Symptomatically, ice 
and local blood-letting are used when there are symptoms of 'local inflammation ; 
and morphine, warm baths, and sometimes mechanical aids, e. g., the catheter, 
when there are symptoms of colic. 

2. Bistoma haematobium (bilharzia hasmatobia — blood-fluke, see Fig. 71) is a 
parasite which belongs to the flukes or trematodes, and which occurs especially in 
Egypt, Abyssinia, and East Africa. Infection is said to take place partly by means 
of the drinking-water and food, and partly, perhaps, by the parasite creeping into 
the urinary passages and the rectum during bathing. Natives are much oftener at- 



* In regard to the general natural history of the echinococcus, compare page 575. 



PARASITES OF THE KIDNEYS AND URINARY PASSAGES 647 



tacked than Europeans. The distoma has its chief abode in the branches of the 
portal vein, and particularly in the venous plexuses of the bladder and the rec- 
tum. Its eggs are often deposited in great numbers in the mucous membrane of 
the pelvis of the kidney, the ureter, and the bladder, and they excite in these 



Fig. 71.— Distoma haematobium (from Leuckart). a. Male and female, the latter in the canalis gynae- 
cophorus of the former. Ten diameters, b. Egg with a terminal spine, c. Egg with a lateral spine. 
150 diameters. 

places a severe inflammation with ulceration and consequent strictures, or the 
formation of concretions. Similar violent inflammation occurs, also, in the rec- 
tum and in the sexual organs. The course of the disease is very chronic. The 
main symptom is persistent haematuria. Many cases of so-called tropical hema- 
turia are due to the distoma, and later we have the symptoms of local inflamma- 
tion and of severe cystitis. The diagnosis may be established by the discovery of 
the eggs in the urine or the faeces. Treatment is merely symptomatic. 

3. Strongylus or Eustrongylus G-igas (palisade worm) is a parasite occurring 
in the pelvis of the kidney in many animals — the dog, the wolf, the marten — and 
very rarely in man. In size and color it is not unlike an ordinary earth-worm. 
It may produce symptoms of severe pyelitis, with haemorrhages, and colicky 
pains. No well-established cases have been reported of late. 

4. Filaria Sanguinis. Chyluria. — The blood filaria of man, belonging to the 
round-worms, has obtained a special clinical interest, since it is recognized, from 
the investigations of Wucherer in Bahia in 1868, and of Lewis in the East Indies 
in 1870, as the cause of the tropical chyluria and some allied diseases, such as 
lymph scrotum, elephantiasis Arabum, and chylous ascites. 

The full-grown filaria, "filaria Bancrofti," a very thin worm, about three or 
four inches long, has been found only a few times in man. Its seat is in the 
larger lymphatics, where it gives rise to chronic stasis of the lymph with its conse- 
quences — chronic hyperplasia of the connective tissue, etc. In chyluria, the para- 
sites are probably situated in the main branches of the thoracic duct — at any 
rate, in such a place that a stasis of the lymph ensues in the lymphatics of the 
bladder, or perhaps, in some cases, of the pelvis of the kidney and the other urinary 
passages. If the distended lymph-sac ruptures, the lymph or chyle is poured out 
into the urinary passages and is evacuated with the urine. Since this process may 
be often repeated, the intermittent course of chyluria is thus explained. The indi- 
vidual attacks of the disease may come on during years at intervals of weeks or 
months. They are often associated with pain and febrile symptoms. 

The condition of the urine, which in many cases may look almost exactly like 
milk, is most characteristic. A creamy layer of fat forms upon the surface. If we 
shake the urine with ether, the greater part of the fat can be removed, and the 
urine rendered clear. The fat in the urine may amount to two or three per cent. 
The chyluria is often associated with a haematuria coming from the ruptured 
veins. The urine then looks bloody red, and shows under the microscope many 
red blood-corpuscles beside the fat-drops. Large clots often form in the urine. 




648 



DISEASES OF THE URINARY ORGANS 



The embryos of filaria, found in the urine in very many cases, although not in 
all, form the most important diagnostic feature in the urine. These (see Fig. 72) 

are objects two to three tenths of a milli- 
metre long, with a diameter about equal 
to that of a red blood-corpuscle. They are 
usually imbedded in a very delicate sheath, 
which often projects at the end of the ani- 
mal, and show a constant, vigorous vibrat- 
ing motion. They have also been found in 
the blood of the patient, as well as in the 
urine, and, strange to say, especially during 
the night. 

The course of the filaria disease may 
vary considerably. Many patients reach an 
advanced age; in others, severe general 
symptoms, like anaemia and emaciation, 
finally come on. The different forms in 
which the disease occurs — chyluria, elephan- 
tiasis, etc. — are combined in manifold ways. 

The region of the geographical distribu- 
tion of the disease lies almost wholly in 
hot countries. It has so far been most fre- 
quently observed in Brazil, the Antilles, the 
East Indies, China, Japan, Egypt, Cape 
Colony, and Australia. Nothing definite is 
yet known of the precise mode of invasion 
of the parasites. According to Hanson's 
investigations, mosquitoes play an important part here. [This view is now well 
established. — V.] 

In regard to treatment, apart from any surgical interference, we may try 
picro-nitrate of potassium, three to ten grains (gramme 0.2-0.5), in pills or cap- 
sules, several times a day (Scheube). 




Fig 



(From Scheube.) Embryos of filaria. 



CHAPTER X 

MOVABLE KIDNEY (FLOATING KIDNEY, REN MOBILIS) 

iEtiology. — With some practice the physician can frequently palpate the kid- 
neys, particularly the right kidney, even under absolutely normal conditions 
("palpable kidney"). This is much oftener the case in women with lax and 
yielding abdominal walls than in men. With every inspiration the kidney is 
pushed somewhat downward. In many cases, therefore, the kidney, or at least its 
lower half, is felt only upon deep inspiration. If the kidney is not only palpable, 
but also capable in greater or less degree of being moved about by the hand, and 
if, consequently, we do not always find the kidney in the same place, then we de- 
scribe it as an abnormally movable kidney; or, if the case is extreme, a floating 
kidney. What may be the causes of this extreme mobility of the kidney is not set- 
tled. Often it may be due to the congenital, anatomical relations of the perito- 
neum, and other tissues around the kidney. This is indicated, particularly, by the 
occasional occurrence of movable kidney in children. Certain external mechan- 
ical factors, however, undoubtedly play the most important role. First among 
these is the distention and relaxation of the abdominal walls as a result of preg- 



MOVABLE KIDNEY (FLOATING KIDNEY, KEN MOBILIS) 649 



nancy; and, secondly, the influence of clothing, waist-bands and corsets. This ex- 
plains the fact that movable kidney is found mainly in women, and particularly in 
married women. At the same time, the abnormal mobility and downward dis- 
placement of the kidney are often merely a part of a general " enteroptosis " (see 
page 465), and are therefore associated with gastroptosis, coloptosis, and cor- 
set liver. That the movable kidney is far more often the right than the left, is 
probably due to the fact that the right kidney is originally less firmly fastened, 
and is placed lower, and also that it is affected by the great mass of the liver which 
lies above it. Numerous other causative influences have been mentioned, but none 
of them is as important as the preceding: they are severe physical labor with 
frequent tension of the abdominal muscles; injuries involving the region of the 
kidneys; diseases of the neighboring organs, particularly displacement of the 
uterus, and finally emaciation, causing absorption of the fat which supports the 
kidneys and makes tense the abdominal walls. After death a movable kidney 
can not be recognized, unless it is found in an abnormal position — e. g., in front 
of the vertebral column, or close to the anterior abdominal walls. In such cases 
its external edge may be directed downward and its inner edge upward. 

Symptoms. — The clinical importance of movable kidney is estimated very dif- 
ferently by different physicians. Many conceive that it is a very frequent cause 
of manifold abdominal disturbances; others are almost inclined to deny it any 
influence on the health. We ourselves believe that a movable kidney as such may, 
in fact, excite disagreeable symptoms, but that this is the exceptional occurrence. 
As we have already mentioned, palpability and slight movability of the right kid- 
ney are so frequent in women that as soon as one's attention is directed to the 
matter, one finds this condition in a large proportion of all cases in which there is 
occasion to make a careful abdominal examination. The pains and abnormal 
sensations in the abdomen, of which women so frequently complain, are difficult 
of interpretation, and it is, of course, very seductive and convenient to refer them 
to a movable kidney; but if we consider how often we find an exactly similar 
movable kidney in women who are entirely free from abdominal symptoms, we 
can not avoid suspicion as to the importance of the condition. 

It is difficult to form a characteristic group of symptoms which may be un- 
hesitatingly referred to movable kidney. First, pain should be named. This is 
to a certain extent local, but it often radiates into the epigastrium and the sacral 
and lumbar regions, and sometimes is colicky. Not infrequently the pain is asso- 
ciated with nausea. The discomfort is aggravated by any decided motion of the 
patient, or by riding, driving, and the like ; but during repose it becomes slight, 
or entirely disappears. In rare cases we have symptoms of strangulation. These 
occur periodically, and are said to be especially frequent at the time of the menses. 
They consist of the sudden onset of violent pain; chilliness which seldom 
amounts to a rigor; great tenderness and tenseness of the abdomen; slight 
fever; vomiting; and collapse. During this time the urine is usually scanty, and 
the amount does not increase again till the attack is over, about three to five days. 
The precise cause of these symptoms is supposed to be a sudden damming up of the 
urine by a kink or twist in the ureter. This occasions acute hydronephrosis, and 
resultant phenomena, which last until the urinary channels are free again. In 
certain cases floating kidney seems actually to be the cause of persistent hydro- 
nephrosis, with secondary pyelitis. 

The discovery of floating kidney by palpation is usually easy. The physician 
examines the patient lying on her back, applying his left hand on the right lum- 
bar region and pressing forward, while his right hand presses from in front in the 
opposite direction. It is then often possible, especially upon deep inspiration 
(vide supra), to catch the kidney between both hands, and so form an opinion 
as to its position and mobility. 



650 



DISEASES OF THE UKINAKY OHGANS 



The next point is to determine whether, in any particular case, the symptoms 
which may be present are actually due to the movable kidney which has been dis- 
covered, or whether the latter is an unimportant matter. This question demands 
a careful and complete physical examination and a consideration of all the symp- 
toms. In the first place, we should determine accurately the position of the stom- 
ach (gastroptosis, etc.), and we should also think of the possibility of gall-stones, 
which may produce a very similar group of symptoms. Gall-stones are especially 
apt to occur in women with corset liver and enteroptosis, and this explains why a 
movable kidney is not infrequently found in cases of biliary colic, although it 
has nothing to do with the attack. 

In a great majority of cases of "floating- kidney" we have to do with those 
familiar and frequent conditions of a " nervous " character which are termed 
hysteria or neurasthenia. Women of this kind suffer very frequently from all 
sorts of painful sensations in the abdomen, and from dyspeptic disturbances and 
the like, and of course we very often find in them a movable kidney. In such 
cases the abdominal symptoms are also of a nervous character, as can usually be 
easily determined from the general condition of the patient, from her psychical 
and cerebral symptoms, and the indications of a cardiac neurosis, and also from 
the results of suggestive treatment. Still, a certain number of cases may be very 
difficult of diagnosis. If we find a movable kidney in a nervous, hysterical 
woman, it is not always advisable to apprise the patient of the fact, for with a 
person of this sort the mere idea of possessing- a " floating kidney " is enough to 
stir up a host of subjective symptoms. On the other hand, it may be said that the 
floating kidney may serve as a very handy instrument for suggestive therapeutics. 
If we say to such a patient that her annoyance would immediately vanish after 
the application of a suitable bandage, we may sometimes attain great therapeutic 
success, although this is apt to be but temporary. 

Treatment. — If we deem that the movable kidney requires treatment, the first 
thing to recommend is the wearing of a suitable support. The bandages, with 
special pads and the like, we regard as usually of no value, while a good elastic 
abdominal bandage, with thigh-straps, or a well-fitted " abdominal corset," is 
sometimes decidedly efficient, particularly in all cases of general enteroptosis. 
We should also see that the patient is properly nourished. If she is emaciated, 
we should prescribe rest with the largest possible amount of food, so-called over- 
feeding. As more and more fat is deposited in the abdomen, the abdominal walls 
regain their tension and the kidneys receive better support. It is also advisable to 
sponge the abdomen with cold water or brandy. 

If there are any symptoms of strangulation, we should of course put the patient 
to bed and order hot poultices and opium. We may also make a cautious attempt 
to replace the organ. If severe attacks of this sort recur, the possibility of surgical 
treatment should be considered (nephrorrhaphy or nephropexy). In a fairly large 
number of cases the patients are said to have been entirely freed of their discom- 
fort by this method. 



APPENDIX 

THE DISEASES OF THE SUPRA-RENAL CAPSULES AND ADDISON'S 
DISEASE (BRONZED SKIN) 

etiology and Pathological Anatomy. — In the year 1855 the English physi- 
cian Addison published for the first time a list of cases in which, besides the symp- 
toms of a general bodily weakness and anaemia, a peculiar dark pigmentation of 



ADDISON'S DISEASE 



651 



the skin had gradually developed. Since disease of the supra-renal capsule was 
found at the autopsy in all cases, Addison concluded that this was the immediate 
cause of the bronze coloring of the skin. Observations similar to Addison's were 
soon made in greater numbers, so that the fact itself can not be doubted; but even 
at present nothing definite is known as to the special cause of the disease or the 
true nature of this remarkable connection between disease of the supra-renal 
capsules and pigmentation of the skin. 

Attempts have been made in different quarters to obtain an explanation from 
experiments on animals. Erom these it has appeared that the complete extirpa- 
tion of both adrenals in animals usually results, after a short time, in death, but 
if vestiges of the adrenals, or if so-called accessory adrenals are left behind, there 
is no unfavorable result; or, if any, it is much delayed, The symptoms of the 
extirpation of the adrenals consist in emaciation, paretic weakness of the muscles, 
indigestion, and nervous disturbance. It has not yet been possible to obtain by 
experimental methods such an abnormal pigmentation of the skin as is seen in 
Addison's disease (JSTothnagel and others). Very many experiments have been 
made with regard to the ehect of extract of the adrenal gland; it affects chiefly 
the vaso-motor system, as shown by the increase of blood-pressure and slowing of 
the heart's action. The results thus obtained do not as yet, however, justify abso- 
lute conclusions. Chemical examination of the gland shows an abundance of 
lecithine, also brenzcatechine, and a substance, sphygmogenine, which raises the 
biood-pressure. ALost investigators are at present inclined to the opinion that the 
adrenals have the task of destroying, or rendering innocuous, certain poisons 
which are formed in the body, particularly in connection with muscular activity. 
It may also be that the adrenal gland secretes some material of physiological 
importance. We are as yet far from a clear understanding of the matter. 

f he anatomical lesions found in man up to the present time are not calculated 
to add clearness to the case, since they seem to contradict one another in various 
points. In the first place, some observations must be mentioned in which the 
supra-renal capsules were found perfectly normal in spite of an existing pigmen- 
tation of the skin. Such cases, however, prove little, since it of course can not be 
put in question that a staining of the skin may sometimes develop from some 
other reason besides disease of the supra-renal capsules. On the other hand, it has 
been asserted that extensive changes are sometimes found in the supra-renal cap- 
sules on autopsy without the existence of the symptom of bronzed skin during the 
patient's life ; but these cases are also open to the objection that the disease has 
perhaps not been extensive and intense enough to cause the bronze coloring of the 
skin. The contradictions just mentioned, however, have led to many other at- 
tempts at an explanation of Addison's disease, of which one especially deserves 
consideration. According to this, the symptoms met with are produced not by the 
disease of the supra-renal capsules themselves but by the invasion of the solar 
plexus and the semilunar ganglia of the sympathetic by the morbid process (Rise], 
Burger, and others). According to this theory, the symptoms of Addison's disease 
may arise when the aforesaid nervous parts are diseased independently, or by the 
extension of a pathological process from some other neighboring organ; but 
pathological anatomy has not furnished any corroboratory evidence of this view. 
On the contrary, the more recent investigations of the sympathetic nervous sys- 
tem in Addison's disease have had ambiguous results. 

Addison himself has pointed with emphasis to the fact that the precise form 
of disease in the supra-renal capsules is by no means always the same. At any 
rate, the disease named from him is not to be regarded as a definite anatomical 
affection, but rather as a particular group of symptoms. By far the most fre- 
quently it is tuberculosis of the supra-renal capsules which lies at the bottom of 
Addison's disease. The capsules then are either enlarged and studded with case- 



652 



DISEASES OE THE URINARY ORGANS 



ous tubercular new growths, or they are in part cicatricially contracted. Other 
tubercular affections are almost always present in the body at the same time, espe- 
cially caseation of the mesenteric lymph-glands and pulmonary tuberculosis. 
Other morbid processes besides tuberculosis may also be found in the supra-renal 
capsules: tumors (adenoma or struma, carcinoma, sarcoma), haemorrhage, atro- 
phy, etc. It is self-evident, from what has been said above, that in every case we 
must consider some implication of the neighboring sympathetic ganglia, by com- 
pression, cicatricial contraction, or chronic inflammation. Both supra-renal cap- 
sules are almost always diseased at the same time, rarely only one is affected. 

Of the lesions in other organs we must also mention that Peyer's patches and 
the solitary follicles of the intestine are as a rule swollen. The spleen is some- 
what enlarged in some cases, but not in others. There is no striking pigmentation 
of the internal organs. The changes in the skin and in certain mucous membranes 
will be mentioned below. 

Considering the variety of the anatomical causes there can be no question of a 
uniform aetiology of the disease. Among the causal factors, those most frequently 
reported are defective nutrition, care and anxiety, and finally injury of the abdo- 
men. The majority of cases are met with in the male sex and in middle life. 
Addison's disease, however, must be regarded as a rare affection, of which but 
few cases are observed even in the larger cliniques. 

Symptomatology. — The purest type of Addison's disease appears in those cases 
where the symptoms are apparently primary in their development, and do not 
come on in the course of some other disease, such as phthisis or cancer. 

The first symptoms of the disease are usually of a general nature, and are 
referable to a gradually increasing anaemia and to general weakness and physical 
lassitude. The anaemia shows itself objectively through the pallor of the skin 
and the diminution in the number of red blood-corpuscles, but without other defi- 
nite anomalies of the blood that can be made out. Moreover, there are a number 
of symptoms which depend in part upon the cerebral anaemia, and in part upon 
nervous disturbance. In this number are the mental torpor and lack of energy, 
the headache and tendency to syncope, and the tinnitus aurium. Sometimes 
there are marked psychical disturbances, such as impairment of memory, feeble- 
ness of mind, or exaltation. The patient's general nutrition often suffers very 
considerably; but it must be added that in Addison's disease, as in other anaemias, 
the fatty layer, especially over the abdomen, often remains remarkably well de- 
veloped. 

The great muscular weakness, asthenia, of the patient is still more character- 
istic than the anaemia. This is shown less in inability to make a few vigorous 
contractions than in extremely rapid exhaustion of the separate muscles. As a 
consequence, all long-continued muscular exertion, such as walking for any length 
of time, standing, continuous labor, becomes absolutely impossible. 

Beside the symptoms which have been enumerated there is often gastric dis- 
turbance. The appetite is poor, and there is very often vomiting. The latter may 
sometimes be almost uncontrollable, and then it is one of the most distressing 
symptoms of the disease. It is usually due not to an anatomical change in the 
stomach, but probably to the anaemia of the brain, or to other nervous influences. 
Cardialgic symptoms are also frequent. The bowels are sluggish as a rule, but 
there is sometimes diarrhoea. We sometimes hear functional murmurs in the 
heart, but as a rule its sounds are pure though feeble. The pulse is usually mod- 
erately accelerated. The liver and spleen do not show any special changes. Albu- 
minuria is exceptional and depends upon complications, such as amyloid kidney; 
the bodily temperature is not elevated, and not infrequently, indeed, it is decid- 
edly subnormal. 

The special characteristic symptom, which alone renders the diagnosis possible, 



ADDISON'S DISEASE 



653 



is the gradual onset of a peculiar pigmentation of the skin. This usually shows 
itself first in the face and on the backs of the hands, and also in those parts which 
normally present a greater pigmentation (the areola of the nipples, the axillae, 
and the genitals), or which are exposed to greater pressure by the clothing, as 
the hips and shoulders. It is especially noteworthy that dark pigmented spots 
and stripes usually develop on the mucous membrane of the lips, particularly at 
the corners of the mouth, and inside the cheeks. The intensity of the coloring 
differs in different cases. It usually increases as the general condition grows 
worse. In the most intense cases almost the whole skin may become dark brown 
or black, like that of a mulatto or negro. Sometimes, however, the pigmentation 
remains limited to separate large or small spots, and in other parts of the skin 
there may then be even a marked loss of pigment. The nails and the sclera always 
remain white, and frequently the palms of the hands and the soles of the feet also. 
The hair is usually not changed. The pigmentation of the skin usually increases 
during the whole disease; only exceptionally does the skin become light again in 
the later stages. 

The real cause of the accumulation of pigment in the skin is wholly unknown. 
We find on microscopic examination of the skin that the pigment lies not only 
in the cells of the rete Malpighii, but also in the corium, especially along its blood- 
vessels. It is probably formed from the blood-pigment, and is carried by wander- 
ing cells from the cutis into the epithelial layers of the skin (Demieville, Noth- 
nagel). 

The course of Addison's disease is almost always chronic, and may last for 
years, but cases have been described with a rather acute course. The disease 
sometimes begins with violent initial febrile symptoms, vomiting, and diarrhoea. 
The disease then has a comparatively rapid termination after a few months, or a 
second chronic stage may follow the first acute one. 

The final termination of Addison's disease is always unfavorable. Temporary 
remissions are often observed, but the disease always becomes worse again after 
them. Death usually ensues gradually amid the signs of increasing general 
uraemia and weakness. In some cases severe nervous symptoms also come on 
toward the end of the disease — coma, delirium, or epileptiform attacks. Condi- 
tions of this sort may develop comparatively suddenly and unexpectedly; indeed, 
they seem to support the hypothesis of toxic influences (vide supra). 

Treatment. — Organo-therapy has been repeatedly tried in Addison's disease, 
on the same lines as the treatment of diseases of the thyroid gland. The 
adrenals of the sheep have been administered, either as fresh glands, finely 
minced and eaten with bread, or as an extract, or in the form of tablets of the 
dried glands. In some cases excellent results seem to have been obtained in this 
manner, even to diminution in pigmentation, but in many other cases this pre- 
scription has no beneficial effect. We ourselves administered adrenal tablets in 
one case for a long time without any advantage. Still, it would be proper to con- 
tinue these trials. Whether treatment with Koch's tuberculine might cause per- 
manent benefit in those cases which are due to tuberculosis, is as yet doubtful. 
A cautious trial might be made under proper circumstances. As to other reme- 
dies, tonics are generally employed — nourishing food, iron, quinine, and arsenic ; 
iodide of potassium, bromide of potassium, and electricity have also been tried, 
but without success. Symptomatic treatment is needed for the vomiting, diar- 
rhoea, and nervous attacks. Experience has shown that great caution should be 
exercised in prescribing laxatives, because in repeated instances such remedies 
have had decidedly unfavorable results. 



654 



DISEASES OF THE UEDs T AEY OEGA1TS 



SECTION II 

Diseases of the Pelvis of the Kidney and of the Bladder 

CHAPTEE I 

INFLAMMATION OF THE PELVIS OF THE KIDNEY. PYELITIS 

Etiology. — Isolated primary pyelitis hardly ever occurs as an independent 
disease. Pyelitis is rather in most cases either a complication or a result of other 
diseases, and in such cases often attracts but little clinical attention. 

We sometimes find a rather moderate pyelitis in the bodies of persons who 
have died of severe general infectious diseases, typhoid fever, small-pox, diph- 
theria, or pyaemia. The affection depends, in all probability, upon the elimination 
by the kidneys of substances that excite inflammation, and is thus to be regarded 
as analogous to the renal changes which often coexist. Toxic substances, such as 
cantharides and copaiba, which pass through the kidneys, may also cause pyelitis 
as well as other disturbances. 

Pyelitis very often arises from a direct extension of inflammation from the 
neighboring organs. In many cases of acute and chronic nephritis the pelvis of 
the kidney takes part in the inflammation to a greater or less degree; but an 
ascending extension of the inflammation from primary diseases of the urethra or 
bladder is still more common. Any case of urethritis or cystitis may, if it lasts 
long, advance upward to the ureters and the pelvis of the kidney, so that in severe 
cases we often find an inflammation of the whole urinary tract, a pyelo-cystitis, 
and even a " ureteritis." It has been already mentioned (page 640) that the in- 
flammation may extend still farther to the kidneys themselves (pyelo-nephritis), 
and we shall refer to this repeatedly. Of all these varieties of ascending inflam- 
mation in the urinary passages, none is so frequent or of so great practical impor- 
tance as that which results from persistent narrowing of the urethra (stricture, 
hypertrophy of the prostate), and the consequent obstruction to the flow of urine. 
We shall revert to this important variety when discussing hydronephrosis. Very 
frequently the ascending pyelitis is a sequel to cystitis in disease of the spinal 
cord, with paralysis of the bladder. 

Another form of pyelitis is that caused by the presence of foreign bodies in 
the pelvis of the kidneys — e. g., calculous pyelitis due to the mechanical irritation 
of renal calculi. This also will have a special consideration below. Much less 
frequent causes are retained blood-clots, parasites {vide supra), and genuine 
foreign bodies. 

Primary idiopathic pyelitis, as a result of catching cold or similar influences, 
is, as we have already said, of extremely infrequent occurrence. We have our- 
selves seen a few cases which did not seem to be capable of any other interpreta- 
tion, and yet we must strongly emphasize the necessity of regarding all such cases 
of pyelitis with great suspicion, from a diagnostic point of view. It is only too 
often that the " simple " pyelitis will prove to be renal tuberculosis, or an inflam- 
mation due to calculi or other causes. The pyelitis coming on in women in child- 
bed, or following different sorts of diseases of the sexual organs, may in all cases 
be referred to an infection of the pelvic mucous membrane from the bladder or 
from the kidneys. 

Pathological Anatomy. — In simple catarrhal inflammation the mucous mem- 
brane of the pelvis of the kidney is reddened, swollen, and covered with an abun- 
dant secretion, which contains varying amounts of pus-corpuscles and epithelium. 



INFLAMMATION OF THE PELVIS OF THE KIDNEY 655 



In severer inflammations we often find quite numerous little haemorrhages in the 
mucous membrane, and sometimes little gray nodules, which correspond to the 
swollen lymph-follicles. 

In severe cases, which are seen almost solely as a complication of a more 
extensive affection of the urinary passages, such as pyelo-cystitis, we have a puru- 
lent, ulcerative inflammation, which may even assume a diphtheritic character. 
In these cases the kidneys are almost always coincidently involved — pyelo-ne- 
phritis. If the nephritic abscesses break into the pelvis of the kidney, there arises 
an ulcerative destruction of the renal tissue, so that the pelvis of the kidney is 
filled with pus and bounded by extensive ulcers, which often penetrate deeply 
into the substance of the kidney — pyonephrosis. The pyelo-nephritic abscesses 
reaching to the outer surface of the kidney, and usually giving a striated appear- 
ance to a section of the organ, have already been described (see page 641), and 
their bacterial origin mentioned. 

The condition differs when the kidney is involved, as in many cases of chronic 
pyelitis. This appears most frequently as a result of retention of urine, and hence 
it is usually associated with a dilatation of the pelvis of the kidney. In these cases 
we sometimes find pronounced processes of contraction in the kidneys — that is, a 
partial atrophy of the renal tissue, increase of the interstitial connective tissue, 
and evident cicatricial depressions on the surface — in a word, a secondary con- 
tracted kidney, arising as a result of pyelitis, which differs from genuine contrac- 
tion of the kidney only in its aetiology. 

Clinical Symptoms. — Since in most cases pyelitis develops only as one symp- 
tom of a more extensive morbid process, its clinical symptoms are usually but 
slightly prominent in the general course of the illness. In what follows, there- 
fore, we can not give any complete description of the clinical course of pyelitis, 
but we must mention only those symptoms from which, when there is an affection 
of the urinary passages, we may conclude 
that the pelvis of the kidney takes part in 
the morbid process. 

The most essential sign which the urine 
presents in all inflammatory affections of the 
urinary passages, the presence of mucus and 
pus, w T ill be described more fully in the chap- 
ter on cystitis (vide infra). In pyelitis, also, 

,i -i ,. j» .-I i • Fig. 73.— Epithelium from the pelvis of the 

the muco-purulent secretion ot the pelvic kidney, 
mucous membrane must mix with the urine, 

and in every severe purulent inflammation the amount of pus in the urine must be 
considerable. We can never decide with certainty, from the mere presence of pus 
in the urine, as to the place where the pus mixes with the urine, whether in the pel- 
vis of the kidney or in the bladder, or even in the urethra. If only we were able to 
demonstrate other morphological elements besides the pus-corpuscles, so charac- 
teristic that their origin might be affirmed with certainty to be the pelvis of the 
kidney, we might, by means of them, make our diagnosis of pyelitis absolute. Un- 
fortunately, however, the microscopic sediment of the urine leaves much in this 
regard to be desired. The greatest weight was formerly ascribed to the discovery 
of pelvic epithelium; especially the triangular, long-tailed epithelial cells, some- 
times arranged one upon the other, like the tiles of a roof (see Fig. 73), were re- 
garded as an indication that the pelvis of the kidney was involved in the inflam- 
mation; but the diagnostic significance of these cells is by no means indubitable, 
for, on the one hand, they may be absent in a severe case of pyelitis ; and, on the 
other hand, precisely similar epithelium comes from the mucous membrane 
of the bladder. Greater value is given of late to the discovery of certain casts 
from the mouths of the urinary canaliculi (ductus papillares) — structures which 




656 



DISEASES OF THE UKINAKY OKGANS 



are almost invariably involved in all but the milder cases of pyelitis. Tubulif orm 
epithelial casts, cylindrical formations composed of pus-corpuscles, and, above all, 
casts composed of micrococci, have been repeatedly found in the urinary sediment 
in cases of pyelitis, and possess some diagnostic importance (Fiirbringer and 
others). 

With regard to the other characteristics of the urine, it should be mentioned 
that it is often remarkably abundant in pyelitis, and that it then of course is 
pale and has a comparatively low specific gravity. The reaction of the urine is 
usually acid, despite the admixture of pus. That this acid reaction is an effectual 
distinction from the urine of cystitis can by no means be maintained (vide infra). 
We may, however, say that the tendency of the urine to ammoniacal fermentation 
is decidedly greater in cases of cystitis than in cases of pyelitis. The amount of 
albumen in the urine corresponds to the amount of pus. If there is a very large 
amount of albumen, it arouses suspicion of a coincident nephritis. The only de- 
cisive proof of such a complication lies in the finding of genuine urinary casts. 
In cases of simple pyelitis it is exceptional for the urine to be bloody, while in 
calculous pyelitis (q.v.) blood is often present. 

Besides the quality of the urine, another symptom is pain in the region of the 
kidneys. This is present in many cases of pyelitis. The pain is often very severe, 
and radiates along the ureters to the bladder. In some cases, however, there may 
be no pain at all, so that while its presence is one symptom of pyelitis, its absence 
does not weigh against the disease. 

All the other symptoms may be directly dependent upon the pyelitis, but they 
may usually be referred in great degree to the other co-existing affections. First 
among these is fever, which either shows an irregularly remitting course, or ap- 
pears in single high elevations of temperature, usually associated with rigors. 
The fever, however, seldom shows this latter pysemic character except in the 
severe purulent forms, where we usually also have the formation of renal abscesses 
— that is, a pyelo-nephritis. Besides the fever there are often, in severe cases, 
general nervous symptoms, such as headache, delirium, and sopor, which are to be 
referred partly to the general pysemie infection of the body and partly, perhaps, 
to the absorption of ammonia from the decomposing urine into the blood — the 
" ammonisemia " of Treitz and Jaksch. 

The whole course of pyelitis differs so much according to the primary disease 
present that nothing of general application can be said about it. The milder 
forms, which often pass off rapidly, are found most commonly in childbed, and 
sometimes in acute infectious diseases, poisonings, and as a result of mild cystitis. 
The severe forms are chiefly, as we have said, pyelo-cystitis and pyelo-nephritis, 
as a result of strictures of the urinary tract (vide infra), of severe cystitis in dis- 
eases of the spinal cord, and in other severe diseases of the kidney and of the pel- 
vis of the kidney, such as new growths, and parasites. They usually constitute a 
very tedious and incurable affection, which lasts until the patient's death. 

The important factors in the diagnosis of pyelitis have been already pointed 
out. The main thing in every case is a careful consideration of the cause and the 
course of the disease, and, with regard to the special involvement of the pelvis of 
the kidney, a study of the changes in the urine, and the local symptoms if there 
be any. If the bladder itself is unaffected there will be no special bladder symp- 
toms, such as tenesmus and frequent micturition. If there is severe disease of the 
urinary passages, and especially if the patient has considerable fever, we may 
often be justified in gliagnosticating pyelitis, or pyelo-nephritis, even when there 
are no direct indications, because experience has shown that such an extension of 
the disease is the rule in all severe and long-continued cases. 

The implication of the kidneys is shown by the presence of casts in the urine 
in addition to the pus-corpuscles. In the cases above mentioned, in which a 



NEPHROLITHIASIS 



657 



chronic pyelo-cystitis is complicated with a contracted kidney, the condition of 
the urine is the same in many respects as in genuine contracted kidney. It is 
abundant, usually has a low specific gravity, and contains, besides the pus-corpus- 
cles, a few short hyaline casts. In such cases there may be developed a secondary 
hypertrophy of the left ventricle, unless the general nutrition of the patient is too 
much impaired. 

Treatment. — The treatment of pyelitis coincides mainly with the treatment of 
the primary disease — for example, renal calculi — and therefore it needs no de- 
tailed description here. Ordinarily only the accompanying cystitis (vide infra) 
is accessible to a direct local treatment, and here an important prophylactic factor 
is discovered, since by a timely treatment of the cystitis we can certainly hinder 
the advance of the inflammation to the pelvis of the kidney. 

Among the internal remedies to which we ascribe a favorable influence on the 
mucous membrane of the urinary tract, which are therefore used in like man- 
ner both in pyelitis and in cystitis, we may mention the astringents, tannin, 
alum, and acetate of lead. Their therapeutic effects, however, are usually very 
slight, and often they are ill-borne, so that certain antiseptic remedies are prefer- 
able, particularly salol in capsules of eight grains (gramme 0.5) three to five times 
a day ; [urotropine, ten grains three times a day] ; also, camphoric acid and chlo- 
rate of potash. Balsamic remedies are sometimes useful, including turpentine, 
sandalwood, and copaiba. The details in regard to all these remedies will be 
found in the treatment of cystitis. The copious ingestion of fluids usually acts 
favorably, especially the use of certain mineral waters, among which the waters of 
Carlsbad, Vichy, Ems, ISTeuenahr, and Wildungen have obtained the most reputa- 
tion. A methodical milk cure is also greatly to be recommended, especially when 
there are symptoms of irritation, such as pain on micturition. 

Local applications to the region of the kidneys, warm poultices, or exception- 
ally local blood-letting, are indicated only when there is severe pain, and then, of 
course, narcotics must also be used under some circumstances. In this respect 
warm baths also do good service at times. 



CHAPTER II 

NEPHROLITHIASIS 

{Renal Calculus. Eenal Gravel. Pyelitis Calculosa) 

Occurrence, Chemical Composition, and JEtiology of Kenal Concretions. — 
The precipitated concretions of the urinary constituents which form in the pelvis 
of the kidney, and which, under some circumstances, may be passed from it with 
the urine, are designated, according to their size and nature, as renal sand, a fine, 
pulverized precipitate; renal gravel, gravel-like, granular concretions about the 
size of the ordinary coarse grains of sand, which can usually pass through the 
ureters without special difficulty; or renal calculi, the larger concretions. The 
last are about the size of a millet seed or a pea, but larger stones are occasionally 
seen which may even resemble actual casts of the pelvis of the kidney. We usually 
find a calculus in only one kidney, although both kidneys may be affected. 

In regard to the chemical nature of renal concretions, they consist most fre- 
quently of uric acid. They then are hard, have a brown-red or blackish color, and 
a crystalline fracture, which in large stones is usually plainly laminated ; and, on 
the whole, a smooth although irregularly-shaped surface. More rarely the renal 
concretions consist of calcic oxalate. The oxalate calculi are extremely hard, 
42 



658 



DISEASES OF THE UKIXAKY OKGAXS 



have a dark-brown color and a rough surface, often furnished with many prickles, 
from which reason they are often called " mulberry calculi." Their fracture 
sometimes has a radiated but never a laminated arrangement. Stones are also 
frequently seen, which consist of alternating layers of uric acid and calcic oxalate, 
or which have a nucleus of uric acid and a coating of calcic oxalate. The phos- 
phatic calculi are another variety of renal concretions. We only rarely have to 
do, however, with stones which consist exclusively of basic calcic phosphate or 
ammonio-magnesic phosphate, but we oftener have secondary deposits of layers 
of phosphate which are precipitated on uric acid or mulberry calculi in urine 
which has become alkaline. The pure phosphatic calculi are grayish-white and 
rather soft, so that they can be crushed with the finger. The largest specimens 
of this kind are not found usually in the pelvis of the kidney, but in the bladder ; 
still, as we have ourselves observed, large and pure phosphatic calculi do occur in 
the pelvis of the kidney, without any uric-acid nucleus. All the other calculous 
formations are so rare that they scarcely possess clinical interest. We may 
mention the light-yellow cystine calculi with a surface of waxy luster, the xanth- 
ine calculi, and the indigo calculi. 

As to the precise causes of all these concretions we have as yet no certain 
knowledge. The uric acid probably originates from the nucleines. An increase 
in the destruction of leucocytes seems to be associated with an increased excretion 
of uric acid. The formation of a solid deposit of uric acid is usually associated 
with marked acidity of the urine. Yet, we do not know at all in what way these 
circumstances bring about the development of renal calculi. There is much prob- 
ability in the assumption that some solid substance or other usually forms the nu- 
cleus, and gives the impulse to the formation of at least the larger renal calculi. 
Such nuclei may be coagulated mucus, bits of epithelium, and perhaps bacteria. 
It is an interesting fact, although we can not completely explain it, that, as 
Meckel, Ebstein, and others have shown, the microscopic examination of minute 
scales of calculi disclose the crystalline uric acid deposited in a supporting struc- 
ture of an albuminous character. With regard to the formation of oxalate cal- 
culi, likewise, we possess no exact knowledge. Oxalic acid in the urine probably 
is due in part to the oxalic acid which is introduced into the system in vegetables, 
and in part is probably formed from the decomposition of albuminous substances. 
The deposits of crystals of calcic oxalate from acid urine is well known to be a 
very frequent occurrence, while the actual formation of calculi is, as has been 
said, comparatively rare. The cause of the deposit of phosphatic concretions must 
lie in the urine becoming alkaline. In such cases, therefore, the development of 
concretions is probably preceded by disease of the pelvis of the kidney, and the 
ingress of bacteria capable of exciting an alkaline fermentation of the urine. 

In regard to the predisposing causes of calculus formation we must mention, 
first of all, that stones are often found in children, and next in frequency in ad- 
vanced life. Men show a greater disposition to renal calculi than women. He- 
redity also seems to play a certain part, since the disease has been repeatedly 
observed in different members of the same family. The many relations which 
have been imagined between the formation of calculi and certain conditions in 
the manner of life and in the food taken, all lack definite proof. As to mode of 
life, the chief blame is laid upon an excessive meat-diet, drinking copiously of 
new sour wines, and drinking water containing lime. It is remarkable that cal- 
culi are much more frequent in some countries (England) and regions than in 
others. In regard to the occurrence of uric-acid concretions in gouty patients, 
compare the chapter on gout. 

The Anatomical Changes caused by Renal Calculi. — The usual change which 
the presence of concretions in the pelvis of the kidney excites is pyelitis. This 
may exhibit all degrees, from a simple catarrhal inflammation to a diphtheritic or 



ISTEPHKOLITHIASIS 



659 



severe purulent inflammation of the pelvic mucous membrane. As a result of 
the mechanical irritation, there are quite frequently large or small haemorrhages. 

If a severe purulent pyelitis has developed, this may bring with it all the 
sequelae with which we have previously become acquainted. In severe cases the 
process may involve the kidneys, when there arises a pyelo-nephritis, with a puru- 
lent breaking down of the renal tissue, and, under some circumstances, even a 
perinephritis, with extensive suppuration in the vicinity of the kidney, and with 
occasional perforation into the neighboring organs. If the renal calculi have 
previously passed outward, they are not found at the autopsy, although they form 
the special starting point of the disease. Sometimes, however, the pus-cavity is 
entirely filled with calculi. 

A second important sequel of a renal calculus, which sometimes develops, is 
hydronephrosis (vide infra). It arises when a large stone blocks the passage from 
the pelvis of the kidney into the ureter, or when a smaller stone remains fast 
in the ureter and completely shuts off the passage of the urine. In the latter case 
there may also arise a pressure necrosis and perforation of the ureter. It goes 
without saying that inflammation and hydronephrosis or pyonephrosis may be 
combined. 

Clinical Symptoms. — If there is merely the formation of renal sand or renal 
gravel in the urinary tract, this condition is sometimes associated with no symp- 
toms at all. The little granules are washed away by the urine and evacuated, 
and at most they may give rise to slight pain in the region of the kidney. 
Larger stones, however, may sometimes be wholly, or almost wholly, without 
symptoms, if their position and their smooth surface are such that they are com- 
paratively harmless. 

The characteristic clinical symptoms of nephrolithiasis do not appear until the 
results of mechanical irritation of the pelvis of the kidney arise, or until there is 
an incarceration of a calculus in the ureter. It is the latter circumstance which, 
after the analogy of gall-stones, causes the most important symptom in the diag- 
nosis of renal calculi — the pain, the so-called renal colic. Such an attack of colic 
sometimes comes on quite suddenly and unexpectedly; in other cases it is pro- 
duced by some exciting cause — jumping, running, walking, or riding. The pain 
often becomes frightful ; it radiates from the lateral portions of the abdomen along 
the course of the ureters upward and downward, spreading particularly toward the 
bladder, testicles, and thighs, and also up the back. In severe attacks there may 
be a general state of collapse with a small rapid pulse, cold sweat, and attacks of 
fainting. The temperature may be somewhat raised. We often see nausea and 
repeated vomiting. The urine is often scanty but sometimes entirely normal, 
inasmuch as it comes exclusively from the other free kidney; but oliguria, or even 
complete anuria, with its consequences, invariably sets in if both ureters be 
stopped. Still, even when one kidney is normal the amount of urine secreted by 
it may be scanty, as a result of a reflex inhibitory influence reaching it in some 
unknown way. If there is at the same time an inflammatory process, the urine 
may contain blood and pus. The duration of renal colic depends upon the dura- 
tion of the incarceration ; it may last for a few hours or several days. The attack 
often ends with the passage of the stone outward into the bladder. 

The other symptoms occurring in nephrolithiasis refer mainly to the results of 
the mechanical irritation of the pelvis of the kidney. In most of the severer cases 
there is pain in the region of the kidneys, which is persistent, although of varying 
severity. The urine then shows an admixture of pus, and contains pelvic epithe- 
lium and often blood. The frequent appearance of blood in the urine, which usu- 
ally has its cause in purely mechanical lesions of the mucous membrane, is a char- 
acteristic symptom of pyelitis calculosa. If we find, as sometimes happens, the 
urine at many times perfectly clear and normal, but at other times purulent, we 



660 



DISEASES OE THE URINARY ORGANS 



may suspect an occasional blocking of the ureter coming- from the diseased kidney 
by a renal calculus. 

The symptoms are much more severe if the trouble goes on to a severe purulent 
pyelitis and pyelo-nephritis. We need not describe the details again here — the 
pain, fever, swelling, and perforation internally or externally — since they agree 
completely with what has been said before (see the previous chapter and Chapter 
VI in the previous section). A special chapter will be devoted to the symptoma- 
tology of hydronephrosis. 

The course of nephrolithiasis is, as a rule, very tedious. Since the disposition 
to the formation of calculi usually persists, and since also the sequelae which have 
once developed may last for a long time, a very chronic state often develops, 
which, in varying ways and with manifold exacerbations and remissions, is com- 
posed of attacks of colic, haemorrhages, and symptoms of pyelo-cystitis. 

In many cases, of course, complete recovery may finally ensue. The calculi 
present are passed, new ones are not formed, the pyelitis that has arisen disappears, 
and all the morbid symptoms cease; but, on the other hand, nephrolithiasis has 
also a number of dangers in itself, which threaten life very seriously. These are, 
besides the rare occurrence of uraemia, first of all the development of pyelo- 
nephritis and of still more extensive suppurations, with a general decline in 
strength, pyaemic states, etc. There is also a possible danger in such chronic 
suppurations that a general amyloid degeneration of the internal organs may 
ensue. With regard to complications on the part of other organs, there is only 
one point of special interest — viz., that sometimes gall-stones and renal calculi 
are found in one and the same patient. 

Diagnosis. — Diagnosis is rendered absolutely certain by the discovery of 
renal calculi in the urine. Eor this purpose the urine must be examined as soon 
as possible after its evacuation, and the best method is by pouring it through a 
fine sieve. In many cases, however, we can make a tolerably certain diagnosis of 
nephrolithiasis, without the direct demonstration of concretions, by means of 
the characteristic clinical symptoms, particularly the periodical renal haemor- 
rhages, the attacks of colic, and in most cases the early appearance of pyelitis. 
If these symptoms are not well marked, it must be confessed that it is not always 
easy to distinguish renal colic from intestinal colic, biliary colic, neuralgia, or 
other painful abdominal diseases. It is possible to confound the condition with 
renal carcinoma and renal echinococcus. It is of great importance, particularly 
with regard to any operative treatment, to determine which kidney is the seat of 
the trouble, and whether one kidney, at any rate, is perfectly healthy or not. In 
considering these questions we must be guided by the chief seat of the pain ; the 
appearance of the urine — for instance, observing whether there is an increase in 
the amount of pus if pressure is made upon the diseased kidney, and whether 
from time to time normal urine is evacuated as a result of occlusion of the ureter 
upon the diseased side; and by the results of external examination with regard 
to tenderness, or the discovery of a tumor due to hydronephrosis. In difficult 
cases the special catheterization of each ureter is sometimes practiced. Numer- 
ous methods of performing this have been devised, some of them involving an 
incision into the bladder, and cystoscopy has of late become so perfected that im- 
portant information may be obtained by its means. With regard to the minutiae 
as to these, methods and their employment, we must refer the reader to special 
monographs. 

In a few cases admirable diagnostic results have been obtained in case of renal 
calculi by examination with the Rontgen rays. It appears, however, that only the 
phosphatic calculi can be recognized in this manner, while the concretions of 
urates, which are of much more frequent occurrence, do not throw any distinct 
shadow. 



NEPHROLITHIASIS 



661 



Treatment. — Since the uric-acid concretions are by far the commonest, the 
methods of treatment most in use for nephrolithiasis refer especially to these. 

If the tendency to the formation of urinary gravel be confirmed in a patient, or 
if the severer symptoms of nephrolithiasis have already appeared, we must first 
give a number of general dietetic directions, in order to check the formation of 
uric acid in general, and promote the solution of the uric acid already formed as 
far as possible. Without entering too much on theoretical reasoning, we will give 
in what follows the measures which have won general approval. In the first place, 
the patient must avoid immoderate indulgence in any sort of food, and particu- 
larly in meat. Articles of diet, such as liver, sweetbread, and calf's kidneys, which 
contain an abundance of nucleine, should be forbidden. The patient should be 
advised to choose a chiefly vegetable diet, with milk and a moderate amount of 
meat; spirituous beverages are to be used little, if at all, and acid viands and 
liquids are inadmissible. It is advantageous to weigh the patient regularly in 
order to keep watch on the nutrition, and to avoid any further increase of weight 
in such individuals as are well nourished; and in the obese, to bring about a 
diminution of weight. Moreover, so far as the general condition of the patient 
allows, he should have regular exercise in the gymnasium, or at sawing wood, or 
gardening. He should also promote the assimilation of his food by the frequent 
use of warm baths or mud baths ; and an abundance of liquid must be ingested, so 
as to dilute the urine, and thus increase its solvent power. 

This last indication is usually met, in conjunction with that of diminishing 
the acid reaction of the urine, by the ingestion of alkalies, so as to prevent, as far 
as possible, the deposit of uric acid; consequently, alkalies and alkaline mineral 
waters are very extensively employed in nephrolithiasis. Pfeiffer and others hive 
been able to demonstrate by direct experiment that the urine secreted after the 
use of such waters and drugs does possess an increased power to dissolve uric acid. 
The simplest way is to have the patient use phosphate of soda in a daily dose of 
one to four drachms (grammes 5-15) ; or, better, carbonate of soda, one drachm 
to two drachms and a half (grammes 5—10) ; or, finally, the specially recommended 
carbonate of lithia, two to eight grains (gramme 0.1-0.5), several times a day, 
dissolved in a large amount of simple water or carbonated water, or lemonade. 
Also, mixtures of these remedies are often used with good results; thus Cantani 
recommends bicarbonate of soda, eight grains (grammes 0.5) ; effervescing car- 
bonate of lithia, four grains (gramme 0.25) ; citrate of potash, fifteen grains 
(gramme 1) ; also the so-called uricedine, which is composed of the citrates of 
sodium and lithium, sulphate of sodium, and chloride of sodium. Of this, fifteen 
grains are to be-given several times a day. Another remedy is borocitrate of mag- 
nesium, of which a teaspoonful may be taken in soda-water with syrup, three 
times a day. Of the natural mineral waters, the results of experiment point out 
the springs of Fachingen, Vichy, and Vals as specially efficient, but good results 
are also obtained in Carlsbad, Salzbrunn, ISTeuenahr, and Wildungen. The natu- 
ral lithia waters of Assmanshausen and Salzschlirf contain such minute amounts 
of lithia salts that, in general, the artificial waters are to be preferred to them. 

The attempt has been often made to promote the solution of uric acid by 
administering certain chemical substances, but unfortunately the results have not 
been brilliant. The conditions which obtain in the human organism are essen- 
tially different from those in a test-tube. Piperazine, fifteen to forty-five grains 
(grammes 1-3) daily, has been much recommended, but has not proved at all effi- 
cient, and the same may be said of lysidine, fifteen to sixty grains (grammes 1-4) 
a day, and urotropine, fifteen to twenty-five grains (gramme 1-1.5) daily, in 
water. Still, further trial of these remedies would not be unjustifiable. 

The symptomatic treatment is very important. In so far as this relates to 
the accompanying pelvic and vesical catarrh, we may refer to the appropriate 



662 



DISEASES OF THE URINARY ORGANS 



chapters in this book. For renal haemorrhages some internal remedies, such 
as ergo tine or tannin, have been recommended, but their action is quite doubtful. 
The treatment of the attacks of colic is of great practical significance. The 
chief remedies are the narcotics, opium, and morphine, internally, or, with very 
severe pains, better subcutaneously. In severe cases chloral and inhalations of 
chloroform may be employed. Warm baths, warm poultices, or narcotic em- 
brocations, such as chloroform liniment, also frequently give relief. Local blood- 
letting is only rarely indicated. An abundant supply of fluid is always advisable, 
in order to aid the washing out of the incarcerated stone by an increased secretion 
of urine. 

Since the initiative of Simon in 1871 the operative treatment of renal disease 
has made continuous progress, and it has been eminently successful in many cases 
of renal calculi. It is, therefore, most important in all instances of nephrolithiasis 
with severe symptoms, and particularly with secondary purulent inflammation, to 
consider the possibility of surgical interference by nephrotomy or nephrectomy. 
Particulars in these matters must be sought in special treatises on renal surgery. 

What has been said thus far refers, as we have stated, chiefly to the treat- 
ment of uric-acid calculi. If there are calculi made up of oxalate, the amount 
of vegetables eaten must be limited, but the use of alkaline waters is advisable. 
We do not know any special directions to give in case there were cystine calculi. 
On the other hand, when phosphatic stones are present, inasmuch as these can 
not be deposited unless the urine is alkaline, we should recommend the employ- 
ment of acids, particularly lactic acid, eight to fifteen grains (gramme 0.5-1), and 
salicylic acid; also, hydrochloric acid and phosphoric acid. Of course, in most 
cases there is some disease of the urinary passages which has occasioned the for- 
mation of the calculi, and if such disease is discovered its treatment is of para- 
mount importance. 



CHAPTER III 

TUBERCULOSIS OF THE GENITQ-URINARY APPARATUS 

^Etiology and Pathological Anatomy. — It does not seem remarkable that, 
with the presence of many tubercular processes in the body, tubercle bacilli should 
quite easily reach the kidneys by way of the blood-current, and there give rise to 
an eruption of tubercle. Accordingly, we quite frequently find a few or many 
miliary tubercles in the kidneys in acute miliary tuberculosis, in pulmonary tuber- 
culosis, etc., which are distributed over the whole kidney, or sometimes only in the 
territory of one arterial branch. 

While miliary tuberculosis of the kidney, however, is without any clinical sig- 
nificance, there is also an extensive local tuberculosis of the kidney, as well as of 
the urinary tract and the sexual organs. Such affections sometimes occur as a 
result of pronounced pre-existing tuberculosis of other organs, especially the 
lungs, or they arise as an apparently independent disease, which is termed genito- 
urinary tuberculosis. In such cases the infection with the tubercle bacilli often 
seems to take place by means of the blood from some previously existing — perhaps 
concealed — tubercular focus in the body, such as a gland, tubercular bone or joint 
disease, etc. In other cases, the tubercle bacilli perhaps enter the urinary tract 
from without, but the point of the first anatomical lesion need not, apparently, 
always be the same. The kidneys often seem to be first diseased, in other cases 
the bladder, and quite frequently, as it seems, the prostate, and sometimes perhaps 
the vesiculse seminales or the testicles. From the organ first affected the process 



TUBEECULOSIS OF THE GEXITO-UKIXAEY APPARATUS 663 



then extends continuously or by leaps to the neighboring parts. If the cases come 
to autopsy, the tuberculosis is often so extensive that we can no longer make out 
with certainty the place where it first began. In women the urinary apparatus is 
only very rarely affected by tuberculosis, while uterine and ovarian tuberculosis 
represents a localization of the tubercular poison of clinical importance. 

In the kidneys the tubercular infiltration develops either chiefly from the pel- 
vis of the kidney or in the renal substance itself. Yellow cheesy nodules arise, 
which finally break down and thus lead to an actual " nephro-phthisis." If the 
disease arise from the pelvis, the infiltrated renal papillse are usually first affected. 
Ulcerative recesses are formed in the pelvis of the kidney, and finally the entire 
lining of the pelvis is transformed into a raw surface covered with necrotic tissue 
and cheesy detritus. In very advanced cases almost the whole kidney is destroyed. 
The process is usually bilateral, but it is often more advanced on one side than on 
the other. 

If the process invade the ureters, their walls also are infiltrated with tubercular 
deposits, and hence they are thickened, while the mucous membrane is often 
changed in great part to a necrotic ulcerating surface. Precisely analogous con- 
ditions are found in the bladder, and in some cases even in the urethra ; while 
in the prostate, the vesiculae seminales, and the testicles there is more frequently 
the formation of cheesy tubercular nodules, and rarely disintegration and per- 
foration. 

Clinical Symptoms. — The picture of genito-urinary tuberculosis corresponds 
in most of its details completely to that of a severe chronic pyelo-cystitis. The 
occasional local symptom is pain in the region of the kidneys and bladder. 
This may sometimes assume great severity, like colic, if the ureter become plugged 
by a broken-down, crumbling mass ; yet in other cases the pain is but slight during 
the whole disease. 

The urine shows the most important changes. It almost invariably contains 
an abundant sediment, consisting of pus-corpuscles and detritus. Its amount 
usually remains normal for a long time ; its reaction is faintly acid, but in severe 
cases it may become alkaline through complication with an alkaline fermentation 
of the urine. The discovery of shreds of tissue in the urine, elastic fibers and 
connective tissue, is sometimes possible, and is of diagnostic value because it is 
direct evidence of an ulcerative process. The discovery of tubercle bacilli in the 
purulent urinary sediment (Rosenstein and others) is, however, far more impor- 
tant. This is possible in almost all cases, and is a reliable and absolutely decisive 
factor in diagnosis. There is, however, one unfortunate circumstance about 
the demonstration of tubercle bacilli in the urine, for not infrequently other ba- 
cilli (smegma bacilli) are stained by the ordinary method of staining, which is 
that employed for sputum, and are thus mistaken for tubercle bacilli. As yet, 
no easy and certain method of distinguishing these two varieties of bacilli has 
been discovered, and hence in doubtful cases it is necessary to resort to pure cul- 
tures and to inoculation, in order to reach a decision. [Stain with carbol-fuch- 
sine ; decolorize with twenty per cent, nitric acid ; wash in water ; and still 
further decolorize in seventy per cent, alcohol for at least ten minutes. This will 
bleach the smegma bacilli. — Y.] 

Admixtures of blood in the urine are also seen in genito-urinary tuberculosis, 
but they may often be entirely absent. In several of our cases a slight hematuria 
was the first symptom which called the patient's attention to the trouble with the 
bladder. 

The local objective examination of the kidneys usually gives a negative result. 
Only in a few cases have we been able to feel the diseased kidney as a tumor 
through the abdominal walls. This is usually due less to the tubercular infiltra- 
tion of the kidney itself than to the dilatation of the pelvis of the kidney from 



664 



DISEASES OE THE ITBINARY ORGAN'S 



hydronephrosis. We can sometimes feel trie thickened walls of the bladder. The 
local examination of the prostate and the testicles is far more important in diag- 
nosis. Especially in the latter we often feel the hardening corresponding to tho 
tubercular infiltration, and manifesting itself chiefly in the epididymis, while the 
hardening and enlargement of the prostate and seminal vesicles can usually be 
easily detected by rectal palpation. 

Among the general symptoms we must mention, first of all, fever, which is 
only exceptionally absent, and usually, in the severe cases, shows a pronounced 
remitting, hectic character. The other general symptoms are the same as in most 
of the other tubercular diseases — anaemia, emaciation, loss of appetite, increasing 
bodily weakness, etc. We have a special sign in the occasional co-existence of 
other tubercular diseases in the body, the lungs, the intestines, the bones, etc., 
but these may also be wholly absent, so that we may have to do with a purely local 
genito-urinary tuberculosis. 

The course of the disease is steadily progressive. Recovery does not occur, at 
least not in any cases where the disease has attained any extent. The disease 
lasts from a few months to a year or two, but sometimes much longer. The fatal 
termination usually ensues from the increasing general weakness, more rarely 
under the symptoms of ammonisemia, or sometimes from a miliary tuberculosis 
or some other tubercular disease, such as pulmonary tuberculosis, tubercular 
meningitis, etc. 

Diagnosis. — The diagnosis of genito-urinary tuberculosis is now seldom diffi- 
cult in fully developed cases, since it can be made with complete certainty by the 
discovery of the tubercle bacilli joined to the presence of pus in the urine. Of 
course this gives no information as to the exact distribution of the process. In 
order to judge of this, we must add the local symptoms and the physical examina- 
tion of the different organs. We are aided in the confirmation of our first sus- 
picion of a tubercular disease chiefly by the consideration of the general condi- 
tion and the habit of the patient ; the discovery of a hereditary taint, or at least 
the probability of tubercular infection; and also the discovery of other tubercu- 
lar affections, especially in the testicles; the hectic fever; and the tedious 
course, upon which nothing has a favorable influence. At any rate we must 
make it a rule, in every case of persistent pyuria which can not be otherwise 
explained, to examine the purulent sediment for tubercle bacilli (vide supra). 
We may then often be able to recognize with certainty the milder and incipient 
cases of this not very rare affection. [Another valuable diagnostic method, briefly 
referred to by the author, is by inoculation of eight to fifteen minims of the 
urinary sediment into the peritoneal cavity of a guinea-pig. If tubercle bacilli 
are present, the animal will develop tuberculosis in six to eight weeks. — V.] 

Treatment. — Whether specific treatment of genito-urinary tuberculosis with 
Koch's tuberculine is likely to have permanent success can not yet be determined, 
as so few trials have been made. Nevertheless, it would be justifiable to make a 
cautious trial of the remedy, although we can hardly cherish the hope that it 
would prove very beneficial. Beyond this we must resort, in the treatment of tu- 
berculosis of the urinary passages, to the same remedies as in ordinary chronic 
pyelitis and cystitis. Of internal remedies we have most frequently used chlorate 
of potassium and turpentine, and have sometimes seen good results, especially from 
the latter. The internal exhibition of creasote sometimes seems to us to act well. 
[TJrotropine has also been recommended. — V.] In vesical tuberculosis it is well 
to wash out the bladder. As an operative procedure we may remove tubercular 
testicles and epididymes and one kidney, but we must remember that in such 
cases there is usually co-existing disease of other parts of the genito-urinary appa- 
ratus, such as the prostate, the other kidney, etc. 



HYDRONEPHROSIS 



665 



CHAPTER IV 

HYDBONEPHROSIS 

{Dilatation of the Pelvis of the Kidney) 

.^Etiology. — If a contraction arises in any part of trie urinary tract and checks 
the flow of urine, there is a stasis of the urine in the portion behind the stenosis, 
which gradually leads to a constantly increasing dilatation of the tract as a result 
of the pressure of the retained fluid. 

In general, it is evident that gradual constrictions of the urinary tract and 
periodic obstructions, as from calculi, interrupted by free intervals, lead to more 
marked degrees of hydronephrosis than rapid and complete obstructions. Under 
the first-named circumstances the renal secretion persists much longer and is more 
abundant than in the latter case, when it usually soon ceases. Nevertheless, there 
may be even then a very slow distention of the pelvis of the kidney, particularly 
if its mucous membrane continues to secrete. If the obstruction is located in the 
ureter, the proximal portion of that canal dilates, and still more the pelvis of the 
kidney, giving rise to what is called hydronephrosis ; but if the obstruction is 
located in the urethra there is a gradual dilatation of the bladder, both ureters, 
and finaly there develops a bilateral hydronephrosis. 

A closure of the ureter arises most frequently in adults from impacted renal 
calculi, and also from new growths in the vicinity, in the uterus or ovaries, which 
compress the ureter from without. So great a pressure may also be exerted on 
the ureters by the gravid uterus as to be followed by a hydronephrosis, which 
is usually bilateral. Cicatricial strictures, valve-formations and bends, also are 
found in the ureter, and form an obstacle to the flow of urine. Finally, in can- 
cer of the bladder the lower opening of the ureter may be contracted or entirely 
closed. Constrictions of the urethra, which finally lead to a bilateral hydronephro- 
sis, arise most frequently from strictures as a result of gonorrhoea, and also from 
enlargements of the prostate. In rare cases phimosis may form the obstacle. 

It is worthy of note that hydronephrosis may also be congenital, and then it is 
usually due to congenital defects of development in the ureters or other urinary 
passages. In later life hydronephrosis is in general more frequently observed in 
women than in men. 

Pathological Anatomy. — The pathological anatomy of hydronephrosis is on 
the whole very simple. We have a dilatation of the pelvis of the kidney, which 
is associated with a pressure atrophy of the renal tissue. The papilla? are flattened, 
the uriniferous tubules and the glomeruli are gradually more and more obliter- 
ated, and finally the whole kidney may be changed to a connective-tissue sac 
filled with fluid, and displaying in its walls a few vestiges of the renal paren- 
chyma. The size of such a hydronephrotic sac may sometimes be sufficient to con- 
tain ten or fifteen quarts (litres) of fluid. The latter consists, of course, at first 
of urine, but the farther the atrophy of the kidney advances, the more it merely 
represents the secretion of the mucous membrane. Inflammatory conditions 
are found in hydronephrosis only when they have existed previously, as in pyelitis 
calculosa, or when excitants of inflammation in addition have reached the pelvis 
of the kidney. We then have a pyonephrosis. 

Clinical Symptoms. — Since the whole type of the disease is, of course, depend- 
ent in many respects upon the nature of the primary disease, we have here to 
describe only those symptoms which point to the development of hydronephrosis. 
Such a condition often causes no special clinical symptoms at all, so that we can 
at most suspect its existence from the presence of an ^etiological factor. 

The appearance of a visible and palpable tumor is the first definite point in the 



666 



DISEASES OE THE URINARY ORGAXS 



diagnosis of hydronephrosis. This first shows itself in the region of the affected 
kidney, but then it gradually enlarges toward the hypochondrium and the median 
line of the body, and it may finally reach very considerable dimensions. Hydro- 
nephrosis on the left side does not usually move with respiration. On the right 
side, however, there may be a distinct downward motion upon deep inspiration. 
The resistance of the hydronephrotic tumor is usually quite considerable, but 
there may sometimes be a distinct sense of fluctuation. On percussion, the tumor 
gives a dull note, from which the tympanitic note of the colon in front of the 
tumor is sometimes distinct (see page 645). It is an important diagnostic sign 
if the tumor show variations in its size at times — decreasing in size with a simul- 
taneous increase in diuresis, and increasing again when the amount of urine be- 
comes smaller ("intermittent hydronephrosis")- In such cases there is usually 
a very peculiar alternation in the other clinical symptoms. At the time of the 
scanty secretion of urine the patient suffers from violent pain, vomiting, chills, 
and similar symptoms, while upon the appearance of an abundant urinary secre- 
tion, all these symptoms quickly vanish. In doubtful cases an exploratory punc- 
ture of the tumor may also be of significance in diagnosis. It of course favors the 
assumption of hydronephrosis if urinary constituents, especially urea, can be 
found in the fluid evacuated; but if the hydronephrosis be of long standing, its 
contents, as we have said, will be simply sero-mucous, and then chemical examina- 
tion gives no definite data for distinguishing hydronephrosis from ovarian tumors, 
or other cystic tumors of the kidney. 

The secretion of urine in unilateral hydronephrosis may be completely normal 
if the other healthy kidney acts vicariously. In stricture of the urethra, and also 
in bilateral constrictions of the ureters, however, there is, of course, an obstacle 
to the passage of urine, so that the amount of urine may be abnormally small. 
There may be at times complete anuria, and even ursemic symptoms. The com- 
position of the urine depends entirely upon the forai of the primary disease. If 
the healthy kidney alone secretes, the urine passed is normal. If there be at the 
same times pyelitis or cystitis, the urine may contain pus or blood. If the urine 
can also come from the diseased kidney at one time and not at another, the urine 
also exhibits a varying composition, as we have said before (page 660). 

In many cases of hydronephrosis quite severe local symptoms are constantly 
present ; there are frequently severe pains in the tumor, which shoot chiefly toward 
the thigh. Still, these local symptoms are sometimes surprisingly slight. In re- 
gard to the symptoms on the part of other org-ans, gastric disturbances appear to 
be of the most frequent occurrence; among them are nausea, loss of appetite, 
vomiting, and eructations. In some cases the bowels are constipated, in others 
there is obstinate diarrhoea. It is a very interesting fact that, particularly in case 
of bilateral hydronephrosis, there may be developed a distinct hypertrophy of 
the left ventricle, with all its sequelae. The explanation of its occurrence, in our 
opinion, is precisely the same in this case as in chronic nephritis (vide supra, page 
602) — viz., the toxic effect of the urinary constituents retained in the blood. 

The whole course of the disease is always chronic. There are often variations 
in its course, but no general statements can be given, because the conditions vary 
in the different cases according to the form of the primary disease. Most cases 
of hydronephrosis end fatally, either in consequence of the primary disease or 
in consequence of secondary pyelonephritic or perinephritic inflammations, of 
uraemia, etc. Recovery takes place in rare cases, especially if one kidney be per- 
fectly normal, and there be no incurable primary disease. Recovery may ensue 
spontaneously from perforation or obliteration, or it may be brought about arti- 
ficially from operative procedures. 

In the diagnosis of hydronephrosis, the points especially to be considered have 
already been mentioned. The diagnosis is usually not easy, especially if the seti- 



CYSTITIS 



667 



ological factors be unknown; and the disease is often confused with other renal 
tumors and echinococci of the kidneys, with ovarian tumors, and even with splenic 
and hepatic tumors. 

Treatment. — Except for the symptomatic treatment of the pain and any ac- 
companying pyelo-cystitis, an efficient treatment of hydronephrosis can be at- 
tempted only by surgical means, the details of which are to be found in the spe- 
cial surgical treatises. 



CHAPTER V 
CYSTITIS 

( Vesical Catarrh) 

^Etiology. — In most cases of vesical catarrh the agents of inflammation reach 
the bladder from without through the urethra. The most unequivocal demonstra- 
tion in this regard is, unfortunately, often made by the physician himself, when 
he excites a cystitis by the use of am insufficiently purified and disinfected cath- 
eter or bougie. The development of the vesical catarrh is generally aided in such 
cases by the fact that there is usually a defective evacuation of urine, from 
stricture of the urethra or paralysis of the detrusor, with a consequent reten- 
tion of urine, in which the bacteria can develop undisturbed. The agents of 
inflammation may also enter from the urethra into the bladder in incontinence 
of urine. On account of the imperfect closure of the sphincter, a stagnating 
column of urine, directly connected with the contents of the bladder, forms in the 
urethra, and to this column the air and the bacteria that excite decomposition of 
the urine have direct access. In this way many cases of cystitis arise in patients 
with nervous disease who have paralysis of the bladder, and also many cases of 
cystitis arise in this way in persons who are severely ill and stupid from some 
other disease, such as typhoid fever. 

Cystitis often follows diseases of the neighboring portions of the urinary tract. 
Among these, gonorrhoeal urethritis is the most common, and this invades the 
bladder directly and leads to a gonorrhoeal cystitis. In this case, it has not yet 
been absolutely determined whether the gonococci themselves invade the bladder 
and occasion cystitis, or whether the inflammation is due to the secondary intro- 
duction and dissemination of other pyogenic cocci, such as staphylococci {vide 
infra). It is, moreover, a fact of great importance that the development of cys- 
titis is decidedly promoted by the unskilful employment of urethral injections. 
In women, the agents of inflammation may quite easily enter the bladder from the 
vagina through the short female urethra. Thus arise especially the frequent 
cases of cystitis in childbed. In some cases communication may develop between 
the bladder and certain neighboring organs, as in vesico-rectal or vesico-vaginal 
fistulse, by which again access to the bladder is opened to the agents of inflam- 
mation. 

Another group of cases is due to the presence of foreign bodies, which irritate 
the vesical mucous membrane mechanically. Among these is, first of all, the cys- 
titis which so often accompanies stone in the bladder. It must be stated, however, 
that probably these cases of vesical catarrh are not directly dependent upon the 
calculi, but are first excited by examination with catheters and sounds, and in 
brief are due to secondary infection. 

In distinction from the methods of origin of cystitis so far described, the pro- 
duction of inflammation by way of the blood-supply is much rarer. Certain 
chemical substances, already mentioned (page 654), which are eliminated by the 



668 



DISEASES OF THE UKECTAKY OKGANS 



kidneys and provoke an inflammation of the urinary tract, are the most important 
in this respect. Cantharides shows the most intense action of this sort, and it may 
cause an actual croupous cystitis. Slight irritative states of the bladder also fre- 
quently appear after taking certain foods and drinks, as after drinking new beer. 
Infectious substances only rarely come under consideration in this regard. Most 
of the cases of cystitis in severe acute infectious diseases are secondary complica- 
tions due to germs reaching the bladder through the urethra (vide supra). It 
can not be doubted that in some cases an apparently idiopathic primary cystitis 
appears after exposure to cold, but it is very rare. In such cases we usually have 
to do with acute exacerbations of an old chronic cystitis — for example, of gonor- 
rhoea! origin. 

As to the special variety of inflammatory germs in cystitis, our knowledge is 
as yet incomplete. In many cases, particularly in the cystitis of puerperal women, 
the germs are perhaps the ordinary pyogenic cocci (streptococcus and staphylo- 
coccus pyogenes). In gonorrheal cystitis the invasion of the gonococcus into 
the bladder has been absolutely demonstrated in some cases. Moreover, the bac- 
terium coli commune seems to play a great role in cystitis. The development of 
ammoniacal fermentation of the urine (vide infra) is, nevertheless, not due to 
the bacterium coli, but in most instances to special micro-organisms (formerly 
termed by Cohn " micrococcus urese "), among which the proteus deserves promi- 
nence. The staphylococcus pyogenes also has the power of exciting ammoniacal 
fermentation. 

It has been stated in the previous chapters how frequently cystitis is only one 
symptom of a more extensive disease of the urinary tract. As cystitis may invade 
the pelvis of the kidney through the ureters, so, on the other hand, any pyelitis 
of primary origin may extend downward and involve the bladder. 

Pathological Anatomy. — The pathological anatomy of cystitis presents the 
same conditions as the inflammation of any other mucous membrane. In simple 
catarrhal cystitis the mucous membrane is swollen and covered with pus, and is 
often studded with haemorrhages. In chronic cystitis the mucous membrane some- 
times takes on a granulated appearance, because of the swelling of numerous fol- 
licles, and in other cases assumes a slaty, grayish-black color, because of the pig- 
mentation resulting from numerous small haemorrhages. The severer forms of 
cystitis, such as are often observed in diseases of the spinal cord, are termed vesi- 
cal diphtheria. These cases come to a necrotic destruction of the superficial lay- 
ers of the mucous membrane, ulcerations, etc. In such severe cases submucous 
and pericystitic abscesses sometimes develop, which may perforate into the sur- 
rounding parts in various ways. The incrustation of the mucous membrane with 
urinary salts, especially with ammonio-magnesic phosphate, is also frequently 
found in chronic cystitis, and is worthy of mention. If the disease of the bladder 
is associated with a stricture of the urethra, the bladder is usually much dilated, 
and the muscular layer is hypertrophied and stands out in ridges on the inner sur- 
face of the bladder. 

Clinical Symptoms. — The local symptoms are sometimes quite severe in cys- 
titis, but in other cases they are only slight. In general, they show a greater in- 
tensity in acute cases than in chronic cystitis. The pain in the region of the 
bladder is rarely continuous; it usually occurs only on micturition, but it is 
often very distressing then, and shoots to the opening of the urethra. Since 
the inflamed vesical mucous membrane shows an increased irritability, and since 
the morbidly altered urine (vide infra) also exerts an abnormal irritation on the 
mucous membrane, there is very often an increased desire to micturate. The 
patient has to empty the bladder much oftener than normal, and in severe cases 
there is an almost constant, painful "vesical tenesmus," and at every attempt 
to micturate, only a very small amount of urine is passed, with severe burning. 



CYSTITIS 



669 



As a result of the increased irritability of the vesical mucous membrane, there 
sometimes comes on a very troublesome reflex spasm of the sphincter, by which 
the symptoms are increased. 

The character of the urine is alone decisive in the diagnosis. This is secreted 
in a perfectly normal amount and quality, in case there is no complication on the 
part of the kidneys ; but in the bladder it is mixed with the products of the dis- 
eased mucous membrane, and it is here exposed to the action of the bacteria in a 
way that will presently be described. The abnormal constituents of the urine are 
chiefly pus-corpuscles, bladder epithelium, and mucus secreted by the mucous 
membrane. As a rule, the urine of cystitis contains innumerable bacteria, under 
the influence of which develops that important chemical transformation of urea 
into carbonate of ammonia, which is characteristic of all severe cases of cystitis, 
and which has been termed the alkaline (ammoniacai) fermentation. This for- 
mation of carbonate of ammonia decidedly aggravates the inflammation. As 
Lepine and Koux have shown, we can produce a severe cystitis, and even nephritis, 
by injecting very small amounts of a pure culture of micrococcus urea? into the 
bladder of a guinea-pig. The stagnation is a factor which greatly aids the whole 
process, since the activity of the bacteria, 
as we have said, can develop much better 
than if the bladder were to a certain de- 
gree constantly purified and washed out 
by the urine; but cystitis can not be pro- 
duced by mere retention of urine. 

As soon as a part of the urea is 
changed to carbonate of ammonia, the 
urine must be less acid in reaction. 
The urine has a faintly acid or neutral 
reaction, and sometimes it is decidedly 
alkaline when passed. The latter, how- 
ever, is only rarely the case, but it is 
often simulated by the fact that the 
urine is not examined until it has stood 
for some time. Since during this time 
the alkaline fermentation makes rapid 
progress, the urine that has stood is very 
often alkaline. Many crystals of am- 

monio-magmesic phosphate and urate of ammonium then form in it ; the former 
are easily recognized by their " coffin-lid shape,'' and the latter by their " thorn- 
apple shape" (see Fig. 74). There is also a deposit of amorphous phosphates. 

If we then briefly sum up what has been said, the urine is passed in about 
the normal amount in cystitis. It usually looks pale, and has an abundant sedi- 
ment, which can often be recognized as purulent with the naked eye, and in which, 
microscopically, we can find pus-corpuscles, often bladder epithelium, and con- 
stantly innumerable bacteria — usually short rods in vigorous motion. The alka- 
line fermentation may usually be recognized by the strong ammoniacai odor, and 
also, as we have said, by the reaction of the urine. In the severe diphtheritic 
forms of cystrtis we find shreds of necrotic tissue in the urine. If there are 
haemorrhages in the bladder, the urine often contains red blood-corpuscles and 
sometimes even large blood-clots. The mucus in the urine appears in milder cases 
as a cloudy opacity — " nubecula:' The viscid masses which can be drawn out into 
threads, and which are usually abundant in the urine in severe cystitis, and some- 
times form gelatinous casts corresponding in shape to the bottom of the vessel 
containing the urine, are not mucine, but they arise from the pus-corpuscles and 
the epithelium, changed and dissolved in the alkaline urine, and hence give the 




Fig. 



4,— Crystals of triple phosphate and am- 
nionic urate. \From Fr>'KE.) 



670 



DISEASES OF THE UEIMEY ORGANS 



reactions for albumen. It goes without saying (compare page 590) that cystitic 
urine is always albuminous from its mixture with pus-serum. The presence of 
slimy threads in the urine — the so-called " clap-threads " (Ti'ipperfaden) — is 
characteristic of gonorrhoea! cystitis. 

There can be no doubt that, as already stated, the decomposing alkaline urine 
acts as a chemical irritant on the vesical mucous membrane. Hence cystitis often 
arises perhaps in this way, that the bacteria which have entered the bladder first 
excite only an alkaline fermentation, and that then the mucous membrane is 
affected by the irritation of the ammonia salts that are formed. Sometimes, how- 
ever, the mucous membrane endures this irritation for a long time, and this ex- 
plains the fact that alkaline fermentation may be observed in cases which, upon 
autopsy, present an almost normal condition of the vesical mucous membrane. 
In addition to the alkaline fermentation of the urine, it seems probable that 
many other processes of disorganization may develop in the urine, as is indicated 
by the various sorts of bad odors which the urine of severe cystitis may have. 
In a few cases there is even a formation of gas (carbonic dioxide, nitrogen, hydro- 
gen), giving rise to pneumaturia. This indicates the development of special bac- 
teria which generate gas. If the patient is also suffering from diabetes mellitus, 
the pneumaturia may be due to the fermentation of the sugar in the bladder. 

The other morbid symptoms associated with cystitis usually depend only in 
part upon the disease itself and in part upon some existing primary disease. The 
most important symptom is the fever, which is often to be referred directly to the 
cystitis. In severe cases it may be very intense, and often assumes a pysemic 
intermittent character, especially if there have arisen pericystitic suppurations or 
if the cystitis has extended to the pelvis and parenchyma of the kidney (see page 
654). An acute cystitis also may begin with a chill and high fever. If the escape 
of the purulent urine, however, is absolutely free, fever may be entirely absent in 
spite of the existence of cystitis. 

Sometimes in severe cystitis with a marked alkaline fermentation certain nerv- 
ous symptoms appear, such as headache, vertigo, stupor, and nausea. The idea has 
been advanced that in these cases we have to do with an auto-intoxication of the 
body, since ammonia and perhaps other products of decomposition, such as sulphu- 
retted hydrogen ('{), are absorbed from the bladder into the blood (ammonisemia), 
and in this way excite the symptoms of poisoning mentioned. 

According to the course of the disease we distinguish an acute and a chronic 
cystitis. The former, which may come on, for example, after catheterization, in 
gonorrhoea, etc., often terminates favorably after a few days or weeks. The 
amount of mucus and pus in the urine is never great. Chronic cystitis is observed 
especially as a complication in other diseases of the urinary tract, such as stric- 
ture, chronic diseases of the spinal cord with paralysis of the bladder, etc. It is 
very often incurable because the primary disease is incapable of improvement and 
the cause of the disease therefore persists. The longer a cystitis lasts, the greater 
is the possibility of the development of severe and dangerous complications, espe- 
cially the development of a pyelo-nephritis, and the formation of pericystitic 
suppurations. In this way cystitis, especially in chronic nervous diseases, may 
become the immediate cause of death. 

Treatment. — The dangers last mentioned must urgently impress upon us the 
prophylaxis of cystitis. Fortunately, a good deal can be done in this respect, in 
the first place, by the avoidance of all unnecessary use of bougies and catheters, 
by the greatest care for cleanliness in the use of all instruments of this sort, and 
by the timely treatment of all those conditions which may lead to cystitis. 

The treatment of cystitis is, in the milder and acute cases, hygienic and medic- 
inal, but the severer cases demand careful local treatment. 

In any severe, and especially in any acute cystitis, the greatest bodily rest (if 



CYSTITIS 



671 



possible rest in bed) is urgently desirable, since otherwise an increase of trie symp- 
toms and a prolongation of the course of the disease is the almost inevitable 
result. The diet must be mild and unirritating. Spiced food and alcoholic drinks 
are to be avoided, but we should recommend an abundant supply of fluid, by 
which the urine is diluted and the bladder washed out. We have the patient 
drink plenty of ordinary water, tea (made from uva ursi, etc.), or a suitable min- 
eral-water, like Wildunger or Fachinger. A diet mainly of milk is very good; 
under it, improvement is often surprisingly rapid. 

Among internal remedies those are to be considered which are eliminated with 
the urine, and are thus able to act on the diseased mucous membrane, or directly 
upon the agents of inflammation and the ammoniacal fermentation. One of the 
most efficient drugs, which never does harm if proper caution is exercised, is chlo- 
rate of potassium, of whose favorable influence on vesical catarrh we have often 
convinced ourselves. It is prescribed in an aqueous solution, forty to seventy-five 
grains a day (grammes 3-5), and it should never be taken on an empty stomach. 
Far less efficient than chlorate of potash are the true astringents, such as tannin 
and uva ursi, which were formerly much employed. The latter drug is said by 
Lewin to contain a glucoside, arbutine, which is itself recommended in doses of 
forty-five to sixty grains a day (grammes 3-4), but its efficacy is doubtful. Of 
metallic astringents, acetate of lead in powders of half a grain to a grain and a 
half (gramme 0.03-0.1), repeated several times a day, is at present seldom em- 
ployed. In cases with a decided purulent secretion, if the initial symptoms of 
irritation have abated, we may often prescribe with good results resinous drugs, 
of which the best are oil of turpentine, in capsules or in milk, or balsam of copaiba. 
If, on the other hand, the ammoniacal fermentation is more prominent, salicylic 
acid in daily doses of thirty to sixty grains or more (grammes 2-4) in capsules, 
and salol, in powders of eight grains (gramme 0.5), repeated several times a day, 
are specially to be recommended; naphthaline, a grain and a half to five grains 
(gramme 0.1-0.3), repeated several times a day, has also been recommended, but 
it may produce decidedly disagreeable symptoms. [In the same class with the 
remedies just named, but far superior to them, is urotropine, which may be given 
in doses of ten to fifteen grains in water, after meals. — V,] 

If there are severe local symptoms, we prescribe warm compresses and poul- 
tices to the region of the bladder. In robust persons with acute cystitis, local 
blood-letting (three to six leeches to the perineum) sometimes has a decidedly 
favorable symptomatic action in such a case. In other respects narcotics, espe- 
cially subcutaneous injections of morphine, are the best remedy when there is 
severe pain and tenesmus. Camphor, extract of belladonna, etc., are much more 
uncertain in their action. The frequent use of protracted warm baths may, how- 
ever, be greatly recommended. 

In chronic cystitis all the remedies previously mentioned are also to be con- 
sidered ; but they are usually not sufficient alone, and at any rate they are far less 
effective than a methodical local treatment. This consists in a regular daily 
washing of the bladder by means of an elastic catheter. A rather long rubber 
tube is attached to the catheter at one end, and to a funnel at the other, and by 
raising or lowering this funnel the bladder can be filled or emptied. We allow a 
moderate amount, say three to seven ounces (100 to 200 cubic centimetres), 
of the warm fluid to run into the bladder and escape, repeating the process 
until the wash-water is clean. For this, perhaps we employ either a simple 
one-half to one-per-cent. solution of common salt, or preferably a warm and weak 
solution of acetate of lead, 1 to 1,000; permanganate of potash, 1 to 1,000; or a 
combination of boracic and salicylic acids. By treatment of this sort many cases 
of chronic vesical catarrh may be cured, while the most obstinate may, at any rate, 
be kept within bounds. In rebellious cases of purulent cystitis it is advantageous 



672 



DISEASES OF THE URIXARY ORGANS 



to employ lunar caustic. The bladder is rinsed out, and then about five ounces 
(grammes 150) of a weak solution of nitrate of silver, at first 1 to 3,000, later as 
strong- as 1 to 1,000 or 1 to 500, are injected through a catheter. The solution is 
allowed to remain two or three minutes in the bladder and then withdrawn. What 
is called the Janet method of irrigating the bladder is also very useful. The 
fluid is placed in a fountain syringe, and made to enter the bladder from the 
urethra, by raising the reservoir high enough to give a pressure which overcomes 
the sphincter of the bladder. The advantage of this method lies in the coincident 
dilatation and lavage of the posterior portion of the urethra. 

It is very important, in treating chronic catarrh of the bladder, to consider 
the possible cause of the condition — for instance, stricture, or vesical calculi, or 
paralysis of the bladder. 

In pericystitis suppuration surgical treatment is only rarely possible. We 
must, therefore, confine ourselves to purely symptomatic procedures. 



CHAPTER VI 
NEW GROWTHS IN THE BLADDER 

1. Cancer of the Bladder. — Primary carcinoma of the bladder is rare. It 
forms localized tumors, sometimes with a pedicle ; or it extends diffusely over the 
wall of the bladder, and in that case leads to such thickening that the bladder can 
sometimes be felt through the abdominal walls as a firm tumor. Secondary car- 
cinoma of the bladder is not infrequently due to direct involvement by extension 
from neighboring parts, such as the uterus, prostate, or rectum. 

The. early symptoms of primary cancer of the bladder consist of disturbances 
of micturition, which are often difficult to explain. Usually the first indication 
of the special local disease consists of a change in the character of the urine, which 
is probably coincident with the beginning of ulceration in the tumor. Then the 
complete picture of severe chronic cystitis is rapidly developed, a particularly 
characteristic symptom being the frequent, though irregular, appearance of blood 
in the urine. The condition becomes most distressing if the vesical termination 
of the urethra is occluded by the new growth. In the cases which we have seen, 
cancerous cachexia did not develop until rather late. One case was in the person 
of a quite young man. In general, the entire course of the disease seldom occu- 
pies more than one or two years. 

The diagnosis of vesical cancer is not always easy, particularly at first. The 
main point is, that when there is a chronic disease of the bladder and no other 
sufficient reason for it is discovered, we should think of the possibility of tuber- 
culosis or cancer, and make a careful examination with these severe conditions in 
mind. It is sometimes possible to confirm the diagnosis by finding bits of the 
tumor in the urine, but this is not invariably possible ; consequently a number of 
methods have been elaborated to facilitate early recognition of vesical tumors by 
means of a direct and careful examination of the bladder — thus we have : cystos- 
copy (Nitze) ; exploratory cystotomy ; and in women dilatation of the urethra 
and digital examination of the bladder. Particulars with regard to these pro- 
cedures and their value are to be found in monographs, and in them the reader 
can also inform himself as to the results of the attempts which have thus far been 
made to remove vesical tumors by operation. 

2. Papilloma of the bladder is usually a very soft fibroma, which is located in 
the trigonum or fundus and has delicate waving papilla?, which are covered with 



EXUEESIS XOCTUEXA 



673 



several layers of cylindrical epithelium. The local discomfort which this not 
very rare form of tumor occasions is often slight, but the haemorrhage it causes 
may be very important, being chronic and obstinate; for months and years the 
iiaeniaturia may be more or less continuous. The clotted blood as it passes through 
the urethra often assumes the shape of a worm. There is not much disturbance of 
micturition unless portions of the tumor obstruct the inner end of the urethra. 
Any one who has had the experience which we have had of seeing an otherwise 
healthy and vigorous man die because of persistent haemorrhage from a papilloma 
hardly as big as a walnut, can not insist enough upon the value of an early and 
certain diagnosis (reached by examining portions of the tumor, or, still better, by 
■cystoscopy) and of surgical treatment. 



CHAPTEE VII 

ENURESIS NOCTURNA 

{Nocturnal Incontinence of Urine) 

Enuresis nocturna is a nervous affection of the bladder by no means rare in 
children of both sexes, and therefore quite important in its practical relations. 
Of course, in small children there is no sharp boundary to be drawn between 
normal and pathological conditions ; but it is decidedly pathological if larger chil- 
dren, from four to ten years of age and even older, pass their urine in bed more 
or less frequently during sleep, in spite of well-developed reasoning powers and 
professedly the best intentions. This may extend to the years of puberty and even 
beyond, and then it frequently produces a very depressing mental influence upon 
the patient. Special causes for it are not to be discovered in most cases. We are 
compelled to assume either an abnormal weakness of the sphincter, which is prob- 
ably sometimes congenital, or an abnormal irritability of the detrusor. Some- 
times, but not invariably, the child has a neurotic constitution. At any rate, in 
wetting the bed at night the process of micturition comes on in a purely reflex 
way, but it is often accompanied by certain ideas in dreams referable to micturi- 
tion. It does not hold in all cases that the sleep is especially deep. Many patients, 
of course, do not notice the mishap till morning, but others almost always wake 
directly after. The involuntary micturition usually occurs in the first hours after 
going to sleep, but sometimes it is later, and even toward morning. By day mic- 
turition is often perfectly normal ; but in many cases there is even then a notice- 
able weakness of the bladder, so that the child has to make water oftener than 
usual, and sometimes even wets its clothes. 

Although, as we have said, we can usually find no special cause for the trouble, 
still, in some cases, certain morbid changes in the urinary organs may give rise to 
the incontinence. We should, therefore, in every case at least think of the pos- 
sibility of stone in the bladder, of congenital phimosis and adhesions of the pre- 
puce to the glans penis, of ascarides, of inflammatory conditions, and foreign 
hodies in the vagina, and make a special examination into these points. We must 
also bear in mind polyuria caused by diabetes or renal disease, and finally, of 
course, in the diagnosis of a purely nervous nocturnal incontinence of urine, we 
must exclude the existence of any actual anatomical spinal affection. 

In all the cases just mentioned, the treatment must be directed first to the 
primary disease ; but in the ordinary nocturnal incontinence the treatment must 
be aimed at the symptom of nocturnal micturition as far as possible. The child 
must take only a very little fluid in the evening, and he should be made to empty 
43 



674 



DISEASES OE THE URIXAKY ORGANS 



his bladder immediately before going to sleep, and perhaps once again later. He 
should not be covered up too warmly, and, if possible, he should not lie on his back 
during sleep. Tying a brush to the back is therefore a well-known domestic rem- 
edy. It is strongly recommended that the child should be made to lie in bed, with 
the hips elevated and the head low. A somewhat strict mental treatment is often 
effective, since thus the attention to the process is increased, although uncon- 
sciously, and the child often learns to wake up at the right time. We have seen 
many cases of enuresis, which did not recover when treated at home, get well 
quite rapidly when the children were isolated in the hospital. The employment 
of the rod is rarely allowable; on the other hand, we often must shield the child 
from injudicious parents. 

Internal remedies, such as belladonna and tincture of nux vomica, were for- 
merly recommended, but they seldom do good. Lately the tincture of rhus aro- 
matica has been employed again ; of this, fifteen drops are given in the afternoon 
and in the evening before going to bed. In anaemic children preparations of iron 
are indicated. It is often useful to employ electricity, although it may be that the 
only influence it has is psychical. We put the broad anode over the lumbar cord, 
and the smaller kathode over the region of the bladder or on the perineum, and 
let quite a strong constant current pass through for two or three minutes. The 
current may also be interrupted and closed a few times. Then we pass the wire 
end of one conducting cord, which we make the kathode, into the mouth of the 
urethra for one or two centimetres, while we place the other broad electrode on the 
perineum or above the symphysis, and let quite a strong and somewhat painful 
faradic current act for one or two minues (Seeligmiiller). The sittings must at 
first be repeated daily. It is also a very good plan to let the whole body be well 
rubbed with cold water before going to sleep. It is said that in obstinate cases 
the introduction of large bougies and the consequent distention of the posterior- 
portion of the urethra are often attended with rapid improvement. 

Even in cases in which, despite careful treatment, no permanent success is 
attained, we have this consolation with regard to the prognosis, that in simple 
enuresis the abnormal condition usually undergoes gradual and spontaneous im- 
provement as the patient grows older. 

[Belladonna, strychnia, or nux vomica, or a combination of the two, are often 
of unquestionable service. If the enuresis is only nocturnal, belladonna alone 
may be used, either in a single dose at bedtime or three times a day. If the 
enuresis is diurnal also, the two drugs should be combined and given three or four 
times a day.] 



DISEASES OF THE ORGANS OF LOCOMOTION 



CHAPTER I 
ACUTE ARTICULAR RHEUMATISM 

^Etiology. — Acute articular rheumatism is an infectious disease. This is 
shown by all its clinical and anatomical characteristics, and although we are not 
yet definitely acquainted with the specific organized poison which gives rise to it 
(vide infra), still, it is impossible to come to a correct understanding of the symp- 
toms and the course of the disease, unless we assume that it is caused by an infec- 
tious germ. 

Like many other infectious diseases, acute articular rheumatism is often indis- 
putably endemic and epidemic. According to Hirsch, the disease is most preva- 
lent in the temperate zones, being much rarer in cold and tropical latitudes ; but 
even in Europe it is by no means uniform in its frequency, and certain districts of 
England, Belgium, and Russia are said to be almost exempt from it. It is also 
possible to observe epidemic influences with regard to the frequency of its appear- 
ance, as already intimated. In Leipsic, where articular rheumatism is one of 
the most frequent of acute diseases, we observed for years that at certain times 
there were only a few cases, while at others there was a striking increase in 
their number. Usually attacks are most prevalent in the winter and spring 
months, but again it is sometimes in summer that the disease is especially 
common. 

Among the exciting causes of the disease, taking cold is always mentioned as 
of first importance ; and in fact it can not be denied that the influence of cold does 
often seem to contribute to the occurrence of the disease. This result, however, 
seldom follows a single severe exposure, but it much more frequently follows long- 
continued " rheumatogenous influences," as we may call them, and in particular 
the long-continued influence of wet and cold, certain occupations — for example, 
washing and scrubbing — inhabiting unhealthy damp dwellings, and the like. 
This explains why those who follow certain callings are especially subject to 
articular rheumatism ; thus servant-girls and coachmen are frequently victims to 
the disease. And yet it is possible to regard all these injurious influences as being 
merely indirect causes, assuming that they favor the development or action of the 
specific micro-organisms ; and, furthermore, it is by no means exceptional to see 
a case of articular rheumatism in which no history of exposure to cold can be 
obtained. 

Sex exerts no special influence upon the frequency of the disease. As to age, 
acute articular rheumatism is most frequent in young adults between fifteen and 
thirty-five years old. In later life, and particularly in old age, it is much rarer. 
In children six years old or more the disease is not especially infrequent, but in 

675 



676 



DISEASES OF THE OKGANS OF LOCOMOTION 



younger children it occurs only exceptionally. We may be permitted to mention 
a single interesting case which we met with in Leipsic, where a child who died 
when only a few days old, and whose mother at the time of its birth was suffering 
from a severe attack of acute articular rheumatism, was found to have multiple 
purulent arthritis. 

Of precisely what variety the special germ of acute rheumatism may be we do 
not yet know. Still, many recent investigations (Sahli and others) seem to prove 
that, at least in many cases, the chief role is played by the staphylococcus pyo- 
genes. If this claim is confirmed it will deprive acute articular rheumatism of the 
most part of its specific character, from an setiological point of view. In that 
case, we would have to regard it merely as a special clinical form of staphylococcus 
infection, and place it among the mild varieties of septic infection. Indeed, upon 
more careful consideration, this conception of articular rheumatism seems very 
probable. It is well known that in all varieties of constitutional sepsis the joints 
are particularly apt to be involved. It has also been shown by numerous observa- 
tions that staphylococci are most frequently found to be the infectious germs in 
cases of acute benign endocarditis, consequently we should expect that a constitu- 
tional infection with the staphylococcus would, as a rule, display itself by fever 
and multiple serous arthritis. Very often there are at the same time other local 
disturbances. These are the so-called " complications " of articular rheumatism, 
which, however, would be more correctly termed special localizations of the infec- 
tious germs (vide supra, endocarditis, pericarditis, pleurisy, etc.). Not infre- 
quently these localizations in the other serous membranes may appear previous to 
the swelling of the joints, or even without any articular swelling*, and yet they 
may be, in an aetiological point of view, precisely analogous to articular rheuma- 
tism. If, however, we are not yet inclined to accept the designation of acute 
articular rheumatism as a mild septic infection, then it would seem advisable to 
speak of all the forms of disease which belong in this class and which are closely 
related to one another, as due to a " rheumatic infection," employing the word 
rheumatic with a special idea of aetiology. 

If we conceive of articular rheumatism in the way just indicated as a clinically 
well-characterized constitutional infection — perhaps with staphylococci — the next 
question is the place of infection, and its gate of entrance. It seems probable 
that the place is not the same in every case. Very often it is impossible to deter- 
mine the path by which infection entered; yet we may sometimes ascertain by 
careful questioning that the arthritis was preceded by a mild sore throat, or a 
laryngitis, or an intestinal disturbance. Indeed, we often find even small abra- 
sions of the skin and similar lesions. It is probable that such statements of the 
patient and discoveries of the physician indicate the starting-point of the infec- 
tion in the individual case. 

Now that we have become clear as to the mode of development of articular 
rheumatism, we have gained also a satisfactory conception of the so-called second- 
ary rheumatism which occurs subsequently to scarlet fever, meningitis, and other 
acute diseases. It is probable that in most instances these are due to secondary 
infection with the staphylococcus, although, of course, it can not be denied a priori 
that other varieties of germs may produce inflammation of the joints — e. g., multi- 
ple purulent arthritis is probably due in most cases to streptococci. Very fre- 
quently, however, the primary disease itself is occasioned by staphylococci. This 
is the case in many instances of chronic valvular disease. If a " secondary " acute 
articular rheumatism occurs in such diseases, as it often does, the process is to be 
regarded merely as a fresh acute infection, starting from the old focus. 

A very noteworthy fact is that acute articular rheumatism can not be num- 
bered among those infectious diseases which usually occur but once in the same 
individual. On the contrary, the disease has the same peculiarity as pneumonia 



ACUTE AETICULAE EHEUMATISM 



077 



and erysipelas, of appearing with noticeable frequency, several times in the same 
individual, so that when a person has once had articular rheumatism, even though 
it has left no sequelae behind it, he seems to be more liable than before to the 
disease. It is not exceptional to meet persons who have had five or more attacks 
of acute articular rheumatism. 

Symptomatology. — The chief symptom of acute articular rheumatism is an 
acute febrile synovitis, which almost always affects several joints. The synovitis 
is associated with the usual local phenomena of swelling and tenderness in the 
parts affected. Often this articular affection is the first symptom, and, indeed, it 
may be the only symptom of the disease. It is, however, by no means exceptional 
for the arthritic trouble to be preceded by certain prodromal or initiatory symp- 
toms, as is true of other infectious diseases. These prodromata consist either of a 
slight general malaise, or of certain local symptoms. It is not rare, as already 
mentioned, to have sore throat, or,, as we have repeatedly had opportunity to ob- 
serve, laryngitis. Still, the precursors are usually mild ; and they may, as we 
have said, fail to appear at all, or at any rate they may easily escape notice. In 
some few cases the only symptoms at first are febrile; there may be no other 
marked constitutional symptoms, or there may be a typhoidal condition with en- 
larged spleen, and diarrhoea. Then, some days later, the characteristic swelling 
of the joints appears (Wagner). Taken in connection with the view of the nature 
of articular rheumatism which we have elaborated above, this behavior has noth- 
ing inexplicable about it — merely, the constitutional symptoms develop some little 
time before the local manifestations of the disease. 

The articular disturbance is almost always very rapid in its development. 
Some of the larger joints are usually first affected, and perhaps those of the lower 
extremities somewhat oftener than those of the upper. It is extremely exceptional 
for all the joints that are affected to be attacked at one and the same time. It is 
somewhat characteristic of acute articular rheumatism that it " jumps from one 
joint to another." To-day this joint will be affected and to-morrow that, while the 
joint first attacked may still remain diseased or undergo rapid recovery. Thus, 
there may be either a few joints affected or many, in varying sequence, and they 
may sometimes be affected rapidly and at other times more slowly. In many 
of the milder cases the disease is an extremely temporary one, while in others it 
may attach itself most persistently to some one or more joints. 

There is usually fever in addition to the arthritis; but it is not usually very 
high, seldom exceeding 103° (39.5° C). The fever, on the whole, corresponds with 
the arthritic phenomena, and does not present an especially typical curve, but 
one which is irregularly remittent. We have scarcely ever seen the disease begin 
with an initial rigor; and the so-called " general febrile symptoms " of headache, 
stupor, and subjective feeling of heat are as a rule ill marked in acute rheuma- 
tism. This indicates that the constitutional infection does not, owing to the 
peculiar nature of rheumatic infection, attain great severity. The skin is notice- 
ably inclined to perspiration, but the perspiration is not at all a result of any 
sudden fall in temperature such as is seen in other diseases. 

The course of the disease is marked by alternate ameliorations and aggrava- 
tions of the local symptoms and of the fever, and lasts, particularly if it is not 
treated, one or more weeks, or a still longer period. Often the entire course of 
the disease under such circumstances is made up of separate " attacks " (vide 
infra), there being repeated improvement followed by articular swelling and fever. 
At last, however, the symptoms entirely disappear, and the patient enters upon a 
tedious but complete convalescence. 

In contrast with this simple course the clinical picture may be, in other cases, 
much more complex, for the peculiar infectious character of articular rheuma- 
tism renders possible many complications and peculiarities. The protean char- 



678 DISEASES OE THE OKGANS OF LOCOMOTION 



acter of the disease will be evident upon a perusal of the following description of 
the symptoms referable to the different organs of the body. 

Symptoms referable to the Different Organs, and Peculiarities in the Course 
of the Disease. — 1. Joints and Sheaths of the Tendons. — The favorable termina- 
tion of most cases of acute articular rheumatism prevents us from often examin- 
ing the anatomical changes in the affected joints; but there can be no doubt that 
in most instances the trouble is merely a simple serous synovitis — that is, an in- 
flammation of the synovial membrane, with an exudation into the cavity of the 
joint, composed mainly of serum with but little admixture of fibrine and pus. The 
synovial membrane itself, in the cases which do come to autopsy, is usually very 
little affected. It is somewhat injected, opaque, and thickened. Necrosis of the 
cartilages is seen only in severe cases, or in those which have lasted a rather long 
time. From a clinical standpoint, the articular disturbance is noticeable chiefly 
for the pain which it causes the patient upon every movement of the joint and 
any pressure upon it. The tenderness is often in striking contrast with the 
slight objective signs of inflammation, for a joint which is extremely sensitive 
may appear to be scarcely at all diseased. Usually, however, the joints exhibit 
the signs of synovitis. The effusion into the joint produces an evident swelling, 
which can be seen particularly well in the knees, but also in the joints of the 
ankle, wrist, shoulder, and elbow, and sometimes even in the smaller joints of the 
fingers and toes, particularly the great toe. It is rather exceptional to detect swell- 
ing of the hip- joint. It should be remembered, however, that the swelling in the 
region of the joint, particularly the ankle or wrist, is often less the result of a 
synovial effusion than of an inflammatory periarticular oedema. This oedema, 
for example, may extend over almost the whole posterior surface of the hand. 
The joints are by no means invariably the only parts attacked. Not infrequently 
there are analogous inflammatory changes visible in the sheaths of the tendons, 
the bursas, and perhaps, in many cases, even the fascise and muscles. The skin 
over the affected joints often has an inflammatory blush, which is usually pale- 
red and spotted, and can be best seen at the ankle, knee, and wrist. It has been 
maintained that the cutaneous sensibility is diminished over the joints affected, 
but we regard this as a mistake. 

As might be expected, the number of joints attacked and the sequence in which 
they are attacked differ greatly in different cases ; but almost invariably a number 
of joints suffer, so that any monarticular arthritis should not be regarded as rheu- 
matic except after careful deliberation (vide infra, diagnosis). It should be said 
that, in mild cases, there may be only two or three joints affected, these being 
usually some of the larger joints of the extremities ; and of these, one may be so 
much worse than the others that their participation in the trouble can be ascer- 
tained only by careful questioning and examination. In severe cases, on the other 
hand, the number of joints attacked is often very great. Such patients become 
extremely helpless, because any movement is possible, if at all, only under the 
penalty of very severe suffering. The patient usually lies with bended knees and 
feet curved so as to be concave on the plantar surface, and screams with pain at 
any attempt to change his position. The joints of the trunk sometimes participate 
in the disease, but hardly ever except in the severe cases ; the articulations of the 
vertebras, the sternoclavicular joint, the articulation of the lower jaw, and the 
symphysis pubis, are then particularly apt to be affected. 

The fugitive character of the arthritis has been spoken of as characteristic of 
acute articular rheumatism, and, indeed, it is not infrequently the case that com- 
paratively large swellings of the joints soon abate and yield to new disturbances in 
other joints ; but, on the other hand, the disease may persist very obstinately in 
a single joint. In this case one joint or rarely several joints are attacked with 
marked severity, either from the start or subsequently to milder affections of 



ACUTE ARTICULAR RHEUMATISM 



679 



other joints, and often remain for weeks swollen or painful, long after all other 
symptoms have vanished. 

2. Cardiac Symptoms. — The condition of the heart in acute articular rheuma- 
tism is next in importance to that of the joints. The physician should therefore, 
in every case, even the mildest, maintain a continuous watch over this organ. In 
1836 Bouillaud made careful auscultatory investigations in this disease, and was 
thus the first to discover that the course of acute articular rheumatism is, with 
noticeable frequency, accompanied by endocarditis, and sometimes even by peri- 
carditis. Complications of this sort may occur in any case, whether mild or severe, 
or may be absent in any case, even the worst. They may develop at the beginning 
or later on in the course of the disease. Their development is often unattended 
by any subjective symptoms, so that they can be recognized only by careful phys- 
ical examination. In many cases, however, the onset of cardiac disease is marked 
by a fresh exacerbation of the fever, or possibly by palpitation, or by painful sen- 
sations in the prsecordia, or by dyspnoea. 

We will consider first rheumatic endocarditis. This is almost always the be- 
nign verrucous variety (see page 306). It is far more prone to attack the mitral 
than the aortic valve, and is accordingly usually betrayed by a blowing systolic 
murmur at the heart's apex. Uncertainty may be cast upon the diagnosis by the 
fact that functional murmurs are not very infrequent at the apex or at the base 
of the heart in cases of acute articular rheumatism. We once observed a case of 
u hyperpyretic rheumatism " (vide infra) in which there was an evident murmur 
of this sort during life, and yet at the autopsy we were able to assure ourselves 
of the normal condition of the cardiac valves. Even an expert may for a time be 
in doubt as to the significance of many cardiac murmurs, and this explains in part 
the conflicting statements as to the frequency of cardiac complications in acute 
rheumatism. In general, one may say that such complications occur in twenty- 
five to thirty-three per cent, of the cases. The ultimate results of this endocar- 
ditis we do not need to describe over again in this connection (see the chapters on 
acute and chronic endocarditis). Complete recovery is possible. Often, however, 
the lesion gives rise to a chronic endocarditis — that is, to a cardiac valvular dis- 
ease, which lasts through life. 

The close connection between endocarditis and the arthritis must formerly 
have seemed very puzzling, despite the many hypotheses made to explain it. Our 
present conception of articular rheumatism as a septic (staphylococcus) infec- 
tion renders the frequent development of endocarditis easily explicable. It is 
due to a settlement of the germs, which are circulating in the blood, upon the 
cardiac valves (see page 304). As a matter of fact, staphylococci are almost 
invariably found in the inflammatory deposits of " rheumatic " endocarditis. 
The endocarditis, therefore, is not strictly a " complication," but a symptom of 
the disease. 

Rheumatic pericarditis is not infrequent, although less common than endocar- 
ditis. The only certain way to recognize it is by a characteristic friction-sound ; 
and even when this is heard there may be a doubt as to its significance, inasmuch 
as functional murmurs are not infrequently heard at the base of the heart. The 
pericarditis is of a sero-fibrinous nature. Sometimes it is of slight severity; but it 
may be extremely severe, with a large effusion and the most urgent dyspnoea 
(see page 359). In rare instances this pericarditis proves fatal. Usually, however, 
recovery ensues, although in severe cases there may be obliteration of the peri- 
cardial sac, with the consequences described on page 364. 

As to the way in which pericarditis develops, it is probable that in most cases 
there is a direct infection of the pericardium from the blood. In some cases, how- 
ever, we are inclined to assume that the infection of the pericardium comes from 
the endocardium, and probably in most instances from the aortic valves (see 



680 DISEASES OE THE ORGANS OF LOCOMOTION 



page 359). We have repeatedly found a distinct aortic insufficiency to have been 
left behind after rheumatic pericarditis, the heart having previously been healthy. 

We should also mention that there may be functional cardiac derangement 
without any grave anatomical lesion. We have already spoken of the functional 
murmurs. There may also be a rapid and irregular pulse, and, in rare instances,, 
attacks of angina pectoris of apparently purely nervous origin. 

3. Serous and Mucous Membranes. — We have not only pericarditis in associa- 
tion with articular rheumatism, but also pleurisy and peritonitis, so that we may 
say that in acute articular rheumatism the incidence of the disease is mainly upon 
all serous membranes, inclusive of the joints. It should be said that rheumatic 
pleurisy, and particularly rheumatic peritonitis, are much less frequent than endo- 
carditis and pericarditis, but we have repeatedly seen in severe cases rheumatic 
pleurisy, with serous effusion, on one or even on both sides. In such severe attacks- 
it is not exceptional to find several serous cavities simultaneously involved — for 
instance, the pericardium and pleura ; so that in such instances the inflammation 
may have extended directly from the pericardium to the pleura, or vice versa? 
although direct infection of the pleura by the blood is perfectly possible. Rheu- 
matic peritonitis, indicated by distention of the abdomen with a moderate exuda- 
tion and by tenderness, has been absolutely diagnosticated in a few cases. Here, 
also, the inflammation may appear independently, or may be due to extension 
from the pleura through the diaphragm. 

The mucous membranes are seldom greatly affected in acute articular rheuma- 
tism. As we have already mentioned, in the beginning of the disease there may 
be catarrhal affections of the pharynx, larynx, stomach, or intestines; which 
lesions probably facilitate the " rheumatic " infection. Bronchitis is spoken of by 
the older authors as frequent, but it is probably in many cases not due directly 
to the rheumatism, but is a complication, just as in any disease attended by great 
prostration. 

4. Skin. — Cutaneous phenomena are not infrequent in the course of acute- 
articular rheumatism. A prominent symptom of the disease is the tendency to 
profuse perspiration. The perspiration often has a strongly acid odor and reac- 
tion. Many patients exhibit an abundant crop of sudamina, the back in particu- 
lar being sometimes entirely covered. Sometimes there are other cutaneous 
eruptions. In a whole series of cases we observed erythema nodosum. This af- 
fected the lower extremities more than the upper. Urticaria is not very infre- 
quent, while herpes labialis has been very rare in our experience. It is well 
known that arthritic affections and the so-called " hgemorrhagic diseases " are in 
many ways related to each other; and it is therefore an interesting fact that 
extensive hemorrhagic disturbance of the skin also occurs in connection with 
acute articular rheumatism, as we have repeatedly had opportunity to observe. 
We have seen several cases of hemorrhagic urticaria : wheals appear upon the 
skin, and a hemorrhage takes place into their centers and spreads gradually. 
There may also be simple cutaneous ecchymoses. These may in severe cases be 
merely one symptom of a general hemorrhagic diathesis, with hemorrhages 
from mucous membranes. The occurrence of all these symptoms shows clearly 
that no sharp dividing line can well be drawn between the various disorders. 

5. The Muscles and Nervous System. — The condition of the muscles is very 
important in many cases of acute polyarthritis. They are often quite painful on 
pressure, and apparently somewhat swollen about a joint that has been long af- 
fected. The muscular atrophies and muscular paralyses that often remain after 
the arthritis has disappeared are especially important. 

According to a general law, there are certain definite trophic relations between 
a joint and the muscles belonging to it, whereby almost every severe and persistent 
disease of the joint is necessarily followed by an atrophy of the affected muscles. 



ACUTE ARTICULAR RHEUMATISM 



681 



The extensors of the joint are often most affected by this atrophy. This atrophy 
has long- been recognized, and it was formerly regarded, particularly by surgeons,, 
as merely the result of inactivity of the muscles — "atrophy from disuse"; but this 
view is certainly erroneous. We do not know its precise cause, but it is without 
doubt the result of the disease of the joint, and may therefore be termed " muscu- 
lar atrophy of arthritic origin." If an attack of acute articular rheumatism 
affects any one joint for a long* period there is a secondary atrophy of the corre- 
sponding- muscles. This is seen most often, and in its most typical form, when 
there is obstinate trouble in the shoulder-joint, the deltoid becoming extremely 
atrophied. This atrophy of the muscles may contribute largely to the sum-total 
of functional derangement. We have repeatedly seen cases where the patient, 
could hardly lift his arm at all, although the inflammation of the shoulder-joint 
had passed away, and that without leaving any anchylosis. It is therefore en- 
tirely justifiable to speak of a rheumatic paralysis. We have seen similar muscu- 
lar paralyses after acute articular rheumatism in the rest of the muscles of the 
upper arm, also in the quadriceps extensor, and once in the serratus magnus. The 
explanation given by Charcot, that the cause of the atrophy is a " reflex " implica- 
tion of the trophic centers in the cord due to the disturbance in the joint, seems to 
us hardly satisfactory. There are probably local disturbances of nutrition, and 
sometimes apparently a direct extension of the inflammatory process from the 
joint to the neighboring muscles. It is noteworthy that the atrophied muscles, 
respond promptly to the f aradic current, and never exhibit the reaction of degen- 
eration. 

Chorea (vide infra, page 1152) may be a sequel of acute articular rheumatism,, 
and it is one of the nervous symptoms which may arise in connection with it. 
This complication is seen most frequently in children. Endocarditis may accom- 
pany it, but it does not always do so. 

There are certain peculiar cases of acute articular rheumatism which excite the 
greatest interest. In these, very severe cerebral symptoms are developed, often 
most acutely. They are therefore called " cerebral rheumatism " ; or, as they are 
almost always characterized by an extraordinarily high temperature, another 
name is " hyperpyretic articular rheumatism." In these cases the disease may 
exhibit severe nervous symptoms from the start, particularly delirium ; or it may 
at first run an apparently favorable course, and not change for the worse until 
after several days, or even at a later period. The change may be quite abrupt. 
The temperature rises to 104° or 106° (40°-41° C). There are great uneasiness,, 
delirium, and sometimes also signs of motor irritation, such as general convul- 
sions, or tonic spasm of the extremities, or trismus. The face grows pale and 
cyanotic, the pulse small and extremely rapid. With slight interruptions, the 
temperature continues to rise, and attains 107.5° to 109.5° (42°-43° C). This 
great rise is most apt to occur just before death, and there may be a still further 
increase of temperature after death occurs. As has -'been implied, the termi- 
nation is usually unfavorable. It is only in exceptional cases that recovery takes- 
place. 

It has been stated that cerebral rheumatism attacks mainly hard drinkers and 
other individuals whose nervous system has been previously impaired; but our 
own experience does not confirm this view. ~No case is absolutely secure from the 
occurrence of hyperpyrexia ; but it is a very rare phenomenon, occurring perhaps 
once in several hundred cases. On post-mortem examination, the brain seldom 
shows any change in these cases of cerebral rheumatism. We are therefore 
obliged to regard the condition as the result of an unusually severe infection,, 
affecting chiefly the intellectual, motor, and thermal centers. 

Cases have also been reported which presented actual anatomical lesions of the 
brain — in particular, purulent meningitis. Probably, however, most of these cases 



682 



DISEASES OF THE OKGANS OF LOCOMOTION 



were falsely diagnosticated, the observer having confounded articular rheumatism 
with epidemic meningitis, pysemia, and similar diseases. Of course, if there be 
endocarditis, cerebral embolism is possible. 

Mental derangements deserve a brief mention. They rarely occur during the 
course of the disease, but are somewhat more frequent after it has terminated. 
We may have either melancholia attended with marked excitement or anxiety, 
or a more general insanity. The prognosis is usually favorable. 

6. Other Viscera. — Other parts of the body than the heart, the serous mem- 
branes, and the brain, are seldom much affected in articular rheumatism. Lobar 
pneumonia occurs only in especially severe cases, but in such it may attain quite a 
considerable development and occasion great dyspnoea. It usually requires quite 
a long while to recover from it. Whether we actually have to do in these cases 
with a specific pneumonia, or with an ordinary lobar pneumonia as a complication, 
has not yet been determined. It is also possible for lobular, deglutition pneumonia 
to develop in severe articular rheumatism. Acute nephritis has been demonstrated 
in some instances, but this is very rare. The spleen, as already mentioned, may 
be somewhat swollen; but as a rule we do not find the distinct splenic tumor 
which is present in other acute infectious diseases. 

7. General Symptoms. — In many cases the general condition of the patient is 
but little affected, but in others the disease seems to exert a peculiar influence 
upon the constitution. This may show itself in a striking anaemia; and we 
have observed this repeatedly where there was no cardiac complication. Ordi- 
narily, there is a slight leucocytosis. A dangerous but extremely rare compli- 
cation has already been briefly referred to, namely, the occurrence of a general 
hemorrhagic diathesis. This is almost always associated with high fever and 
great prostration, and is usually fatal. In all such cases there is probably pro- 
found sepsis. 

Course, Duration, and Prognosis. — Acute articular rheumatism may be de- 
scribed as generally a benign disease, for it usually terminates in recovery. It is 
only in very few cases that an unfavorable termination takes place immediately, 
whether as the result of pericarditis or other severe cardiac complication, or from 
hyperpyrexia, or the development of a general hemorrhagic diathesis. 

The entire duration of the disease varies greatly according to its severity. 
There are mild cases, which terminate in a few days ; and, on the other hand, the 
disease may be very tedious, lasting for weeks and months. This latter form 
is seen, upon careful consideration of the whole course of the disease, and par- 
ticularly of the temperature-curve, to be made up of separate attacks, which can 
often be very clearly distinguished. In each attack of this sort (see Fig. 75) the 
temperature rises for some days and then slowly abates, so that the entire length 
of an attack is about seven to thirteen days. Then there is an afebrile interval of 
a few days, followed by a fresh rise of temperature, etc. The recurrence of the 
fever is usually associated with new trouble in one or more joints, or with some 
additional rheumatic disorder, such as endocarditis or pleurisy, while during the 
afebrile period the local symptoms abate, and the patient feels almost well. Fried- 
lander has tried to deduce a series of general laws about the course of the disease, 
based upon this typical behavior of articular rheumatism, but in our opinion he 
has gone too far in this direction, although we have ourselves frequently observed 
this interesting course of acute articular rheumatism, with a series of separate 
attacks, and regard it as very characteristic of individual cases; still, there are 
many other forms which the disease may assume. 

Quite often the violent symptoms experienced at first disappear promptly, 
but only to be replaced by such milder ones as pain and stiffness of the joints — 
these latter persisting for a long time. It is a general rule, that the severity and 
persistency of the case correspond with the number of joints affected; but to this 



ACUTE ARTICULAR RHEUMATISM 



683 



rule there are numerous exceptions. Th 
nacy in a single joint. It need hardly be 
greatly modified by the occurrence of 
complications, cardiac or otherwise, and 
such sequelae as muscular atrophy, an- 
chylosis of the joints, or chorea. The 
most important of all sequelae is cardiac 
disease, and this must always be consid- 
ered in giving a prognosis ; for, although 
the disease as such does in most in- 
stances terminate in recovery, yet too 
often it gives rise to a tedious and usu- 
ally incurable disease of the heart. It 
is, however, true that complete recovery 
from the acute endocarditis seen in 
articular rheumatism is possible, but in 
a large majority of cases recovery is not 
complete, and the acute passes into a 
chronic endocarditis. In these cases the 
cardiac symptoms may be developed di- 
rectly, so that the patient at once begins 
to complain of palpitation and shortness 
of breath; or he may seem to regain his 
health completely, and a murmur which 
the physician alone can detect may be 
the only sign of the incurable injury 
which the body has suffered. The pa- 
tient may feel perfectly well for years 
after, and then at last begin to suffer 
from the failure of compensation (see 
page 326 et seq.). Finally, we should 
again call attention to the important 
fact that after recovery from rheuma- 
tism, there may be a tendency to fresh 
attacks of arthritis for the rest of the 
patient's life. 

Diagnosis. — Most cases of articular 
rheumatism can be easily recognized, 
for the acute occurrence of pain and 
swelling in several joints is sufficiently 
characteristic of the disease. It should 
nevertheless be borne in mind that ar- 
ticular swelling may also take place in 
the course of other diseases, and that 
mistakes in diagnosis are by no means 
impossible. When there are grave con- 
stitutional symptoms with fever from 
the start, we should not forget the pos- 
sibility of pyaemia, or of acute osteomye- 
litis, since these affections occasionally 
give rise to the swelling of several 
joints. In such cases, however, careful 
attention to the further course of the 
disease will generally enable us to see 



i disease may .persist with great obsti- 
said that the duration of the disease is 




o c © © © 

i-H o os oo r- 



684 DISEASES OF THE OKGANS OF LOCOMOTION 



that we can not be dealing with a simple acute articular rheumatism. Again,, 
after childbirth there may be swelling of the joints, of septic origin, and but 
distantly related to genuine rheumatism. 

If a single joint be attacked, the diagnosis of articular rheumatism must be 
made with extreme caution. These monarticular inflammations often prove to be 
something entirely different, namely, fungous disease of the joint, or an osteo- 
myelitis. The arthritis which follows gonorrhoea is usually [though not invari- 
ably] monarticular (affecting especially the knee-joint or wrist). In conclusion, 
it should be stated that it is not very rare to observe pain and swelling in various 
muscles and joints at the commencement of the secondary stage of syphilis, simu- 
lating an acute articular rheumatism. 

Sometimes the diagnosis is doubtful in those cases which present cutaneous 
ecchymoses (purpura and peliosis) and erythema nodosum, because we may be 
unable to determine which should be regarded as the primary symptoms and 
which the secondary. Fntil we become acquainted with the specific germs which 
cause all these diseases, it will be merely a dispute about words, whether we shall 
call a particular case by one name or another. In our opinion, all these conditions- 
have a close serological relation to one another. 

Genuine gout (q. v.) can usually be readily diagnosticated from articular rheu- 
matism by its localization in the toe, and by the gastric and other symptoms- 
which attend it. 

Finally, we must mention that acute multiple neuritis (q. v.), beginning with 
fever and severe pain in the extremities, may sometimes, if we are not sufficiently 
careful, be mistaken for polyarthritis. 

Treatment. — Acute articular rheumatism is one of the few diseases for whichi 
we possess an undoubtedly specific and universally accepted remedy. Kolbe sug- 
gested its use, and since 1876 it has been largely employed upon the recommenda- 
tion of Strieker, Buss, and others, for articular rheumatism. This remedy is sali- 
cylic acid. Although this medicine does not in all cases produce its surprisingly 
favorable results with equal rapidity and completeness, yet it almost invariably 
does produce a decided and beneficial effect upon the disease. We might even 
say that this influence is so constant that when salicylic acid proves entirely 
inefficient in a fresh case, such failure throws doubt upon the correctness of the 
diagnosis. Thus, where there is monarticular arthritis dependent upon some local 
cause, the remedy has hardly any beneficial influence. The same is true with 
regard to affections of the joints connected with gonorrhoea, pyaemia, and similar 
troubles. In genuine acute articular rheumatism, on the other hand, the salicylic- 
acid treatment is so superior to any other that it is the first duty of the physician 
in every case to give this remedy a fair trial. 

There are but two preparations of salicylic acid used in rheumatism — the pure- 
acid and its sodium salt, salicylate of sodium. Each of these two remedies has its 
peculiar advantages, but the specific influence of each is about the same. Sali- 
cylic acid should never be prescribed in solution, but always in wafers or capsules^ 
usually containing ten grains (gramme 0.50). In this way the salicylic acid can 
be taken by almost any patient quite easily, especially if a little water or milk be 
drunk after each dose. Adults should receive ten grains every hour until about 
one or two drachms (grammes 5-8) have been administered. Usually there will by 
this time be a very decided abatement of the articular pain and swelling, while on 
the other hand there will also usually be such toxic " salicylic symptoms " (vide 
infra) as to forbid its further use. The salicylate of sodium is best exhibited in 
single large doses of a drachm to a drachm and a half (grammes 4—6), each dose 
being given with about an ounce (grammes 20-30) of peppermint water, or still 
better, in wafers. The quite disagreeable taste of the medicine is only exagger- 
ated by the addition of such substances as syrup or fluid extract of licorice, added 



ACUTE ARTICULAR RHEUMATISM 



:f or the sake of elegance ; but the simple solution in peppermint water is quite well 
taken, at least by most patients. It is a very good plan to give salicylate of 
.sodium in a glass of Hungarian wine, or in strong black coffee without sugar. 
The advantage of the salicylate over the pure acid consists in its being possible 
to give a larger dose at one time, so that it need not be taken more than two or 
three times a day. In general, the amount given in twenty-four hours should not 
exceed two and a half drachms (grammes 10) ; one and a half to two drachms 
(grammes 6—8) may suffice. For children the dose is, of course, smaller, about five 
_grains of salicylic acid (gramme 0.30), or in twenty-four hours, half a drachm to 
a drachm (grammes 2-5) of the sodium salt. 

Which of these two preparations shall be employed is, as has been stated, of 
little consequence. We ourselves usually prescribe, at first, capsules of salicylic 
acid to be taken hourly, as being most agreeable to the patient ; but if our first 
visit be made in the evening, we prescribe a single large dose of a drachm to a 
drachm and a half (grammes 1-6) of salicylate of sodium, so that the patient may 
not be disturbed every hour through the night in order to take medicine. It is 
often possible to give the two remedies in alternation. This is a good way later 
on in the disease, when the patient has already acquired a distaste for the medi- 
cine. In such cases also it may be desirable to give the salicylate of sodium as an 
enema. About two and a half drachms (grammes 10) should be given, in two 
ounces of water (grammes 60). There is no doubt that the specific effects can be 
obtained in this manner. 

The benign influence of this remedy upon the disease is apparent in many 
fresh cases as early as ten to eighteen hours after treatment begins ; and it is often 
astonishing to see how soon a patient, who before lay helpless and complaining, 
becomes free from pain and able to move his limbs. It must be confessed, how- 
ever, that, apart from its taste, salicylic acid may produce disagreeable incidental 
effects. In the first place, there may be nausea with epigastric distress, and even 
vomiting. Tinnitus aurium may be exceedingly troublesome, and may be at- 
tended with marked vertigo. In somewhat rarer instances the mind is especially 
affected. Young girls in particular are often peculiarly excited; but the frame 
of mind is, however, in general a cheerful one. After large doses there may be 
an actual " salicylic delirium/' It should also be said that respiration may be 
affected, becoming very deep and rapid (salicylic dyspnoea). All these incidental 
effects, and particularly the nausea and ringing in the ears, render difficult the 
employment of the remedy in those large doses which alone are of any benefit. 
This is the more unfortunate, as it is often very desirable to employ salicylic acid 
persistently. 

Although it is not exceptional to have the symptoms almost entirely vanish 
at the end of one or two days, yet it is only in the minority of cases that the 
entire process ends with this release from pain. There is very often, sooner or 
later, a relapse, with fresh pain or even fresh swelling in one or more joints. It 
has been recommended to continue the salicylic acid in smaller doses for some 
time, in order to avert such relapses; but of late we have rather abandoned this 
method, for the reason that these small doses do not prevent the return of the 
disorder, but are calculated to give the patient a strong dislike to the remedy, 
and lessen his confidence in it. We therefore recommend to stop the medicine 
entirely as soon as the pain is wholly gone, and to guard the patient as much as 
possible from relapses by preventing his catching cold (vide infra). If there be 
fresh pain, we should at once resume the acid or its salt in large doses, and thus 
we shall very frequently be able to cut short the relapse at once. In case there is 
persistent discomfort in the joints, small doses may be kept up for some time. 

[One other salicylic compound deserves mention — the oil of wintergreen; this 
has been used largely by Kinnicutt, who finds it efficacious, easy to take, and not 



686 DISEASES OE THE OBGANS OF LOCOMOTION 



likely to produce the unpleasant symptoms which sometimes follow the com- 
pounds in more general use. It is given in doses of ten to fifteen minims every two 
houps, either in milk, on sugar, or in capsules. 

The salicylic treatment markedly diminishes the pain and fever, shortens the 
time spent in bed by four or five days, does not shorten the time spent in hospital, 
and seems to have little or no influence on the cardiac complications. The full 
alkaline treatment does not curtail the pain and fever in the same degree, but 
does seem to afford some protection against the heart affection, and to shorten the 
stay in hospital several days. 

A combination of the salicylic and alkaline treatments seems therefore ra- 
tional, and it has been adopted by the editor for some years. Citrate of potash is 
given in sufficient doses to produce and maintain alkalinity of the urine. The 
salicylic compound is given at first in full doses, which are diminished in size and 
frequency with the control of the articular symptoms, but are not omitted entirely 
until recovery is practically complete. The editor is inclined to believe that re- 
lapse is less common if the system be kept somewhat under the influence of the 
drug. Salicine is often perfectly well borne when the sodium salt causes gastric 
irritability, and the oil of wintergreen is another form which has advantages in 
some cases.] 

Despite the admirable qualities of salicylic acid, it must be confessed that we 
can not always bring about a rapid and complete cure of the disease by this rem- 
edy. There are cases in which, although at first evident improvement follows its 
use, relapses continually recur, or the disease fastens itself obstinately in single 
joints. In such, the continued use of salicylic acid proves almost unavailing, and 
indeed the patient can hardly be persuaded to take it. In these cases, and also 
when the salicylic preparations are ill borne or cause unpleasant attendant symp- 
toms, antipyrine is the best substitute. Many physicians therefore often prescribe 
it from the first in place of salicylic acid, although we think the action of the 
latter upon acute articular rheumatism is greater than that of antipyrine. We 
should give antipyrine in doses of fifteen to thirty grains (grammes 1-2) several 
times a day in water or wine. Its attendant symptoms (sweating, nausea, and 
sometimes an eruption like measles) are usually without special significance, and 
its influence on the articular pains is often so favorable that the remedy is of much 
value in the treatment of protracted rheumatism. We have also often used sali- 
pyrine (salicylate of antipyrine) with good results, and likewise phenacetine, and 
salol (phenyl-salicylate), which last was recommended by Sahli, and which is ad- 
ministered in powders up to fifteen grains (gramme 1) several times a day, the total 
daily dose being seventy-five to ninety grains (grammes 5-6). Antifebrine or acet- 
anilide is decidedly less efficient, but it has the advantage of being inexpensive. 

From the other remedies which may be sometimes tried in obstinate cases, 
we can seldom expect satisfactory results ; at least, we have ourselves never seen 
any decided benefit from iodide of potassium, preparations of colchicum, the 
alkalies, trimethylamine, or veratrine. Far more important in refractory cases is 
the local treatment of the diseased joints. This means chiefly massage, the re- 
sults of which, when scientifically performed, are often adrnirable. Electricity 
also may have a beneficial effect, particularly the galvanic current. We would 
caution against the too early use of warm baths, as these often aggravate the 
pain instead of mitigating it. Steam baths are sometimes very beneficial, but 
they may also do harm, and they should therefore be given only when the acute 
inflammatory symptoms have entirely vanished, leaving behind only stiffness and 
tenderness in the joints. On the other hand, it is advantageous to give the patient 
a sweat in bed. This is a favorite remedy of the author's, and may be accom- 
plished by introducing heated air under the bed-clothes, or in other ways. 

The application of an ice-bag in genuine articular rheumatism is seldom neces- 



ACUTE ARTICULAR RHEUMATISM 



687 



sary, but it may sometimes be desirable when there are violent and obstinate symp- 
toms of acute inflammation. Warm, moist applications are seldom beneficial in 
acute cases. In the advanced stages of subacute cases poultices or a wet-pack may 
afford some relief. Painting the skin over the joints with tincture of iodine pro- 
duces no effect in acute cases, and even in the chronic ones it is probably mainly 
a subjective remedy. Some observers report that injections of carbolic acid be- 
neath the skin of the affected joints greatly relieve the pain. A Pravaz's syringe- 
ful (thirteen minims) of a one-per-cent. solution may be injected one to three 
times a day. We have had no personal experience with this remedy. In all severe 
cases careful attention should be given from the start to maintaining a correct 
position of the diseased joints, because of the possibility of anchylosis. Before 
salicylic acid was introduced, " the treatment of articular rheumatism with 
splints " was largely and very advantageously employed. The use of salicylic acid 
has greatly diminished the necessity of such procedure, but even now it is some- 
times required. It is often possible to give the patient great relief by applying a 
suitable pasteboard or wooden splint to an affected extremity. 

General hygienic and dietetic treatment should not be undervalued. An 
equable temperature should be carefully maintained in the sick-room, inasmuch 
as cold, or draughts, or moisture have very often been found to exert an evil 
influence upon the disease and excite fresh pain. The patient should therefore 
be kept warm, and it is sometimes advantageous to wrap up the affected joints in 
cotton batting. It is of great importance that even in the mildest cases the pa- 
tient should be strictly confined to bed, and he should by no means get up too soon. 
If possible, we keep our own patients in bed for a week after the pain has ceased. 
Getting up too early will very often bring on a relapse. With regard to diet^ 
milk is the best food. We may also allow soup, eggs, and a little meat. In 
France, great weight is laid upon an exclusive milk diet ; but this would seem to 
us an extreme view. 

We do not need to speak at length about the treatment of the complications 
and sequelae, since we should merely repeat what has already been said in the 
appropriate chapters of this work. There has been much said on both sides as to 
the influence of salicylic acid in preventing complications, particularly cardiac 
complications. This much is certain, that cardiac complications are not abso- 
lutely prevented by the salicylic treatment, and that they too frequently occur 
while it is being employed; but we do believe that this treatment decidedly 
shortens the course of the disease as a whole, in many instances, and thus lessens 
the liability to endocarditis. If, however, a cardiac complication has made its. 
appearance, salicylic acid does not exert any appreciable influence upon it. 

Another important question is in regard to the efficiency of salicylic acid in 
the graver forms of articular rheumatism, particularly in cerebral rheumatism. 
It may be stated, in the first place, that in Leipsic cerebral rheumatism has 
apparently become much less frequent since the salicylic treatment was intro- 
duced. At any rate, not a single case of hyperpyrexia occurred in the clinique in 
that city out of many hundred cases treated, where the salicylic acid was properly 
employed from the first. We had an opportunity to observe a case in which hyper- 
pyretic symptoms had already appeared when we first saw it, and which had not 
been treated with salicylic acid. Here large doses of that remedy produced no 
effect. We should nevertheless be inclined to employ it, first of all, in such cases ; 
and the energetic use of cool baths would probably be the most speedy way of 
modifying the dangerously high temperature. Stimulants, in particular camphor, 
are also required in these severe cases. 

In the severe haamorrhagic varieties of rheumatism we should also give sali- 
cylic acid a trial. The milder hsemorrhagic cases (hsemorrhagic urticaria) do well 
under ordinary methods of treatment. 



688 



DISEASES OF THE ORGANS OF LOCOMOTION 



If the acute affection merge into a chronic condition of stiffness and swelling 
of certain joints, such as the wrist or shoulder, we must employ the same remedies 
as in chronic articular rheumatism. Passive movements and massage furnish the 
best results. Warm baths may also be ordered in such cases (see the following 
chapter). The patient might be sent to Teplitz or Wiesbaden. These baths are 
good resorts for convalescents. The subsequent muscular atrophies and paralyses 
recover most rapidly under electricity. 

Prophylaxis requires, first of all, that one should avoid cold or wet, and other 
" rheumatogenous influences." Persons who have already had one attack of 
articular rheumatism must be especially careful, inasmuch as they are more than 
■ever liable to the disease, as has already been said. It is not inconsistent, how- 
ever, with the exercise of due caution, to endeavor to lessen the sensitiveness of 
the skin by such procedures as cold sponging, followed by friction. 



CHAPTER II 

CHRONIC ARTICULAR RHEUMATISM (CHRONIC POLYARTHRITIS) 
AND ARTHRITIS DEFORMANS 

^Etiology. — The two diseases known as " chronic articular rheumatism" and 
4i arthritis deformans " are considered together here, because it is impossible to 
•draw a sharp distinction between them. It is, indeed, not unlikely that the above 
names are sometimes applied to diseases which differ essentially from each other ; 
but as we do not yet understand the nature or the aetiology of many chronic 
•diseases of the joints, we must provisionally be guided by the external changes 
they produce. We shall therefore embrace all chronic inflammatory processes 
affecting the joints under the name of chronic arthritis. It is not intended to in- 
clude traumatic arthritis, much less those chronic affections of the joints which 
are evidently of tubercular origin, and which have ordinarily been termed fungous 
arthritis. These belong to the domain of surgery. We would also exclude chronic 
syphilitic diseases of the joints, about which, indeed, there is still less known than 
about the tubercular affections; besides, they are rare. Chronic articular affec- 
tions from gonorrhoea are more frequent, and of great practical importance. 

The aetiology of those cases of chronic arthritis where the disease is a direct 
sequel of acute articular rheumatism is evident enough. Tt is hardly possible to 
•doubt that the same specific poison which excited the acute arthritis maintains 
possession of the joints, and produces the chronic inflammatory changes. Cases 
of this sort especially deserve the name of chronic articular rheumatism. They 
are not very infrequent, and may be of slight or great severity. The worst cases 
produce macroscopic changes which fully justify the other appellation of arthritis 
•deformans. 

It is also possible that many cases which are chronic from the start have the 
same aetiology — that is, are due to the same pathogenic agents. This might be 
inferred from analogy with numerous other diseases, and it is rendered still 
more probable by the fact that the same exciting causes which promote acute 
articular rheumatism often play a conspicuous part in chronic arthritis. Such 
causes are exposure to cold and wet, and working in cold or draughty places, or 
dwelling in newly built and damp houses. This explains why those who follow 
certain callings — for instance, washerwomen — are more apt to suffer from the 
disease than others, and why arthritis deformans has, with some justice, been 
called a disease of the poor, in contrast with the gout of the wealthy. Many of the 



CHRONIC EHEUMATISM AND AETHRITIS DEFORMANS 689 



laity, and even some physicians, believe that gout and arthritis deformans are in 
some way related, but this view is erroneous. 

It is very questionable whether all cases of chronic multiple arthritis are refer- 
able to the causes already enumerated. Such other influences, however, as are 
concerned in its production are not at all understood. Various authorities have 
maintained that arthritis deformans is the result of a primary disease of the nerv- 
ous centers, and in particular of the spinal cord. We regard this statement as 
•entirely unwarranted. It originated at a time when there was a tendency to 
ascribe all sorts of ills to disease of the " trophic centers," but there is no doubt 
that this tendency was carried very much too far. We may state in this connec- 
tion that a careful microscopic examination of the spinal cord in one case of very 
severe arthritis deformans yielded an entirely negative result. 

[Some striking cases are reported by Blake, which go to show that the arthritic 
changes may be set up by chronic, though slight, suppuration, in analogy, perhaps, 
with the synovitis of gonorrhoea. Careful examination should consequently be 
made of all the mucous membranes, especially in cases which seem to have no 
connection with true rheumatism.] 

Chronic arthritis is mainly a disease of advanced years. Certain monarticular 
varieties, about whose aetiology, it must be confessed, we know little as yet, have 
I)een termed arthritis senilis — in particular the malum coxce senile. Even the 
common and, in a certain sense, typical form of arthritis deformans {vide infra) 
is not apt to occur in people under thirty-five years of age. This rule, however, 
lias exceptions, and we have ourselves seen a few perfectly characteristic cases of 
arthritis deformans in children between ten and fifteen years of age. Women are 
much oftener attacked than men. It is often said that trouble, anxiety, and other 
•emotional influences favor the outbreak of the disease; but the proof of this is 
lacking. The disease does not often seem to be hereditary. 

Pathology. — The process is described as simple chronic arthritis (or synovitis) 
so long as it is confined mainly to the synovial membrane of the joint and the 
periarticular connective tissue. These parts often undergo decided inflammatory 
thickening {synovitis hy per plastic a) ; the synovial membrane becomes cloudy; 
and the amount of synovial fluid is more or less increased {synovitis serosa) — 
that is, we have chronic dropsy of the joint. Sometimes different parts of the 
synovial membrane are connected by adhesions, which considerably interfere with 
the movements of the joint. There may even be complete anchylosis : for exam- 
ple, in the shoulder or knee. 

Chronic synovitis may pass imperceptibly into arthritis deformans. In this, 
not only the capsules of the joint, but the articular cartilages and the articular 
extremities of the bones, are so much affected as to produce the most striking 
deformity. These changes almost always originate in the articular cartilages. 
In many cases the morbid process consists merely in a fibrillation, destruction 
and wearing away of the articular cartilage, beginning usually on its outer edge ; 
finally, the bone is exposed and itself undergoes ulceration. All this while, the 
articular capsule may escape involvement, and there may be no serous effusion 
into the joint {arthritis sicca). In other cases, however, there are soon added 
proliferative changes affecting not only the cartilage itself, but also the synovial 
membrane. The inner surface of the synovial membrane becomes tufted, and 
many of these tufts may undergo secondary calcification, break off, and become 
loose bodies in the joint. The articular cartilages are also affected by inflamma- 
tory new growth and proliferation ; these in part become disintegrated, and lead 
to deeper and deeper excavations of the cartilage. From the cartilage the pro- 
cess extends to the bones, and thus at last the articular extremities of the bones 
become almost completely destroyed. Sometimes, also, the periosteum near the 
joints undergoes ossific periostitis. On microscopic examination, we find fibrous 
44 



690 DISEASES OE THE OEGANS OE LOCOMOTION 



disintegration of the matrix of the cartilage, and proliferation and subdivision of 
the cartilage-cells, at the same time that there is destruction of the newly formed 
cells by simple or fatty degeneration. 

Of course the normal structure of the joint is at last completely destroyed by 
these various processes. The articular extremities of the bones waste away more 
and more, and take new relative positions, as the parts which impinge upon each 
other are worn away. Externally, the joint usually becomes larger and larger; 
and this is the more evident because the surrounding muscles undergo great 
atrophy. There is often no collection of synovial fluid in the joints during the 
entire illness, but sometimes the joints are swollen — e. g., the knee joint — and 
even to a considerable degree. There is a tendency for the affected joints to 
suffer more or less complete anchylosis and contracture (vide infra). 

Symptomatology. — The clinical symptoms of chronic arthritis are very simple 
and uniform. They relate almost exclusively to the local disturbances, and to 

these they are directly due. The gen- 
eral course of the disease, however, pre- 
sents great diversities. Often the ar- 
thritis limits itself to a single joint or 
to a few joints; in other cases almost 
all the joints become finally involved. 

Except in the cases which are pre- 
ceded by acute articular rheumatism, 
the disease usually begins quite gradu- 
ally and insidiously. The first subjec- 
tive symptoms are stiffness and pain in 
the joints, the pain being aggravated by 
pressure or movement. The stiffness is 
most noticeable when the joint has re- 
mained quiet for some time previous, 
and is therefore ordinarily greatest on 
waking up in the morning. The pain 
often shoots from the joints upward and 
downward, and is of a burning character, 
or less often neuralgic. Even in ad- 
vanced cases the pain usually occurs 
only when the affected joints are moved, 
although then it may be very severe. 
When the body is entirely at rest there 
is little or no pain. Besides actual pain 
there are apt to be at the onset of the 
disease peculiar paresthesias and other 
nervous symptoms, particularly in the 
fingers. Motion is impaired very early. 
This is due at first to the pain, and to 
a certain reflex inhibition and ataxia of the muscles ; to which are later added the 
purely mechanical hindrances and the ever-increasing atrophy of the muscles. 

The objective changes in the affected joints begin to appear soon after the 
symptoms just mentioned, at least in cases of any severity. The joints often seem 
enlarged and thickened. If we attempt to move them, we not only cause pain 
and meet with mechanical obstruction, but we may hear and feel the cracking and 
grating produced by the rubbing of the denuded and uneven surfaces upon each 
other. This is often noticed by the patient himself. In chronic arthritis sicca 
there may be no great swelling of the joints; still, there are usually marked 
pain, crepitation, and impairment of motion. 




Fig. 76.— Appearance of the hand in a case of pro- 
tracted arthritis deformans (personal observation). 



CHRONIC RHEUMATISM AJ$D ARTHRITIS DEFORMANS 691 



As the disease gradually progresses, there are usually developed certain char- 
acteristic deformities, which are apt to be most strikingly exhibited in the hands 
(see Eig. 76). The metacarpo-phalangeal joints are thickened and swollen, and 
are made all the more prominent because the interossei upon the back of the hand 
are atrophied. The bases of the first phalanges are directed obliquely toward one 
side, so that the fingers assume more and more the appearance of subluxation. 
They are bent over toward the back of the hand, and are also displaced toward 
the ulnar side, so that they often actually come to rest one upon the other. The 
palm of the hand is frequently deeply hollowed out. Often the phalangeal joints 
also are distorted, so that, for example, there will be an obtuse angle on the dorsal 
surface of the fingers between the first and second phalanx, while the terminal 
phalanx is apt to be flexed, although the second phalanx preserves a position of 
extension. Despite these changes, many patients, if only the thumb remains 
tolerably movable, are able to use their hands for quite delicate work, although 
at the expense of much time and effort. Arthritis deformans scarcely ever causes 
anchylosis of the small joints of the fingers. The elbow- joints are often decidedly 
enlarged. The forearms usually assume a position of pronation, combined with 
more or less flexion. Even the mobility of the shoulder-joints progressively 
diminishes, so that at last the arms can not be raised at all. At the same time 
there is contracture of the adductor muscles. 

With regard to the lower extremities, the hip- and knee-joints usually suffer 
more than the ankle. Sometimes there are thickenings of the joints and serous 
effusions, and sometimes arthritis sicca. If the joints of the lower extremities 
are much involved, of course standing and walking grow more and more painful 
and difficult, and finally require crutches, or an assistant. Yery often there is 
marked contracture of the flexor muscles of the hip, and still oftener, of the 
knee. This is not associated with anchylosis of the joints, but is of purely mus- 
cular origin. In such cases the patient can not sit in bed with the knees ex- 
tended (see Fig. 77). There is sometimes subluxation of the hip-joints, so that 
the head of the femur slides backward and upward. The same thing is observed 
also in very severe cases in the knee-joint. 

There are monarticular and polyarticular forms of the disease. The mon- 
articular form is usually regarded as a surgical trouble, and is most often located 
in the hip-joint (malum coxae senile), or more rarely in the knee- and shoulder- 
joints. The polyarticular form is the characteristic one. In most of the typical 
cases it begins in the small joints of the hand and fingers. At a later period 
the larger joints are also invaded, one after the other, the invasion taking place 
symmetrically on both sides of the body, although the disturbance is not in- 
frequently greater on one side than on the other. In severe cases the joints of 
the spinal column also aTe involved. This impairs particularly the movement 
of the head. The articulation of the lower jaw is usually very little affected, 
if at all. 

In less frequent instances the arthritis is confined principally to the lower 
extremities, while the upper escape intact for a long while, or even permanently. 
It is very possible that such cases often have a different aetiology from ordinary 
arthritis deformans ; and the same is true of the cases which are confined mainly 
to the vertebral column, and are termed spondylitis deformans. A remarkable 
and, as it seems to us, unique disorder may be mentioned in passing. It leads 
very gradually and painlessly to a complete anchylosis of the entire spinal column 
and the hip-joints (chronic spondylitis and coxitis, with anchylosis), so that head, 
trunk, and thighs are firmly united and completely stiffened, while all the other 
joints retain their normal mobility. It need scarcely be said that this necessarily 
causes a peculiar modification of the carriage and gait of the sufferer. We have 
ourselves seen two typical cases of this peculiar disease, and recently other physi- 



692 DISEASES OF THE ORGANS OF LOCOMOTION 



cians have reported precisely similar observations. Marie has proposed for them 
the name " spondylose rhizomelique." 

There is hardly any affection of parts of the body other than the joints in 
arthritis deformans. The muscles should be excepted, for they always undergo 
that muscular atrophy which we have already described (vide page 680) as the 
result of joint disease. This atrophy is most marked in the interossei, the shoulder 




Fig. 77.— Chronic arthritis deformans with contracture of the hip- and knee-joints. 



muscles, and the muscles of the calf and thigh. The associated muscular con- 
tractures (vide supra) are also of great importance. Sometimes the skin over the 
wrist and other affected joints appears peculiarly wrinkled and flabby. The inter- 
nal organs almost always perform their functions in a perfectly normal manner. 
Appetite and digestion remain good, although there is often some tendency to 
constipation. Rarely there is valvular disease of the heart, but usually only in 
such cases as originate in an acute articular rheumatism. Still, we have seen 
valvular disease, exceptionally, in cases which had been chronic from the start, a 
fact which is not without interest from an serological point of view. Certain 
attendant symptoms which are sometimes observed, such as headache, congestive 
states, psychical depression, and bronchitis, probably are not directly connected 
with the disease, but are easily explicable sequelae. 

General Course of the Disease. — Arthritis deformans is an extremely chronic 
trouble. It may last even ten or twenty years, or more. Sometimes there is an 



CHRONIC RHEUMATISM AND AKTHKITIS DEFORMANS 693 



apparent arrest of the process extending- over months, or even longer. Sometimes 
the progress of the disease is marked by remissions and exacerbations, affecting 
either the general or the local manifestations. In general, however, the disease 
continually advances. 

The prognosis is therefore unfavorable. Recovery, if it ever occurs, is ex- 
tremely rare, and is possible only in the early stages. For the encouragement of 
the patient, it may be said that, under proper care and treatment, the disease often 
runs so gradual a course that the general condition remains at least bearable for a 
very long while, although there may be considerable local disturbance. The dis- 
ease is not directly dangerous to life. The eventual fatal termination ensues 
either from general debility, or because of some intercurrent disease. 

The prognosis is somewhat more favorable in the milder cases of " chronic 
articular rheumatism," where the anatomical changes are less severe, and are 
completely limited to the synovial membrane. Even here, however, recovery is 
by no means frequent, and it is always to be feared that grave deformities of the 
joints will gradually be developed. 

Treatment. — With regard to regimen, it is requisite in the first place to avoid 
all unfavorable external influences. If possible, the dwelling should be dry and 
warm ; and it may often seem advisable 16 make a change of climate. The patient 
must dress warmly, without, however, undermining his powers of resistance too 
much, as he will be in danger of doing. The diet must be abundant and nutritious. 

Internal remedies may be tried, with the hope of modifying the disease, but our 
chief reliance must be upon local treatment of the joints. Among internal reme- 
dies, the most important are iodine and arsenic. Iodine may be given in the form 
of tincture (a few drops in mucilage several times a day), or a better form is in 
combination with potassium. As yet, we ourselves have not seen any great benefit 
from iodine, but we have in repeated instances witnessed a quite striking result 
from the use of arsenic. It is best administered in pills containing one thirtieth 
to one fifteenth of a grain (gramme 0.002-0.004) of arsenious acid, one pill two 
or three times a day. If this remedy prove beneficial, it must be continued for at 
least months, perhaps with occasional brief intermissions. The persistent use of 
small doses of salicylic acid or salicylate of soda, thirty to forty-five grains a day 
(grammes 2-3), and similar remedies, is recommended by many physicians. We 
have ourselves seen no special advantage from their employment, and therefore 
usually prescribe them only during acute exacerbations of the disease. The prep- 
arations of colchicum may be tried, but they will seldom be found efficient. Iron, 
quinine, and cod-liver oil are sometimes indicated by the general condition. 

First among local methods of treatment comes massage, although the good it 
accomplishes is, of course, apt to be evanescent. It will, however, do much to 
hasten the absorption of inflammatory exudations, and also to loosen up the 
joints, invigorate the muscles, and improve the general health. The Swedish 
movement cure will be found of great benefit in all cases if begun early and 
methodically persevered in. It preserves the mobility of the joints as long- as 
anything can. Electricity also has a beneficial influence. The galvanic current 
is applied to the affected joints, and the faradic current to the atrophied muscles. 

Baths are universally employed in chronic arthritis. Their value should not be 
overestimated, but, notwithstanding, their usefulness is undeniable in many cases. 
Simple warm baths, or salt-baths (five to ten pounds of salt for each bath), are 
practicable in almost any household. As health-resorts in arthritis deformans, ex- 
perience shows the following to be most desirable : The simple warm baths, such 
as Teplitz, Wildbad, Ragatz, and Baden in Switzerland; the warm chloride-of- 
sodium baths in Wiesbaden ; the acidulated baths of Oeynhausen and Nauheim ; 
and the mud-baths of Elster, Marienbad, Franzensbad, and Schmiedeberg. 
Steam-baths are admissible only in the early stages of the disease, and for pa- 



694 DISEASES OF THE ORGANS OF LOCOMOTION 



tients whose general condition is still vigorous. Even then they should be em- 
ployed cautiously. 

[The mineral springs within the limits of our own country chiefly to be recom- 
mended are Sharon and Richfield, in New York State, the Sulphur Springs and 
Hot Springs of Virginia, and the Hot Springs of Arkansas. At the two former, 
particularly, there is every provision for comfort as well as for the use of the 
waters.] 

We have repeatedly seen quite excellent results follow the employment of hot 
sand-baths. These also can be easily used at home, particularly if applied merely 
to the hands or feet. They are employed more elaborately in Kostritz and Blase- 
witz. These hot sand-baths seem to do good, not only from the temperature, 
but also from the uniform and persistent compression which they exert. Some- 
times, also, the long-continued local application of warmth, of hot compresses and 
packs, is very effective. Recently special apparatus has been constructed (first in 
England) for the local application of hot air. The diseased parts are thus ex- 
posed for about an hour, in closed copper chambers, to a heat of 150°-212° (65°- 
100° C.) and higher. The reports as to the success obtained in this way are very 
favorable [but, unfortunately, they are not fully confirmed by experience. — V.] . 

Stimulating or narcotic remedies may be rubbed into the joints, but they are 
beneficial only because of the massage which accompanies their employment. In 
practice it is not always possible to omit their use. The application of tincture of 
iodine is usually entirely without effect. As to morphine and other narcotics, the 
disease is so chronic that it is desirable to employ them as little as possible. A 
considerable number of those who suffer from chronic arthritis become opium- 
eaters. We should try, therefore, if there is severe pain, to give relief as long as 
possible with antipyrine, phenacetine, and similar remedies. 

We may say, therefore, that the use of the various remedies which have been 
suggested one after another will enable us to oppose some obstacles to the progress 
of the disease. Persistent treatment will, in many cases, be rewarded by consider- 
able, at least temporary, improvement. 



CHAPTER III 

ACUTE AND CHRONIC MUSCULAR RHEUMATISM 

(Myositis, or Myalgia, RTieumatica) 

Definition and -ZEtiology. — Certain acute affections may originate primarily 
in the muscles. These are to all appearance inflammatory in their nature, and 
not infrequently result from taking cold, or other causes similar to those which 
produce acute articular rheumatism. These affections are classed as " acute mus- 
cular rheumatism " or rheumatic myositis. It is possible that this disease also is 
an infectious one, but the question remains entirely undecided. The analogy 
which this trouble bears to acute articular rheumatism is not complete. It is sel- 
dom that the two processes are seen in combination; and, furthermore, acute 
myositis is not " polymuscular," but is usually confined to one muscle, or to a sin- 
gle group of muscles; it is attended with little if any fever; and it is never fol- 
lowed by acute endocarditis. The two diseases, therefore, are alike only in certain 
symptoms (pain and impairment of motion), and in the fact that they are often, 
although not always, ascribable to cold or the like. 

There are many cases in which pain suddenly occurs in the muscles ("my- 
algia ") without any attendant objective change. These cases can not be called 



ACUTE AKD CHRONIC MUSCULAR RHEUMATISM 



695 



genuine acute myositis. Indeed, it is sometimes difficult to know how to regard 
them. In practice they are usually termed muscular rheumatism, especially when 
they are referable to exposure; and it is possible that many such cases are really 
a very mild form of the genuine inflammatory disease. Yet in our opinion it is 
perfectly possible that some chemical change in the substance of the muscle occa- 
sions the local disturbance. That the influence of cold is often, though not always, 
important in this connection, seems to us indubitable. There are individuals who 
are almost certain to have a stiff neck if they are exposed to any decided draught 
upon the back of the neck ; and others who, every time they get chilled, are liable 
to lumbago. However, other injurious influences may, of course, be important. 
Thus, traumatic pain in the muscles is the result of some excessive strain, and in 
many instances is apparently due to laceration of some of the muscular fibers. 
This is generally occasioned by too violent muscular exertion. Any physician 
who sees many patients from the laboring classes meets with an abundance of 
cases of this sort.* 

The limitations of acute muscular rheumatism are obscure; but still more so 
are those of " chronic muscular rheumatism." This disease also is a frequent one, 
and only imperfectly understood. It does not bear a close analogy to chronic 
articular rheumatism, except in this unimportant point, that chronic muscular 
rheumatism seems to be quite often occasioned by meteorological influences. 
While the anatomical changes in chronic articular rheumatism are almost always 
striking, analogous lesions are very exceptional in chronic muscular rheumatism. 
On the contrary, the name is usually applied to cases where there is pain in various 
muscles all over the body, but where there is no discoverable objective disturb- 
ance. Older authorities used to speak of " rheumatic induration " of the muscles, 
but this or any other actual anatomical change is very exceptional. 

These facts justify a doubt as to whether all cases of chronic muscular rheu- 
matism actually deserve their name. It is certainly quite appropriate in those 
not infrequent cases which seem to be due to " rheumatogenous influences," and 
are so evidently aggravated upon every exposure to cold, or every period of bad 
weather, that the patient often asserts that he carries in his bones the best of 
barometers. Such is the " old rheumatism " of those who have passed a large part 
of their lives in the open air, regardless of wind or weather. There are other cases, 
the character of which is different. In them the muscular pain is associated with 
a general neurasthenic condition, or with corpulence (when it is, perhaps, the 
Tesult of circulatory disturbance), or possibly with chronic poisoning. An 
important instance is the " rheumatic pain " sometimes complained of by topers, 
which we are inclined to ascribe not to changes in the muscles but to nutritive 
disturbances of the nerves. Eor these and similar disorders there are no special 
names, and the practicing physician often terms them all " muscular rheuma- 
tism," a diagnosis with which the patient is usually quite contented. 

Clinical History. — Genuine acute muscular rheumatism is ordinarily, as has 
heen said, limited to some one definite group of muscles. The affected muscles 
often seem somewhat swollen and infiltrated, are very sensitive to pressure, and, 
if not quite useless, are nearly so, greatly impairing the motion of the correspond- 
ing member of the body. All these symptoms are best illustrated in acute myo- 
sitis of the deltoid (omalgia). The whole shoulder is swollen, the muscle is very 
painful, and the upper arm is almost incapable of voluntary motion, although, if 
-caution be exercised, passive movement can be made without causing any pain. 

The various forms of acute muscular rheumatism have received names descrip- 



* Some time ago the author saw an organ- player who had to work the pedals for many hours a 
day; he had an extremely painful affection of the lower extremities associated with swelling, which 
<?ould be regarded only as an acute myositis. 



696 



DISEASES OE THE ORGANS OE LOCOMOTION 



tive of the locality of the affection. We have, besides the omalgia already men- 
tioned — k 

1. Rheumatism of the cervical muscles (splenius, trapezius, sterno-cleido-mas- 
toid, etc.), Myalgia cervicalis, or rheumatic torticollis. The pain is located in 
the back and side of the neck, and is usually unilateral. The head is held stiffly 
to one side, the occiput inclines toward the painful side, and the chin is turned 
toward the healthy side. All active and passive motions which tend to stretch the 
painful parts are much impaired, and cause suffering. 

2. Myalgia lumbalis, or lumbago. This, the most acute form of muscular rheu- 
matism, known among the common people in Germany because of its sudden onset 
as " witch's shot," or " dragon shot," is a well-known disease. The region of the 
sacrum and loins in a greater or less extent (erector spinas, quadratus lumborum, 
etc.) is very sensitive. All motions of the trunk, such as bending and twisting, are 
very painful and difficult. The disease is more frequent in men than in women. 
Certain persons seem to be especially predisposed to it. It should also be stated 
that lumbago is not always of a rheumatic character, but of traumatic origin, as 
from lifting a heavy weight, or from sudden stooping.* [It is very common in 
the traumatic neuroses, where it was once regarded as indicative of spinal in- 
jury. — K] 

3. Rheumatism of the thoracic muscles, and particularly of the intercostals. 
This may cause great discomfort, as it renders breathing, coughing, and sneezing 
very painful. It is comparatively rare ; and caution should be exercised in diag- 
nosticating it, to avoid confusion with pleurisy and periostitis of the ribs. Very 
often, also, thoracic disturbance is regarded as rheumatic when it is really trau- 
matic, being the result of stretching or laceration of the fibers of the pectoral or 
other muscles. 

4. Rheumatism of the head also, probably, belongs in this category, although 
the affection is seldom confined to the muscles of the scalp, but involves also the 
f ascise, and may even be almost confined to them. It is not infrequently excited 
by exposure to cold. The pain is quite violent, and greatly increased by any 
movement of the scalp. Of course, the diagnosis requires the previous exclusion 
of the various forms of headache described on pages 824 and 905. 

The duration of acute muscular rheumatism is brief. Usually the pain abates 
in a few days; but a tendency to relapse persists for some time. Constitutional 
symptoms in addition to the local disorder are, as a rule, absent or slight ; still, we 
sometimes meet cases in which acute muscular rheumatism is associated with 
fever and marked general disturbance. 

In chronic muscular rheumatism there are, as a rule, no objective lesions dis- 
coverable. The statements of masseurs as to palpable nodes and indurations are,, 
in our opinion, to be received with very great skepticism. The pain is seldom 
located permanently in any one place, but it is felt first here and then there. It 
is usually increased during bad weather, and is less severe when the weather is 
warm. The pains are often described as "wandering." Motion is seldom much 
impaired. Sometimes, however, there may be a certain stiffness of the muscles, 
most marked after a period of repose. 

The diagnosis of chronic muscular rheumatism rests, therefore, mainly upon 
the rational signs. Hence it is often impossible to avoid the suspicion of malin- 



* Lately, S. Erben has sought to prove that lumbago and torticollis are not at all muscular diseases, 
but probably in most cases due to an affection of the joints of the vertebrae. He bases this belief upon 
the result of painstaking investigations. One who, like the author of this text-book, has often him- 
self suffered from acute muscular rheumatism, will be scarcely inclined to adopt this view, for the sub- 
jective sensation of pain is referred decidedly to the muscles, or to the attachments and fascia? of the 
muscles. 



ACUTE AND CHRONIC MUSCULAR RHEUMATISM 697 



gering, particularly where certain applicants for hospital care are concerned. We 
should not, however, be too uncharitable, since without doubt there are cases 
in which quite severe pain is felt, now in one set of muscles and now in another, 
without any anatomical basis for such pain being discoverable. Nor should we 
ever forget that other diseases may have pain for their first symptom. It is not 
at all exceptional for the lancinating pains of locomotor ataxia to be for a long 
time regarded as " rheumatic." Lumbago may be confounded with insidiously 
developing tumors, diseases of the vertebrae, renal calculi, or with various hypo- 
gastric disorders (particularly in women). We should therefore never omit to 
make a careful physical examination. 

Treatment. — Acute muscular rheumatism has this in common with acute 
articular rheumatism, that it is usually very favorably affected by salicylic acid. 
In cases of genuine acute rheumatic myositis the employment of this remedy in 
the manner already described will often give surprising relief in as short a time 
as twelve or twenty-four hours. We also see good results from antipyrine or sali- 
pyrine, etc. Local treatment of the affected muscles also may be followed by great 
and speedy improvement. Massage is particularly valuable. It is not infrequently 
the case that a single properly conducted massage will cause a violent lumbago or 
omalgia to disappear almost completely, and like favorable results are witnessed 
when there is traumatic pain in the muscles. Most of the external applications 
which are so frequently prescribed for rheumatism — such as spirits of camphor or 
chloroform liniment — accomplish less through the cutaneous irritation they pro- 
duce than by the massage incident to their employment. Next in value comes 
electricity. Both the constant and the faradic current may be employed. Often,, 
also, the local application of warmth is very beneficial ; thus hot dry cloths or hot 
poultices may be applied. Simple stimulation of the skin by mustard is often 
palliative, but less so than the first-mentioned remedies. Often great relief is- 
given by sweating, by means of a hot wet-pack, or by a steam-bath, the employ- 
ment of which is so common that patients often use it of their own accord. 

In chronic muscular rheumatism the benefit of salicylic acid and antipyrine is 
merely temporary, and therefore is to be sought, if at all, only when there is an 
acute exacerbation. Massage and electricity are more effective, and, if persevered 
in for some time, will often accomplish good results even in obstinate cases. 
Treatment by sweating and bathing is frequently prescribed with advantage. 
Steam-baths are often beneficial, but their use requires great caution when the 
patient is corpulent and has a tendency to congestion or cardiac failure. There 
is also value in mud-baths, pine-needle-baths, and in the baths given at Teplitz, 
Wiesbaden, and other places. 

In many case of chronic muscular rheumatism constitutional treatment is of 
great importance. Particularly when the patient is overfed, and intemperate in 
the use of alcohol, much benefit will often be accomplished by a proper regulation 
of the ingesta and the prescription of a sufficient amount of muscular exercise. 
Such patients may also be helped by a cautiously conducted cold-water treatment. 
This lessens their great sensitiveness to cold. 

[In acute cases with localized pain I have found useful a thick flaxseed poul- 
tice, applied as hot as it can be borne, renewed once or twice, and followed by 
the application of a thick layer of cotton. A dry cup or two is also often pro- 
ductive of great relief. In chronic cases, plasters and the iodide of potassium are 
often of benefit. 

Muscular rheumatism is a common and often very troublesome affection in 
those whose occupation calls for decided muscular exertion. A muscle is strained,, 
pain settles in and is apt to recur in the part ; and, while the general health is suf- 
ficiently good, the man is compelled to remain idle. Quack advertisements dwell 
so much upon pain in the back as a symptom of Bright's disease, that we are fre- 



698 DISEASES OF THE OKGANS OF LOCOMOTION 



quently consulted by those who, suffering from muscular pain and soreness, think 
themselves the subjects of serious disease of the kidneys.] 



CHAPTEE IV 
ACUTE POLYMYOSITIS 

From some recent observations (E. Wagner, ITnverricht, and others) we have 
obtained knowledge of a disease which consists essentially in an acute inflamma- 
tion of most, or even of all, the muscles of the body. The disease appears chiefly 
in persons in early or middle life, but it has also been repeatedly observed in the 
elderly. The disease may begin either quite suddenly or gradually. Sometimes 
polymyositis is a sequel of some other disease, most often, as it seems, of septic 
infections, such as puerperal fever and erysipelas. This circumstance seems to 
indicate that polymyositis is associated with severe constitutional intoxication. 

The disease usually begins with decided constitutional disturbance, including 
languor, headache, anorexia, and vomiting. Very soon the characteristic muscu- 
lar pains commence, there are dragging pains, and often cramps in the arms, legs, 
and trunk, and these sooner or later decidedly impede motion. If we examine 
the painful places we find a marked tenderness upon pressure and upon passive 
motion. Soon we can perceive a distinct swelling of the parts involved. This de- 
pends somewhat upon the inflammatory swelling of the muscle, and still more upon 
a firm inflammatory oedema of the corresponding skin, which usually appears very 
early. As a rule, the upper extremities are most severely attacked, and in them, 
too, the inflammatory oedema is most marked. The forearm swells, particularly 
in the region of the belly of the muscles, and so comes to have a characteristic 
spindle shape, provided the region of the wrist-joint is not involved. The face, 
the trunk, and the lower extremities also present similar though less marked 
swellings of the skin, or of the different soft parts, particularly on the extensor 
surfaces. At the same time, the skin is apt to be distinctly reddened with inflam- 
mation, so that it almost suggests erysipelas (" dermatomyositis ")• Other ex- 
anthems also may appear — viz., erythema, urticaria, and herpes. If the disease 
lasts some time the swelling gradually disappears, and there may be distinct 
atrophy of the muscles. The patellar reflex is usually abolished from the start. 
The electric excitability of the muscles rapidly diminishes, and is finally de- 
stroyed. In some few muscles we sometimes observe the reaction of degeneration, 
but a careful electrical examination is always very difficult because of the great 
pain it causes. The sensibility of the skin in cases of polymyositis (vide infra) 
remains unimpaired. 

The general condition becomes very much aggravated if the muscles of deg- 
lutition and respiration are attacked ; the ingestion of food is rendered more and 
more difficult, and there is severe dyspnoea. Soon bronchitis, and lobular pneu- 
monia develop, and these are the more distressing to the patient because expec- 
toration grows increasingly difficult and finally quite impossible. Nutrition is 
often interfered with by stomatitis. Tonsillitis has been repeatedly observed. 
Perspiration is decidedly increased, and the urine may contain a small amount 
of albumen. Splenic tumor has been repeatedly found in the acute cases. The 
bodily temperature is often elevated, 101°-103° (38.5°-39.5° C.) ; the pulse-rate 
may rise to 100 or 120 beats per minute. 

With regard to the clinical course of the disease, we should make a distinc- 
tion between the acute and the more chronic cases. The acute may end in recovery 



EACHITIS 



699 



after two or three weeks. Often, however, after a shorter or longer course of from 
three weeks to three months, a fatal termination occurs, probably in most instances 
the result of respiratory disturbances, secondary pneumonia, and the like. 
Chronic cases may last a year or more. 

In the cases observed thus far there has been found on examination a true 
acute inflammation of the muscles. Not only do the muscular fibers show all 
forms of degeneration and destruction, but also in the interstitial connective 
tissue we find true inflammatory foci (accumulation of nuclei about the vessels, 
etc.). In a case which we examined these changes were apparently to be found in 
all the muscles, even in the tongue, the ocular muscles, etc. In genuine poly- 
myositis the peripheral nerves are perfectly normal. Yet recently there have been 
repeated observations of cases in which a genuine polyneuritis was demonstrated 
along with genuine polymyositic lesions (neuro-myositis) . These cases indicate a 
close serological relation between polymyositis and polyneuritis (q.v.). At the 
bedside the appearance of polyneuritis as a complication may be recognized by 
slight disturbances in sensation, and by tenderness along the nerve-trunks. 

The diagnosis of polymyositis is not difficult, on the whole. The pain in the 
muscles, their swelling, the impairment of motion, the inflammatory changes in 
the skin, etc., present a characteristic clinical picture. It is important to exclude 
a possible trichinosis. In this regard we must consider the aetiology, the initial 
gastro-intestinal symptoms, and the oedema of the face. [It is not yet certain 
whether eosinophilia is peculiar to the myositis occasioned by trichinae or common 
to all forms of it. — V.] That there does not seem to be any sharp dividing line 
between polymyositis and polyneuritis has been already noted. We would like 
to point out, also, that a group of symptoms very similar to polymyositis is some- 
times excited by a peculiar disease first described by Kussmaul and Maier, which 
is as yet very imperfectly understood. It attacks the small arteries and is termed 
" periarteritis nodosa." If the smaller arteries of the muscles are attacked, with 
resultant inflammation of the vascular wall, thrombosis, and similar changes, 
then degeneration of the muscular fibers ensues, with consequent swelling, pain, 
and impairment of function. At the same time there are usually severe con- 
stitutional symptoms, such as fever, anaemia, nephritis, and severe abdominal pain. 

Treatment. — In early cases of acute polymyositis trial should be made of 
salicylic acid and its compounds, antipyrine, and similar remedies; beyond this, 
treatment must be purely symptomatic, including inunctions of chloroform oil, 
the administration of narcotics, and the like. Some cases may be benefited by 
galvanism. 



CHAPTEE V 

RACHITIS 

{Rickets) 

iEtiology. — The first accurate description and the now universal name of 
" rachitis " (from pdxis, the spinal column) is to be ascribed to the Englishman 
Glisson, who published a comprehensive monograph upon this disease in 1650. It 
was his opinion that it first appeared in England, in the beginning of the seven- 
teenth century; and for this reason rachitis is still often called by Germans " the 
English disease." 

Although the clinical and anatomical phenomena of rachitis have been often 
and accurately investigated since Glisson's time, its true cause still remains en- 
tirely unknown. It is certain only that its development is promoted by all unfa- 



700 DISEASES OF THE ORGANS OF LOCOMOTION 



vorable external circumstances affecting the nourishment and health of the child.. 
It is therefore more frequent among- the poor than the wealthy, in the damp and 
crowded quarters of large cities than in the country, and among artificially fed ? . 
and therefore weakly and anaemic children, than such as receive the mother's 
milk. Nevertheless, the essential cause of the disease is not to be sought among 
these various influences, for rickets undoubtedly does occur, although rarely, in 
children whose circumstances seem in every respect most favorable. 

Guerin, Friedleben, E. Voit, Wagner, Baginsky, and many others have made 
very exhaustive experimental researches with regard to the development of 
rachitis. It has been found possible to produce certain changes in the bones of 
growing animals by giving them as little lime as possible in their ingesta, or by 
administering very large amounts of lactic acid, with the purpose of dissolving 
the calcium salts, or by giving small quantities of phosphorus. The changes thus 
caused have been, with more or less correctness, regarded as analogous to those 
of rachitis. These investigations are of great interest .with regard to the physiol- 
ogy of bony structures in general, but in our opinion they throw little light upon 
the clinical question which here concerns us. It is indeed natural enough to sup- 
pose that rachitis in childhood may be due to an insufficient proportion of lime in 
the food; or to a defective absorption of the lime-salts, on account of intestinal 
catarrh; or to an abnormally abundant production of lactic acid, or even of car- 
bonic acid, which may dissolve the lime-salts in the system; but every one of 
these theories is contradicted by the facts of experience, for it is wholly improper 
to assume that the food of children with rachitis contains less lime than the food 
of healthy children, and the hypothesis of a mere poverty in lime of the bony tis- 
sues is by no means adequate to explain the whole complicated rachitic process. 
In our opinion everything seems to indicate that some special, specific, serological 
factor is requisite for the development of rachitis. This factor, however, is as yet 
entirely unknown to us. The thought had occurred to many that the disease 
bears some relation to congenital syphilis; but this assumption has long since 
been proven to be entirely without foundation. It is also claimed that heredity 
plays an important part in rachitis. The proof of this is lacking. It is, however,,, 
noteworthy that quite often several children of the same family are attacked by 
the disease. 

Rickets is most common in children two or three years old. According to- 
Kassowitz, the disease usually begins in the first months of life, while the severe 
symptoms, of course, appear only at the age of two or three years. Congenital 
rachitic changes (foetal rachitis) have been repeatedly observed, but the cases of 
so-called rachitis tarda, where the disease is said to develop in children of eight 
or ten years of age and over, are at least extremely rare. 

Sex exercises no great influence upon the occurrence of the disease. 

Pathology. — Rachitis consists of a peculiar disturbance of the processes con- 
nected with the growth of the bones. As a result of an increased absorption of the- 
already formed bony tissue, and especially as a result of an insufficient or an 
almost wholly deficient deposition of lime-salts, the bones become or remain 
abnormally flexible and soft, so that they can easily be cut with a knife. 

Upon minute examination, we find both the periosteum and the marrow much 
reddened and congested. If we try to detach the thickened periosteum from the' 
bone, not infrequently a few bits of bone adhere to the membrane. The most 
striking changes, however, are exposed upon making a longitudinal section of the 
bone. They are located at the bases of the epiphyses, because here is the place 
where the normal, and therefore the abnormal, processes of ossification are most 
active. Under normal circumstances, the epiphyseal cartilage of the bones in 
childhood is separated from the main shaft by two narrow layers : first, an outer- 
one, nearest the epiphyseal cartilage, of a bluish color, and one or two millimetres 



EACHITIS 



701 



"thick; this is the proliferative layer, or hyperplastic zone, where the cartilage-cells 
lecome divided and arrange themselves in rows. Secondly, an inner, dnll yellow 
layer, only about half a millimetre thick, known as the ossific layer, or zone 
-of calcification, in which the real process of ossification takes place — that is, 
olood-vessels grow into it, osteoblasts develop, lime is deposited, and medullary 
-spaces are hollowed out. In healthy bone these two layers are parallel to each 
other, and are limited by perfectly straight lines. In rachitic bone, on the other 
hand, they are both much enlarged, and their naturally sharp boundaries are 
replaced by an irregular serrated edge, so that the two zones encroach mutually 
upon each other. These changes affect both layers, but are most marked in the 
proliferative layer. Upon microscopical examination, the details of which can 
not be given here, we can see most plainly the complete confusion, if we may be 
permitted to use the expression, into which the growth of the bone has fallen. 
The proliferation of the cartilage-cells has increased beyond all bounds, and the 
-scanty matrix of the cartilage displays a fibrous character. In the bony layer are 
-seen irregularly scattered foci, which are already undergoing incomplete calcifica- 
tion, or else marrow formation, breaking down the cartilage. The latter is due to 
an invasion of the vessels, which always undergo an active new growth; they per- 
meate the cartilage like lacunar spaces, and are surrounded by a so-called osteoid 
tissue. 

The periosteum presents analogous changes. The in nermost osteoblastic layer 
of the periosteum is thickened ; but the newly formed tissue does not become com- 
pletely calcified, but remains in large part soft and spongy. Finally an increased 
absorption of bone takes place inside the bones. The bony partitions disappear, 
and the cortical layer of bone often becomes much thinner than normal. 

These various processes furnish a direct explanation of the macroscopic changes 
presented by rachitic bones. The proliferative process causes marked swelling of 
the epiphyses of the long bones, and thickening of the flat bones of the skull. 
The abnormal softness of the bones is due to the increased absorption of bone, 
their insufficient calcification, and it in turn causes various deformities, which 
are, for the most part, very characteristic (vide infra). If recovery takes place, 
the whole bone becomes firm at last, but often remains permanently deformed. 

The deficient development of rachitic bones can also be recognized upon chem- 
ical examination. While normal bones in a dry state contain about sixty-three 
to sixty-five per cent, of lime, rachitic bones have only about twenty to thirty 
per cent. 

Clinical History. — Rachitis often begins so insidiously that it can hardly be 
detected. Attention is not called to the disease until the deformity of the bones 
becomes very obvious, or it is noticed that the child does not learn to walk as 
•early as other children, or, having already learned, is no longer able to do so. 
At last the anxiety of the parents is excited ; and, on seeking medical advice, they 
find their fears only too well grounded. 

In other cases the appearance of the characteristic changes in the bones is 
preceded by certain prodromes, either inflammatory symptoms, referable to the 
respiratory tract, or, what is especially frequent, signs of acute intestinal disease. 
'The child suffers from diarrhoea, has some fever, looks pale, and grows weak and 
wretched. At night he is restless, screams, bores the back of his head into the 
pillow, and evinces a tendency to excessive perspiration. Often there is a slight 
■enlargement of the spleen even at this period (Oppenheim). 

The diagnosis of rachitis can not be definitely established until the character- 
istic changes in the bones have been developed. These anomalies vary, of course, 
in their severity and extent in different cases. We append a list of the most 
important : 

The head is often noticeable for its great size and somewhat square shape, 



702 



DISEASES OE THE ORGANS OF LOCOMOTION 



due to the thickening- of the parietal and frontal eminences. In striking contrast 
with this the occiput is often thin and soft, so that it can be pressed in like parch- 
ment (Elsasser's cranio tabes). This is particularly noticeable in places near the 
lambdoidal suture. At the same time the occiput usually becomes bald, because of 
its pressure against the pillow. The fontanelles remain open till the second or 
third year of life, and their edges seem soft and yielding. There is often a pecul- 
iar change in the shape of the jaws, particularly of the lower jaw. This is not 
rounded, but angular, being sharply bent in the neighborhood of the canine teeth ; 
so that the incisors stand in a perfectly straight line, besides being somewhat 
inclined inward. Eleischmann was the first to describe this condition, and re- 
ferred it to the action of the mylohyoid and masseter muscles upon the soft bone. 
Dentition in rachitic children is usually tardy, irregular, and tedious. More- 
over, the teeth are soft and easily worn away. 

The thorax presents, even in the mildest cases, very characteristic and notice- 
able changes. There is a swelling at the junction of the cartilages with the ribs, 
which can be felt and seen through the skin, and produces what is called the 
" rosary of rickets." In severe cases the lateral portions of the thorax are often 
drawn inward, particularly at the parts which correspond with the insertion of 
the diaphragm. This change is due mainly to the action of the diaphragm during 
inspiration upon the abnormally soft and therefore yielding ribs. The changes 
are greatest when the respiratory efforts, and particularly abdominal respiration, 
are exaggerated because of bronchitis, pneumonia, or some other disease of the 
air-passages. In such cases the entrance of air into the lungs is impeded, so that 
it is possible that the external atmospheric pressure also contributes to produce 
the deformity of the thorax. Deep hollows may finally be developed on each side 
of the chest, while the sternum becomes unusually prominent, giving the whole 
chest that shape which has been termed pigeon-breast, or pectus carinatum. 
When once this deformity has been developed, of course it in turn contributes to 
render respiration difficult. 

The clavicles are sometimes distorted, and may even be partially fractured 
(vide infra). The spinal column is usually unaffected if the child remains quiet 
in bed; but if it sits up, or is carried about, or tries to walk, the traction and 
pressure thus exerted often produce curvature of the spinal column (rachitic scoli- 
osis and kyphosis). These deformities may become extreme. Changes in the 
bones of the pelvis are of no special clinical importance at this period of the 
patient's life; but in women the consequent shortening of the antero-posterior 
diameter of the pelvis may, as is well known, prove a great obstacle to childbirth. 

The extremities not only present swelling of the epiphyses, but are liable to 
curvature. This latter change is most marked in the lower limbs, inasmuch as 
they have to support the weight of the body. The swelling is especially well 
developed at the lower ends of the bones of the forearm and of the tibia and fibula. 
The curvature is almost invariably greatest, and therefore most easily recognized, 
in the tibia, which becomes convex outward, giving the rachitic child its " bow- 
legs." Similar curvature of the femur is less often seen, although it may be 
obvious enough in severe cases. The same is true of the humerus. The deformity 
of the lower limbs causes that waddling gait which can be so often seen on the 
streets of any large city. Sometimes the limbs present a sharp bend, the result of 
partial fracture. These " green-stick fractures of rachitis " are invariably refer- 
able to some slight traumatism, and are most often seen in the lower third of the 
tibia, although sometimes visible in the clavicles, ribs, and bones of the lower arm. 
The infraction usually takes place upon one — generally the concave — side, so that 
it is often compared to the partial fracture of a quill or an osier rod. 

Symptoms in Other Parts of the Body. — Apart from the changes in the bones, 
a rachitic child may seem to be perfectly well. Even the general nutrition may 



EACHITIS 



703 



be unimpaired. As a rule, however, rickets is associated with anaemia and im- 
paired nutrition. The muscles, in particular, are small and flabby. The child 
seems pale, thin, and feeble, and may present swollen lymph-glands and other 
" scrofulous " symptoms. Sometimes there is a tendency to profuse perspiration, 
especially from the scalp. Very frequently there is chronic intestinal catarrh, 
and sometimes there is chronic bronchitis or lobular pneumonia. The abdomen 
is usually prominent, the liver and spleen are frequently, but not invariably, en- 
larged. The reader should also be reminded that rachitic children are particularly 
liable to spasm of the glottis (laryngismus stridulus) and convulsions, due per- 
haps to the rachitic lesions of the skull. 

The fasces and urine have been repeatedly subjected to careful chemical inves- 
tigation in the hope of gaining some information as to the pathogenesis of the 
disease. The results have been, however, in many respects, contradictory; the 
most accurate of these investigations have shown that the absorption and excre- 
tion of the calcium salts ingested with the food are not much different in healthy 
and in rachitic children. 

The disease almost invariably runs a chronic course. Usually months, or even 
years, pass before the process ends. Its termination is to be recognized by closure 
of the f ontanelles, increase in the length of the bones, and, above all, by the fact 
that the patient becomes stronger and makes attempts to walk. Unfortunately, 
many results of the disease persist through life. The legs are crooked, the thorax 
deformed, the spinal column curved, and the pelvis narrowed. Even in the most 
favorable cases persons who have once had rachitis usually remain somewhat 
smaller than those who are perfectly healthy. 

Some authorities describe an " acute rachitis," in which painful swelling of the 
epiphyses is said to be developed in the course of a few weeks. At the same time 
the child becomes emaciated, and it may also suffer from diarrhoea or ulcerative 
stomatitis. Recovery takes place in a few months. How far cases of this sort are 
related to genuine rickets has not yet been determined. 

Rachitis does not involve direct danger to life, although many rachitic chil- 
dren fall victims to the attendant intestinal catarrh, or to such complications as 
catarrhal pneumonia or tuberculosis. The prognosis is, therefore, not unfavorable 
when the worldly circumstances of the child permit of good care and nourish- 
ment. The remote influences of the thoracic, spinal, and pelvic deformities can 
be readily inferred. 

The diagnosis of rachitis is but seldom difficult if the characteristic changes in 
the bones exist. In case cranial changes have occurred, we should guard against 
confounding rickets with hydrocephalus, but we can usually avoid error. The 
rachitic child holds its head erect, and is free from mental or other functional 
nervous disturbances. 

Treatment. — The most experienced specialists agree that the first aim in treat- 
ing most cases of rachitis is to improve the general nutrition. It is often possible 
to bring about recovery simply by means of proper diet (milk, the yolk of eggs, 
and perhaps meat), good air (in the country), and baths (brine, malt, and medi- 
cated baths). Digestive disturbances should be corrected by such remedies as 
hydrochloric acid or tincture of rhubarb ; and iron should be administered if the 
patient be anaemic. 

It is very important that the child should be placed upon a good mattress, and 
should neither attempt to walk too early, nor be needlessly taken up and carried 
about. The best way to avoid the development of deformities in the bones is to 
avoid all such unfavorable mechanical influences. 

Attempts have also been made to check the disease by specific remedies. Upon 
doubtful theoretical grounds, lime has been very frequently prescribed, in the 
form of phosphate of calcium, of which fifteen to forty-five grains may be given in 



704: 



DISEASES OE THE ORGANS OF LOCOMOTION 



powder several times a day ; or in the form of lime-water, of which, one or two tea- 
spoonfuls are added to the milk which the child drinks. The benefit of these reme- 
dies is seldom very obvious. Kassowitz has given a fresh impetus to the employ- 
ment of phosphorus. To support his belief he brings forward numerous clinical 
observations, as well as facts obtained from experiment. We may either dissolve 
the phosphorus in cod-liver oil (0.01-100), giving one or two small teaspoonfuls of 
this solution every day, or we may write for the following mixture, which is more 
elegant, but is also more apt to spoil : 



I£ Phosphori 0.01; 

Olei amygdala? expressi 10.0. 

Misce, deinde adde: 

Pulv. acacise, 

Syrupi simplicis aa 5.0; 

Aquae destillatse 80.0. 

M. Sig. : Two to four small teaspoonfuls a day. 



We can state from our own experience that the remedy is usually very well borne, 
and, in fact, often shows its beneficial action after a few weeks, the fontanelles 
growing smaller and the bones becoming firm. Yet there are cases in which phos- 
phorus does not seem to do any good. 

It may be eventually necessary to resort to orthopaedic or surgical treatment 
in order to correct the deformities of the bones. 

[The comparative rarity of rickets, especially in its extreme degrees, in this 
■country strikes all observers who have studied in Germany. With a fairly exten- 
sive experience among the poorer classes of the city, the writer can recall scarcely 
half a dozen cases of craniotabes. The colored race furnishes a large contingent 
■of cases of rickets, although, as is shown by Haven, in attention to diet and fresh 
air its members are superior to the Irish laboring classes, as a rule. The more 
pure the negro blood, the greater does the liability to rickets seem to be in this 
latitude — an indication, perhaps, that a northern climate is unsuitable to the 
African race.] 



\ 

CHAPTER VI 
OSTEOMALACIA 

^Etiology and Pathology. — Osteomalacia does not, like rachitis, consist in a 
-disturbance of development. The growing bones are not prevented from ossifying, 
Dut, having already undergone normal development and acquired normal firmness, 
they afterward become soft. It is mainly a disease of adults, occurring between 
thirty and forty years * of age, but sometimes earlier. The female sex is notice- 
ably predisposed to the disease, although occasionally it has been observed in men. 

The true cause of osteomalacia has not yet been ascertained. It is a remark- 
able fact that the disease is much more frequent in certain regions than in others. 
Tt is very common along the Rhine, and in Westphalia, in eastern Flanders, and 
northern Italy. This suggests that there is some specific cause for the disease, 
■endemic in certain localities. Among exciting causes, child-bearing is certainly 
the most important, for both the first signs of osteomalacia, and also fresh exacer- 



* Eehn maintains that genuine osteomalacia may occur in children ; but his statement has not yet 
been fully corroborated. 



OSTEOMALACIA 



705 



bations of the disease, usually date from a pregnancy. There is no doubt, how- 
ever, that occasionally a case of osteomalacia occurs in a woman who has never 
had children. In such instances the appearance of menstruation seems invariably 
to have an unfavorable influence upon the disease. In brief, the relations of osteo- 
malacia to the sexual processes are so close that there is some justification for the 
supposition that osteomalacia is directly dependent for its development upon dis- 
turbances of metabolism in the ovaries. Moreover, certain therapeutic experi- 
ences (vide infra) can well be reconciled with this assumption. It should also be 
mentioned that unfavorable hygienic surroundings, damp houses, and the like, 
promote the development of the disease. 

The anatomical process of osteomalacia consists of a disappearance of the 
earthy salts of the bone, which begins interiorly and spreads outward, and causes 
a corresponding softening of the bony structure. The marrow is at first extremely 
hypersemic;- and extravasations of blood are not infrequently found here and 
there. The bony substance surrounding the myeloid spaces and the Haversian 
canals becomes transformed into a soft fibrous tissue, while the irregularly 
arranged bone-corpuscles either are destroyed or lose their characteristic shape. 
The softening process gradually extends from the spongy substance outward to the 
cortex. The central cavity grows larger and larger, so that finally the cortical 
substance is as thin as paper, and the whole bone like an " inflated and dried coil 
of intestine." At this stage the original hyperemia of the marrow has vanished. 
The marrow acquires a yellow color, and may finally be entirely transformed into 
a yellow, viscid fluid. The affected bones are now flexible and soft, they can be 
easily cut, and they are of less specific gravity than normal. The periosteum is 
also at first thickened and hypersemic, as if inflamed. When it is removed, the 
surface of the bone beneath it is found to be rough and uneven. The attendant 
alterations in the shape of the bones which can be seen during life will be men- 
tioned below. 

Upon chemical examination of the bones in osteomalacia, we naturally find a 
marked diminution in the proportion of lime-salts. It is also stated that lactic 
acid has been discovered in the bones. This is an interesting fact, as it may be 
that the acid plays an important chemical part in the process of decalcification. 

Clinical History. — Osteomalacia begins very gradually in most cases. Usually 
the first thing noticed is an ill-defined, deep-seated pain, most often felt in the 
sacral region, the nape of the neck, and the back and thighs. The affected parts 
are also sensitive upon pressure. 

The pain is persistent. While it still keeps on, motion becomes gradually 
impaired. The patient experiences more and more difficulty in walking, partly 
because of the pain and partly because of muscular weakness. The gait is either 
uncertain and slow, or characterized by short painful steps, the lower limb and 
the pelvis being jerked forward as if in one piece. This peculiar gait in which, 
with every short, hobbling step, the body makes a slight twist inward, is so char- 
acteristic that often the disease may be immediately recognized by this alone. In 
other instances the gait is more waddling. After a shorter or longer time walking 
becomes absolutely impossible, and the patient is permanently bedridden. Even 
then severe pain persists in most cases. It is not precisely spontaneous, but is 
produced by the mere pressure of the mattress or the bed-clothes, and similar 
causes. 

In the meanwhile, there has probably been distortion of many of the bones, 
sufficient to occasion a decided alteration in the appearance of the skeleton. Usu- 
ally the first to be noticed is the deformity of the spinal column (see Fig. 78). 
As a rule, there is kyphosis, less often some other deformity, and the head gen- 
erally becomes more and more bent forward upon the sternum. As a result, the 
patient grows decidedly shorter, and this very shortening may be an important 
45 



706 DISEASES OF THE OKGAXS OF LOCOMOTION 




-j 



factor in diagnosis. The sick woman is apt to remark it, because she has to keep 
shortening- her gown in front. The thorax, also, is apt to be much distorted in 
severe cases. It is compressed laterally, while the sternum becomes very promi- 
nent, and is sharply bent. The change in the shape of the pelvis in osteomalacia 

is less obvious externally, but it can be detected on 
internal examination. It is, of course, of great 
importance from an obstetrical point of view. The 
pelvis, like the chest, is compressed laterally, while 
the symphysis is made to project forward like a 
beak. The sacrum and its promontory are also 
pushed forward, and the superior strait thus ac- 
quires somewhat of a heart shape. This change 
in the pelvis is apt to appear very early. It is 
probably the chief cause of the peculiar gait (vide 
supra). 

The extremities are less often distorted, par- 
ticularly if the patient becomes bed-ridden at an 
early period. Manifold changes are, however, 
possible. Sometimes there is also fracture. In a 
few reported cases the softness of the bones of 
the extremities was so extreme that one could bend 
the limbs at will, like wax, and give them the most 
extraordinary positions. In cases so far advanced 
as these, the pain in the bones seems finally to 
cease. The bones of the head and face seldom un- 
dergo noticeable change, but we often find that the 
teeth are carious or lost. In the muscles, several 
observers have noticed trembling and fibrillary 
contractions, also paresis and complete paralysis. 
It is also said that sometimes even a slight irrita- 
tation of the skin suffices to excite painful con- 
tractions of the underlying muscles. These phe- 
nomena have not yet been thoroughly investi- 
gated. 

The general condition of the patient is often 
unimpaired for a long while, except for the pain 
and the impairment of motion. The internal 
organs perform their functions in a normal man- 
ner, and the appetite is good. Fever is observed 
only when the disease is undergoing some tem- 
porary exacerbation. With regard to changes 
in the urine, there have been a good many 
statements made, but their significance is extremely doubtful. It is said that 
the amount of phosphoric acid excreted is diminished. With regard to the 
amount of lime, no definite statement can be made. Lactic acid has been 
repeatedly detected in the urine, as has also albumen. Concretions of lime have 
been found in the bladder and the kidneys. 

The disease runs a chronic course, occupying seldom less than two or three 
years, and sometimes even five to ten or even longer. Apparent improvement is 
not infrequently observed, but this is followed by fresh exacerbations, especially 
after confinement. The most frequent termination is in death. This results 
either from general debility, or, more often still, from the dyspnoea caused by the 
compression of the lungs, or by some such disease as lobular pneumonia. In milder 
cases, however, particularly if they receive prompt and suitable attention, there 




Fig. 78. -Puerperal osteomalacia. 
(Erlangen Medical Clinique.) 



OSTEOMALACIA 



707 



may be complete recovery ; or in severe cases, even if deformity has occurred, there 
may be, at any rate, a permanent cessation of the disease. 

Diagnosis. — In well-developed cases it is not difficult to recognize the disease, 
but at first a correct diagnosis is often impossible, unless the endemic frequency 
of osteomalacia suggests it. In the onset of the disease we may often be led to the 
false belief that there is incipient disease of the cord or the vertebrae. We our- 
selves, as well as other observers, have repeatedly seen cases in which women as a 
sequel to pregnancy, or even apparently spontaneously, have developed paresis in 
the lower extremities, particularly in the psoas and iliacus muscles, associated with 
pain and exaggerated tendon reflex, and in which diagnosis at first was very diffi- 
cult. Xot very infrequently the complaint of the patient at the start was re- 
garded as hysterical. Later, the peculiar hobbling and waddling gait (" like a 
duck") would suggest the possibility of osteomalacia, and this diagnosis would 
be established by the results of a careful examination of the pelvis. At any rate, 
it is important to know that even before there are demonstrable changes in the 
bones, there may be paralysis, probably referable to an early involvement of the 
muscles in the morbid process. As the disease is almost entirely confined to 
adults, we are seldom in danger of confounding it with rachitis. Besides, osteo- 
malacia does not produce swelling of the epiphyses, nor changes in the bones of 
the skull. It is said that osteomalacia is occasionally confounded with diffuse 
carcinosis of the bones, as this may produce similar symptoms and deformities. 

Treatment. — As has been already implied, therapeutic efforts have thus far 
proved in severe cases 'almost unavailing in this disease. In the onset of the dis- 
ease we can obtain a distinct improvement by the use of hygienic remedies, good 
air, proper food, etc. Internally we give cod-liver oil and also iron. Many pa- 
tients praise warm baths, with or without salt. The exhibition of lime seems to be 
of no special use. On the other hand, personal experience leads us earnestly to 
recommend a trial of small doses of phosphorus, either in the form of phosphorized 
cod-liver oil (vide supra), or in pills of one sixtieth of a grain (gramme 0.001) 
several times a day. Particularly in the above-mentioned forms of incipient 
osteomalacia with paresis of the legs, and even also in cases with distinct changes 
in the pelvis already developed, we have seen, repeatedly, striking benefit from 
treatment with phosphorus. Yet sometimes even this remedy proves disap- 
pointing. 

The changes in the bony pelvis produced by osteomalacia may eventually 
demand obstetrical interference, but we need not discuss such procedures here. 
We should invariably warn women who suffer from the disease of the dangers of 
becoming pregnant. Recently, therefore, castration has been repeatedly per- 
formed in cases in which an aggravation of the disease was invariably associated 
with fresh pregnancies. ITnder these circumstances, it has been shown that the 
removal of the ovaries has resulted in a remarkably rapid recovery from the dis- 
ease, a fact which suggests an intimate connection between the processes in the 
ovaries and the symptoms of osteomalacia (vide supra). Certainly, these rela- 
tions should receive the greatest consideration in the future. 



DISEASES AFFECTING THE BLOOD AND 
TISSUE-METAMORPHOSIS 



{CONSTITUTIONAL DISEASES) 



CHAPTER I 

ANAEMIA AND CHLOROSIS 

1. General Preliminary Remarks as to the Classification and -Etiology of 
the Various Forms of Angemia. — The word "anaemia" (or, more strictly, oli- 
gemia) might properly be taken to signify diminution of the total volume of the 
blood, such as, for example, is directly brought about by a severe haemorrhage. 
Usually, however, the word is employed to signify not so much diminution in 
quantity as deterioration in quality. The total volume of the blood is not liable 
to nearly so great variations as is the number of its most important constituents 
— the red corpuscles — inasmuch as the total volume is dependent merely upon the 
amount of watery constituents, and even after large haemorrhages the water is 
quite rapidly replaced by absorption. This is undoubtedly the case in most in- 
stances of sudden loss of blood. Even in chronic anaemia there is usually no rea- 
son to assume that the total amount of blood is diminished, although it may be 
when there is general emaciation, or diminished supply of liquids (persistent 
vomiting, dysphagia), or large watery discharges (as in cholera). The essential 
element in anaemia is, therefore, a diminution in the number of the red blood- 
corpuscles, or so-called oligocythemia. Changes in the character of the red 
blood-corpuscles are not taken into consideration here. On the other hand, how- 
ever, we shall see later that, even in spite of a normal number of red blood-cor- 
puscles, their abnormal condition, particularly their poverty in haemoglobin, may 
lead to well-marked " anaemic " conditions. 

The circumstances under which anaemia is observed ' are manifold. They 
admit, however, of our distinguishing two great classes of anaemia — primary 
and secondary. Primary anaemia is developed as an apparently primary and 
idiopathic disease in persons previously healthy, while secondary anaemia is 
merely a symptom of some already existing disease. However simple this theoret- 
ical distinction, yet in actual practice it is often quite difficult to determine 
whether the particular case before us should be regarded as primary or secondary. 
A secondary anaemia may occur where the true primary cause can not be at all 
readily determined. There are, nevertheless, quite a large number of cases which 
would seem to deserve the name of primary or essential, in which we feel com- 
pelled to assume that some pathogenic influence acts directly upon the blood and 
the haematopoietic processes. 
708 



ANEMIA AND CHLOKOSIS 



709 



In the first place, we would class as primary, cases which may best be described 
as " simple constitutional anaemia." These often stand close to the borderland 
between health and disease. There are not a few individuals who present a strik- 
ing pallor for a large part, if not all, of their lives. These persons may feel so 
well and vigorous that we scarcely have a right to regard the existent anaemia 
(usually moderate) as an actual disease. Sometimes, however, such individuals 
do betray some diminution of energy, are easily fatigued, and are subject to head- 
ache. We may then regard the conditions as certainly pathological. In many 
instances the cause of this simple anaemia is found in the general hygienic sur- 
roundings of the patient, for such cases are most often met with among the poorer 
classes. Deficient nutrition, bad air, unhealthy occupation in factories or the 
like, not only affect the general health, but more especially interfere with the 
processes of normal blood-making. Other cases of constitutional anaemia, appar- 
ently primary, occur in individuals who are entirely beyond the reach of such 
influences as have just been mentioned, in whom the anaemia has developed and 
persists despite the best of food and air. Here we are forced to the conclusion 
that the organs engaged in the manufacture of the blood are in some way pre- 
vented from performing their proper functions. The trouble often seems to be 
congenital, for such individuals may present the symptoms of anaemia in their 
earliest infancy. There are persons who have always been pale and feeble. Or, 
again, anaemia does not develop urjtil later on, in which case it not infrequently 
associates itself with certain phases of physiological development, as when growth 
is particularly rapid, or when adolescence occurs. Yirchow has directed atten- 
tion to another factor, which he regards as potent in many of these cases of con- 
genital anaemia. He has found that the arteries may be congenitally small, or 
that the whole arterial system may be imperfectly developed. The condition may 
be associated with a congenitally weak and small heart. The importance of this 
factor has not yet been fully determined. Possibly the condition of the circula- 
tory system just mentioned may be the result rather than the cause of the anaemia. 

A second division of primary anaemia includes cases which present a far more 
definite and distinct group of symptoms. They quite often appear in persons pre- 
viously healthy, last for a certain length of time, and then end in complete recov- 
ery. The typical form of this variety is chlorosis (x^«pos = greenish yellow), or 
" green sickness." This well-known disease is especially frequent in young girls 
fourteen to twenty years of age — that is, at puberty. It often comes on quite rap- 
idly without any ascertainable cause. There are not infrequently predisposing 
influences in the outward circumstances of the patient, Thus it is promoted by 
an unhealthy sedentary mode of life, as in seamstresses ; bad air, as in factory 
operatives; mental and physical over-exertion, as in teachers, governesses, and 
students; and, finally, by mental influences (excitement, etc.). It is, neverthe- 
less, true that chlorosis also appears in girls who have lived under the most favor- 
able hygienic conditions possible. Sometimes the disease seems to be merely a 
temporary exacerbation of a simple constitutional anaemia which has existed a 
long time; but it may also appear in young women who have been previously 
healthy, and even robust. 

The true cause of chlorosis is unknown. Perhaps the interesting investiga- 
tions of Bunge with regard to the amount of iron in milk and in new-born ani- 
mals afford at least a starting-point for some future theory as to chlorosis. Bunge 
found that the constituents of the ash of milk, and the constituents of the total 
ashes of young suckling animals, correspond precisely in their proportions. The 
suckling animal, therefore, receives with his mother's milk all the salts that are 
needed for his body, in a proper amount — the single exception being the iron 
compounds. The amount of iron in milk is very small compared with the amount 
of iron in the suckling. Indeed, the proportion of iron in the new-born animal is 



no 



CONSTITUTIONAL DISEASES 



decidedly large, but it diminishes gradually as the creature develops. This in- 
dicates that the animal comes into the world with a supply of iron, which can 
originate only in the maternal organism; and in the first part of his life, so 
long as he has milk for his exclusive nourishment, he draws upon this supply. 
If, therefore, we consider that it is a function of the female organism in some 
way to store up iron for the next generation, there might be some disturbance 
of this function, either an imperfect assimilation or an abnormal conversion of 
the assimilated iron, and this might very likely rob the blood of haemoglobine. 
It must be confessed that as yet we have no thorough understanding at all of 
the internal processes of metabolism which relate to the matter. Still, the 
facts and conditions which we have mentioned explain to a certain degree the 
fact that genuine chlorosis is found exclusively in the female sex and, indeed, 
precisely at the time of puberty — -i. e., the time of preparation for the sexual life. 
Perhaps, also, the fact that disturbances of menstruation are so frequent in asso- 
ciation with chlorosis is connected with the conditions above mentioned, but it 
is also possible that the menstrual disturbances may be a result of chlorosis. 

A third form of primary essential anaemia is the so-called pernicious anaemia. 
This, likewise, appears independently of other diseases, and is characterized by 
its steady progress, as a rule leading finally to death. We do not regard pernicious 
anaemia as a very severe form of chlorosis, but as an entirely separate disease. 
It is distinguished from chlorosis not merely by the much more definite morpho- 
logical changes in the blood, but still more by the circumstance that it is not con- 
fined to women, but appears also in men, both in early and advanced life. Cases 
of " severe essential anaemia " also have many points in common with certain other 
diseases, such as pseudo-leukaemia and splenic anaemia. These will be discussed 
later. 

The forms of secondary anaemia offer a contrast to the forms of primary or 
essential anaemia just described in the much greater number of their causes. 
Under this head come cases of anaemia which do not occur idiopathically, but as 
a result of other abnormal processes. The simplest variety is anaemia from 
haemorrhage. This is produced by profuse loss of blood, whether from the stom- 
ach, lungs, uterus, intestines, kidneys, or some wound. Repeated small haemor- 
rhages finally produce the same result as a single large one. Thus the most pro- 
found anaemia may be observed where there is a very frequent epistaxis (haemor- 
rhagic diathesis, contracted kidney), 'or where cancer of the womb gives rise to a 
constant oozing of blood. 

Other cases of secondary anaemia may be divided into two great groups. In 
one class the anaemia is a symptom of impaired nutrition. This is seen in almost 
every severe disease, acute or chronic, and is usually associated with more or less 
emaciation and loss of strength. The bad appetite, the lack of fresh air and exer- 
cise, and perhaps an impairment of digestion, or fever, or some abnormal drain 
upon the system, as in suppuration — these injure the entire body. It is not sur- 
prising that the blood shares in the universal misfortune. This is why most 
chronic invalids seem pale, particularly if they suffer from disease of the stomach, 
kidneys, chest, or nervous system. In the second class, the anaemia is secondary 
to some other disease, but assumes especial prominence as a symptom, independ- 
ently of any general impairment of nutrition. Of course, it is often associated 
with emaciation, but nevertheless its extraordinary intensity offers a striking con- 
trast to the condition of the rest of the body. This " specific secondary anaemia " 
must, like essential anaemia, be due to a special lesion of the blood itself, and is, 
therefore, to be regarded as in a certain sense a special complication or localiza- 
tion of the primary disease. General malnutrition never produces anaemia of 
this grade directly. This fact is illustrated in stenosis of the oesophagus. Here 
the ingestion of food is very greatly, if not completely, hindered, and there is 



ANiEMIA AND CHLOROSIS 



711 



the greatest emaciation, with a subnormal temperature and slow pulse. Of course, 
such a patient appears pale and wretched, but he does not present that peculiar 
waxy pallor which is the sign of genuine anaemia. 

The exact mode of origin of specific secondary anaemia is often obscure. We 
Jiave already reported, in a preceding chapter, a very instructive example. In 
cancer of the stomach we find usually emaciation and pallor. This is natural 
enough; but sometimes the carcinoma is complicated by an extraordinarily pro- 
found anaemia, comparable only to the pernicious variety. In one such case we 
found, at the autopsy, an extensive secondary carcinosis of the bone-marrow. 
Here, therefore, the anaemia certainly was not the result merely of the general im- 
pairment of nutrition occasioned by the gastric carcinoma, but of the disease of 
the marrow, which tissue undoubtedly plays an important part in the manufac- 
ture of the blood. 

Some cases of specific secondary anaemia deserve special mention, although it 
is seldom possible to demonstrate their precise cause. In the first place come such 
cases as develop after certain acute diseases, usually of an infectious character. 
Tor example, there may be great anaemia after typhoid fever, or less often after 
acute articular rheumatism. A peculiar form of anaemia is often observed during 
the secondary stage of syphilis, although nutrition seems to be otherwise well 
maintained. This is known as " syphilitic chlorosis." Tuberculosis, chronic 
malarial poisoning, chronic septic infection, and other forms of chronic poisoning 
(lead), as well as amyloid disease, renal disease, etc., may also be attended by 
anaemia of such intensity as to justify the conclusion that there is some special 
disturbance of secondary origin affecting the manufacture of the blood or the blood 
itself. Of great importance is the striking anaemia which occurs in association 
with many intestinal parasites (vide supra, page 512 et seq.), sometimes as a re- 
sult of actual loss of blood, but probably more often because of the action upon 
the blood of certain poisons generated by the entozoa. 

[Chronic arsenical poisoning from wall papers, dress fabrics, furniture cover- 
ing, and the like, is a not infrequent cause of anaemia and debility, which resists 
treatment as long as the exposure to the toxic influence lasts. The classical 
symptoms of chronic arsenical poisoning are not necessarily present. The num- 
ber of cases in which prompt recovery has taken place after the removal of the 
poison which was proved to exist in the surroundings as well as in the urine of the 
patient is too large and too striking to explain by simple coincidence. Recovery 
may, however, be slow in those whose toleration of arsenic is slight, or in whom 
the cause of the symptoms has remained long undetected.] 

We shall now proceed to describe the symptoms directly dependent upon the 
anaemia, and therefore common to all its forms. Upon this will follow a sketch of 
chlorosis. A special chapter is assigned to the grave form of essential anaemia 
known as progressive pernicious anaemia ; and in the same connection will be set 
forth the little that is known with regard to the relations of anaemia to patho- 
logical changes in the haematopoietic organs. 

2. Symptomatology of Anaemia. — The first symptom which attracts the at- 
tention of the physician in any case of anaemia is the altered appearance, the 
pallor of the skin and visible mucous membranes. This is especially striking in 
the face, but it is sufficiently evident everywhere. Special value is usually as- 
signed to pallor of the mucous membranes, for example, of the lips and conjunc- 
tivae, inasmuch as their color is not liable to be interfered with by pigmentation 
-or opacity of the epidermis. The degree of pallor, of course, varies greatly. The 
whole body may present a waxy appearance. A pallor of this kind implies, of 
course, a very considerable diminution in the amount of coloring matter in the 
"blood — that is, of hsemoglobine. The diminution of haemoglobine in simple anae- 
:mia is usually a direct result of diminution in the number of red blood-corpuscles, 



712 



CONSTITUTIONAL DISEASES 



each one remaining normal ; but the red corpuscles themselves may show a dimi- 
nution in the amount of haemoglobine, although their number is normal. In order 
to determine these important facts we must in every case of decided anaemia find 
out not merely the relative number of blood-corpuscles — i. e., the number of blood- 
corpuscles in a cubic millimetre of blood — but also the proportion of haemoglobine 
in the blood (the simplest way being by the well-known methods of Gowers and 
Fleischl), and compare the two. 

Besides the alteration in complexion, there is always a group of symptoms ref- 
erable ultimately to an impairment of the normal processes of innervation result- 
ing from a lack of arterial blood. First among these phenomena comes general 
weakness of the motor system. The voluntary muscles are easily fatigued, and 
the patient suffers from constant languor. When the anaemia is very great, as 
after severe haemorrhage, this weakness may be so pronounced that the patient 
can neither walk nor stand; but even in moderate anaemia there is more or less 
impairment of strength. 

This diminished nervous energy is shown also by the mental condition. There 
is no intellectual vigor. The patient is incapable of any great mental exertion, 
and experiences a constant feeling of weariness and sleepiness. In cases of severe 
anaemia there is not infrequently a decided tendency to faintness, or actual syn- 
cope, as the result of cerebral anaemia. — It is very common to have such subjective 
symptoms as impaired vision, specks before the eyes, and pain in the eyes. In 
occasional instances, particularly after a great loss of blood (for example, after 
haematemesis), total amaurosis develops. Examination with the ophthalmoscope 
shows nothing abnormal, beyond the anaemia of the retina. — Impairment of hear- 
ing is exceptional ; on the other hand, there is often great annoyance from marked 
tinnitus aurium, which of course is due to the irritated condition of the auditory 
nerve, or perhaps also of the auditory center. 

The processes of secretion are much less affected. It is true that there is often 
dryness of the tongue and mouth, but this is mainly subsequent to the loss of 
large amounts of blood, and probably, therefore, is occasioned less by a diminution 
in the activity of the mucous and salivary glands than by the desiccation of the 
tissues. As relates to other secretory functions, the only one which has been care- 
fully investigated is the formation of gastric juice. The earlier experiments on 
animals caused the opinion to be held for a long while that in anaemia the propor- 
tion of hydrochloric acid in the gastric juice was diminished. Numerous more 
recent experiments, however, have shown that this assumption is subject to excep- 
tions. Although the amount of hydrochloric acid in the gastric juice may be 
small in anaemia and chlorosis, and although there may be complete absence of free 
hydrochloric acid in the gastric juice; yet, on the other hand, it is a very fre- 
quent experience to find a fully normal or even excessive amount of hydrochloric 
acid ; nor are the motor functions of the stomach, as a rule, disturbed ; but it may 
be that the constipation which is so often present in anaemia is, at least in part,, 
connected with an impairment of the energy of intestinal peristalsis. 

The symptoms thus far described are referable partly to diminished functional 
activity. On the other hand, anaemia gives rise to certain symptoms of irritation 
in the nervous system. These are, in all probability, expressive of the irritation 
excited in certain portions of the nervous system by the products of abnormal 
metabolism, perhaps due to incomplete oxidation. Some of these symptoms, such 
as the annoying tinnitus, the specks before the eyes, and the vertigo, have been 
already mentioned. We should also note especially eructations and vomiting as 
anaemic symptoms; these are in most cases of central origin, and in severe anae- 
mia they may be very annoying. In the same way may be explained the occasional 
occurrence of annoying hiccough, the frequent spasmodic yawning, and similar 
symptoms. Anaemic headache may be very severe. It is usually referred either 



ANEMIA AND CHLOEOSIS 



713 



to the entire head or to the forehead ; there is a painful feeling of pressure, which 
may attain great severity. 

Other important evidences of irritation are to be found in the behavior of the 
pulse and the respiration. The changes here are apparently in part of a compen- 
satory character. The pulse is accelerated in most cases of any severity, reaching 
80 to 100 beats per minute, or even more. It is also very excitable, so that com- 
paratively slight external influences suffice to increase its rapidity for the time 
being. This increase in frequency would not, of course, necessitate an increase of 
intra-vascular tension, or of the rapidity of the circulation; but it may exert a 
favorable influence in this direction, and so be compensatory. Respiration also is 
usually accelerated in anaemia. In cases of great severity the breathing may be so 
deep and noisy as to justify the term " anaemic dyspnoea." This is the direct ex- 
pression of the body's hunger for oxygen. It is obvious that this increase in the 
number of respirations favors, to a certain extent, the absorption of that gas. 

There are still other symptoms referable to the circulatory system. It has 
been already stated that the total volume of the blood is not diminished in anaemia 
unless, of course, there has just been an actual haemorrhage. This explains why 
the pulse in ansemia is often comparatively full and strong. Quite frequently 
there is a peculiar quickness of the pulse. This seems to be due to a vigorous 
cardiac systole, in conjunction with a low intra-arterial tension. Akin to these 
phenomena is the fact that in severe anaemia it is not exceptional to hear a dis- 
tinct pistol-shot sound in the femoral artery, or, in rare cases, even a distinct 
double sound, just as in aortic insufficiency. 

It has long been known that anaemia may produce functional cardiac mur- 
murs, often called " anaemic murmurs." Their mode of origin is not yet fully 
explained. They are usually heard loudest over the base of the heart, in the 
neighborhood of the pulmonary valves, and at the apex of the heart. As a rule, 
they are purely systolic in time, but we certainly heard in one case of pernicious 
anaemia a loud diastolic murmur of anaemic origin. The murmurs are of a blow- 
ing character. Sometimes they are so rough as to simulate pericardial friction- 
murmurs ; it has therefore been suggested that many anaemic murmurs are ac- 
tually due to the rubbing upon each other of the abnormally dry folds of the peri- 
cardial sac. Another explanation of their occurrence is, that the movements of the 
cardiac valves are interfered with, as a result, perhaps, of fatty degeneration of the 
myocardium (vide infra). It is also possible that there may be sometimes relative 
insufficiency of the valves — e. g., due to dilatation of the heart or to imperfect 
action of the papillary muscles. Still, the question has not yet been settled 
whether genuine dilatation of the heart is at all frequent in anaemia. Increase in 
the cardiac dullness is observed, but it is due mainly to retraction of the lungs. 

Murmurs in the large veins of the neck are very often heard in anaemia, either 
with or without cardiac murmurs. They are often called bruit de diable. No 
less an authority than A. Weil has maintained that murmurs in the jugular veins 
are just as frequent in healthy persons as in the anaemic; but our experience 
compels us to differ from this view. We believe that the loud venous murmurs are 
more frequent in the anaemic than in other persons, so that they possess a certain 
diagnostic value. 

The processes of metabolism in profound anaemia are of great interest, but, un- 
fortunately, they have not yet been thoroughly investigated. A priori, we should 
expect that the absorption of oxygen would be diminished in severe anaemia ; but 
it has not yet been possible to confirm this surmise, at least in the cases of medium 
severity, doubtless because the compensatory acceleration of the respiration and 
pulse (vide supra) equalizes matters. Whether, even in severe anaemia, there 
is any diminution in the absorption of oxygen, has not yet been proved ; yet many 
facts seem to favor this idea. One is that in severe anaemia there is usually a 



714 



CONSTITUTIONAL DISEASES 



somewhat increased destruction of albumen, as compared with the amount of nour- 
ishment ingested. This can be recognized by the increase in the excretion of nitro- 
gen in the urine. This circumstance, which accords with the results of experi- 
ments as to the consequences of a diminution in the supply of oxygen, assumes the 
more importance if we associate it with certain anatomical results of anaemia, 
there being almost always a marked fatty degeneration of many organs, particu- 
larly the heart and kidneys. This fatty degeneration is the direct result of the 
abnormal destruction of albuminoid structures. The fat represents the non-nitro- 
genous remnants of the decomposed albuminoids. The reason the fat itself does 
not undergo oxidation is the lack of oxygen. It is perhaps for the same reason 
that the panniculus adiposus is for a long while preserved in many cases of 
ansemia. 

It is evident that the fatty degeneration once produced must, in its turn, lead 
to unfavorable results. It has already been suggested that the fatty degeneration 
of the heart may be the cause of certain irregularities in its functional activity; 
but it should be said that this is not invariably the case, for often the heart 
exhibits a surprising energy despite marked fatty degeneration of its muscular 
tissue. The corresponding changes in the walls of the blood-vessels are, how- 
ever, of great importance, as they frequently occasion disturbance, above all by 
haemorrhage. In many instances (for example, in leukaemia, vide infra) an 
actual hemorrhagic diathesis is developed; but we shall find later (see the chapter 
on pernicious anaemia) that other factors may also play a part in producing capil- 
lary haemorrhages in severe anaemia. There is strong evidence in many cases of 
an abnormal permeability of the vascular walls. From this results the mild grade 
of oedema frequently seen in anaemic patients, although in some few cases this 
oedema may be ascribed to passive congestion, resulting from the cardiac debility 
{vide supra). The increased permeability of the renal blood-vessels is sometimes 
shown by polyuria. 

The urine is usually rather light-colored, if the anaemia be at all marked. It is 
evident that there is a diminished production of urinary pigment, the material for 
which is the coloring matter of the blood. Another reason for the light color of 
the secretion is the polyuria above mentioned. There may be fifty to seventy 
ounces (1,500-2,000 cubic centimetres), or more, secreted in twenty-four hours. 
The specific gravity may nevertheless be comparatively high, and higher than one 
would expect from the appearance of the urine, not infrequently ranging between 
1015 and 1021. This indicates, of course, that the amount of solid constituents is 
comparatively large ; and in fact we find a corresponding amount of urea, perhaps 
four or five hundred grains (grammes 25-32) in twenty-four hours. This is a large 
figure when we consider the amount of ingesta. As to the other constituents of the 
urine, we possess as yet little definite knowledge. The amount of phosphoric 
acid is sometimes surprisingly small, compared with the amount of nitrogen. 
Albuminuria is exceptional in cases of simple anaemia. 

The bodily temperature is very often affected in anaemia. An " anaemic 
fever " is very frequently associated with pernicious anaemia, and even with cases 
of profound secondary anaemia, as after a large haemorrhage from the stomach. 
There are irregular elevations of temperature, usually occurring in the evening, 
and attaining 101°-102° (38.5°-39° C), or even still higher figures. This fever 
is not due to inflammatory organic changes, but, in all probability, is rather the 
result of the presence in the blood of matter due to the disintegration of the blood- 
globules (perhaps fibrine ferment). 

Clinical History of Chlorosis. — Chlorosis, or " green sickness," is a definite 
form of primary essential anaemia, which appears exclusively in the female sex 
and in the years of adolescence, mainly from the fifteenth to about the twentieth 
year of life. The disease either may appear quite suddenly in a previously healthy 



ANZEMIA AND CHLOEOSIS 



715 



girl, and in such a case may completely disappear again after a few weeks or 
months ; or the entire course may be a chronic one without sharp limits, so that the 
condition approaches more nearly to a constitutional anaemia. In many cases, 
also, it would be proper to say that there are recurrences of chlorosis, for severe at- 
tacks of the disease may be seen more than once in the same girl. As a rule, there 
is no definite cause to be found for the appearance of chlorosis, except that some- 
times it seems to be promoted by an unhygienic mode of life, too many social 
demands, or long-continued mental excitement. 

The various symptoms of chlorosis are almost all direct results of the anaemia, 
so that they have already been described. Their intensity and variety are, how- 
ever, very different in different cases. There are mild cases where the patient 
can hardly be called ill. She feels perfectly well, but is " a little pale." From 
these cases there is a gradual and unbroken transition to the other extreme of 
severity. 

A constant and essential symptom is the greater or less pallor of the face as 
well as of the rest of the surface of the body, and of the mucous membranes so 
far as visible. This pallor sometimes really has a greenish tint. There is almost 
invariably general languor; the patient is easily fatigued, and has neither the 
desire nor the ability to make any great bodily or mental exertion. There is also 
a tendency to headache and vertigo. Chlorotic patients often complain of dys- 
pepsia. The appetite is usually diminished, and there is often a sense of pressure 
in the epigastrium after meals. There may be severe cardialgia. It is not 
always easy to determine its cause, often it seems to be purely nervous. Some- 
times there may be myalgia. Moreover, chlorosis may be associated with a genu- 
ine ulcer of the stomach, as has been already mentioned. We believe, however, 
that this combination is much less frequent than is commonly supposed, for many 
physicians make a diagnosis of gastric ulcer upon insufficient data. The earlier 
assumption that the dyspeptic symptoms of chlorosis are associated with a lack 
of hydrochloric acid in the gastric juice is entirely incorrect. If we make a care- 
ful investigation of the gastric functions in chlorotic girls, we shall find that the 
amount of hydrochloric acid in the gastric juice is normal or even excessive. That 
gastroptosis may often be found in conjunction with chlorosis is not surprising 
(vide supra, page 462). An attempt has even been made to regard chlorosis as a 
result of gastroptosis, although of course this is entirely incorrect. The bowels 
are usually constipated in chlorosis, which is explained by the impaired appetite 
and the sluggish intestinal peristalsis. 

Over the cervical veins we often hear a loud murmur, which has been above 
mentioned as the bruit de diable. Examination of the heart often shows a slight 
increase in the area of cardiac dullness, although this does not seem due in most 
cases to an actual dilatation of the heart, but merely to a retraction of the borders 
of the lung. Anaemic cardiac murmurs are often heard, the pulse is accelerated 
and easily excited. Otherwise physical examination does not reveal any abnormal 
condition of the internal organs. It is a very great exception to find any indica- 
tions of disturbance in the spleen or lymph-glands, or the bone-marrow. Fever is 
rare in mild cases of chlorosis, but in severe cases we sometimes see, especially at 
night, a slight rise of temperature, up to 101° F. (38.5° C). The urine is usually 
pale, but seldom differs greatly, either in amount or constituents, from the normal 
character. It is noteworthy that chlorotic girls are very apt to suffer from disor- 
ders of menstruation. The menses may not appear until late, or they are very 
scanty. Even complete and long-continued amenorrhcea is often seen in chlorosis. 
All these disturbances seem to point to an essential relation between the appear- 
ance of chlorosis and the phenomena of sexual life. It is only in exceptional in- 
stances that chlorotic patients have menorrhagia. 

Examinations of the blood have been made, in the hope of gaining a clearer 



716 



CONSTITUTIONAL DISEASES 



insight into the true character of chlorosis. The blood is usually pale. Upon 
microscopic examination, we notice that the red blood-corpuscles do not tend to 
form rouleaux so much as normally, and sometimes we can perceive that the glob- 
ules are comparatively light-colored, and are not all of the same size. Some 
are of the normal dimensions, others are notably small (microcytes), while there 
are a few which are unusually large (macrocytes). Irregularities in the shape 
(poikilocytosis) are also seen, particularly in severe cases. In mild chlorosis all 
these changes in the form of the red blood-corpuscles are slight, or scarcely appre- 
ciable. The white blood-corpuscles are present in normal amount, or sometimes 
somewhat above normal, so that there is a slight leucocytosis. In occasional 
instances there are considerable numbers of " granular bodies " in the blood. 
These are usually regarded as products of the disintegration of white blood-cor- 
puscles. 

Malassez, Hayem, Thoma, and others have endeavored to determine the num- 
ber of blood-corpuscles in chlorosis and allied diseases by means of special meth- 
ods of counting. In general, we may say that in many cases of severe chlorosis 
the number of red blood-corpuscles is decidedly diminished. In a cubic milli- 
metre of blood we find perhaps only 3,000,000 to 3,500,000 red blood-corpuscles, 
instead of the normal number of 5,000,000. The diminution may be even greater 
than this. On the other hand, it should be noted that Duncan, Hayem, and 
Laache have met with cases where the number of corpuscles was not diminished; 
but the amount of haemoglobine in the blood-corpuscles was diminished. Not in- 
frequently, when the number of red blood-corpuscles is but slightly diminished, 
perhaps the amount of haemoglobine in the blood is much reduced, to thirty or 
forty per cent, of normal. This justifies the conclusion that in chlorosis the num- 
ber of red corpuscles is less affected than is their constitution, particularly the 
proportion of haemoglobine contained in them. How this lack of haemoglobine in 
the red corpuscles comes about we do not yet know. 

We have already intimated that there is great variety in the general course of 
chlorosis. Many cases which seem severe at first terminate in complete recovery 
by the end of four to six weeks, or within a few months. Other cases are much 
more obstinate, resist all modes of treatment, and undergo frequent relapses ; so 
that with its manifold variations, improvements, and exacerbations, the disease 
may occupy one or two years or more. The prognosis may be regarded as favor- 
able on the whole, but it should always be given with a certain degree of reserve. 
It is true that ordinary chlorosis never involves direct danger to life. We shall, 
however, find that, so far as symptoms go, there is no sharp dividing-line between 
" simple chlorosis " and " pernicious anaemia " ; and in any individual case it 
may not at first be possible to decide which variety of anaemia is before us. 

There are hardly any true complications of chlorosis. If other organic diseases, 
such as pulmonary tuberculosis or gastric ulcer, exist along with chlorosis, one 
should always consider that the anaemia may have developed secondarily, or that 
the diseases may be present from mere coincidence. All the varieties of nervous- 
ness and hysteria are frequently found in association with chlorosis, and yet it 
can not be assumed in every case that there is an essential causative relation 
between them. ' 

Diagnosis. — The diagnosis of chlorosis is, in a certain sense, easy, for the char- 
acteristic symptoms, the pallor, and the ordinary phenomena consequent on consti- 
tutional ansemia, are always easy to appreciate ; but, on the other hand, the diag- 
nosis is not perfectly simple, for the anaemia must be actually a primary essential 
anaemia in order to justify the name chlorosis. We therefore have no right to 
declare the diagnosis of chlorosis until we have made a careful and thorough phys- 
ical examination, and have found that no factors are present which might pro- 
duce a secondary anaemia. We should, above all, bear in mind the possibility of 



AlSTiEMIA AND CHLOROSIS 



717 



incipient tuberculosis, and examine the lungs, the expectoration, and the general 
condition of the. patient, and also consider hereditary and other predisposing in- 
fluences. We should bear in mind the possibility of some organic disease of the 
stomach, such as ulcer, catarrh, or dilatation, or chronic renal disease, or possibly 
constitutional syphilis, giving rise to the syphilitic chlorosis before mentioned. 
In many cases it is easy to exclude all these secondary forms of anaemia, but occa- 
sionally the task is a very difficult one. In making a diagnosis of chlorosis it is 
very important, also, to consider the entire course of the disease, particularly the 
rapid onset of the anaemia at the time of adolescence in young girls, and the 
greater or less disturbance of menstruation. 

Treatment of Anaemia and Chlorosis. — The first indication in treating chlo- 
rosis, as well as every other form of anaemia, is to promote the regeneration of the 
blood. There are two ways in which we can endeavor to fulfill this indication: 
first, by general hygienic and dietetic measures, and, secondly, by employing 
certain internal remedies. 

First among general measures comes a care for pure air, sunlight, and proper 
food. Many a pale city girl regains her ruddy cheeks after a few weeks spent 
either in the country, or on the mountains, or at the seashore. The choice of a 
place must, of course, depend mainly upon the circumstances of the patient. In 
many instances, boarding in any suitable country place answers as well as a long 
and expensive journey. If the seashore be chosen, some bathing resort on the 
North Sea will usually be preferable. There are other places, where the patient 
can combine the advantages of pure forest air and ferruginous mineral water; 
these will be mentioned below. 

The diet of anaemic patients should be easily digestible and rich in albumen; 
carbohydrates and fat should be given in but limited amounts to patients in 
whom the panniculus adiposus is already well developed. Lean patients, on the 
other hand, require such ingredients in their diet, and should be recommended to 
take simple puddings, extract of malt, butter, and cod-liver oil. Milk, if well 
borne, is certainly not an unsuitable food for anaemic patients, but we do not 
ascribe any special value to the drinking of large amounts of milk as a cure 
for chlorosis. In the first place, milk contains an extremely small amount of iron, 
and secondly, it is very apt to cause troublesome constipation. Formerly it was 
not uncommon to order " milk-cures," but we regard this as decidedly unsuitable. 
On the other hand, we would especially advise the use of the yolks of eggs, pro- 
vided eggs are well borne by the patient, and are not the object of strong aversion. 
The yolk of egg is comparatively rich in haematogen, which is a nucleine-like com- 
pound of iron from which it is probable that haemoglobine is formed; emphasis 
should likewise be laid upon the use of an abundance of green vegetables, such as 
spinach, for these all contain a large amount of iron. Some authors ascribe an 
exaggerated value to alcoholic beverages. They may be allowed in moderate 
amount if the patient asks for them and finds the appetite improve under their 
use. The best to choose for an emaciated patient are porter and other varieties of 
beer rich in extractive principles, but wine is often ill borne by chlorotic girls, 
being apt to cause palpitation, etc. 

Many physicians also insist upon " abundant exercise in the open air." This 
can, however, be carried too far. A chlorotic girl is often made to take long 
walks in spite of her own reluctance to do so, with the result of becoming more 
languid and exhausted than she was before. We even believe that a case of pro- 
found anaemia will be benefited by a certain degree of bodily rest. Thus any 
needless tax upon the muscles is avoided. The most brilliant results we have 
ever observed in the treatment of chlorosis have been within the hospital. The 
patients, who are usually factory operatives and servant girls, are often kept in 
bed for the first two or three weeks. We admit that pure country air may be very 



T1S 



CONSTITUTIONAL DISEASES 



beneficial, but we would strongly advise moderation in bodily exercise. If the 
patient begins to feel more vigorous, she will of herself take more exercise. 

Of internal remedies, the preparations of iron have long occupied the first 
place in the treatment of all varieties of anaemia. How these exert their influence 
is at present quite uncertain, for the body needs so small an amount of iron that 
the iron contained in ordinary food seems to be quite sufficient for the demands 
of the system ; still, the therapeutic efficiency of iron, particularly in chlorosis, has 
been established by so many instances that there is scarcely room for doubt. On 
the other hand, in simple constitutional anaemia the efficacy of preparations of 
iron is much more uncertain and doubtful. 

The number of iron preparations that are recommended and are used is very 
large, and is continually being increased by the commercial manufacturers of 
drugs, although there is no actual need of such increase. Almost every physician 
has his favorite prescription, to which he ascribes the greatest efficiency. We 
ourselves employ most frequently in chlorosis the long- and well-known Blaud's 
pills. We can assure the reader that they are almost always well borne, and often 
cause a surprisingly rapid and decided improvement in chlorosis. We usually pre- 
scribe them in the following form : Dried sulphate of iron, pure carbonate of potas- 
sium, each one hundred and fifty to two hundred and twenty-five grains (grammes 
10-15) ; tragacanth, q. s. This makes one hundred pills, of which two to four are to 
be given three times a day after meals. Other ferruginous remedies which are 
likewise often useful are reduced iron, which is absolutely pure iron in a very 
finely divided powder, and is prescribed as such or in pills, from one to three 
grains (grammes 0.05 or 0.2), to be given several times a day; two prepara- 
tions, ferri carbonas saccharata (U.S. P.), and ferrum oxydatum saccharatum 
solubile (Ph. G.), are prescribed as loose powders, of which one half to one tea- 
spoonful may be given in water three times a day. The last named has a special 
advantage in that it does not blacken the teeth. Another good preparation of iron 
is the lactate, which may be given in powders and pills, in the dose of five to twelve 
grains (gramme 0.3-0.75). The tinctures of iron are, in general, scarcely to be 
recommended, and are usually employed only for children. The liquor ferri albu- 
minati (Ph. G.) deserves praise; a teaspoonful of it is given three times a day. 
It often has a good effect upon the appetite. Of late there have been repeated trials 
of the internal administration of organic compounds of iron. Eirst, haernoglobine 
itself was tried (Pfeufer's haernoglobine tablets or haernoglobine extract) ; also 
Schmiedeberg's " ferratine " ; hsemagallol, which was recommended by Kobert ; 
hsematogen, haemalbumen, and many others. All these preparations have found 
their champions, but it is by no means certain that they act better than the old 
approved inorganic forms of iron. Often iron is given in combination with other 
remedies, of which quinine is chief. This is said not only to increase the tonic 
action, but to lessen the headaches to which anaemic patients are subject. Sto- 
machic tonics, such as gentian, or laxatives, such as aloes, are also combined with 
iron. 

Exceptionally iron is not well borne, and causes digestive disturbances or diar- 
rhoea. We must then try another preparation or diminish the dose. It is usual 
to forbid the ingestion of sour articles of diet while taking iron, but the injunc- 
tion is due mainly to prejudice. 

The use of mineral waters containing iron is quite common, although the 
amount of iron thus introduced into the system is so small that it is hard to under- 
stand their therapeutic value. Of those artificially produced, that which contains 
the pyrophosphate of iron is the best, and seldom irritates even a delicate stom- 
ach. The natural chalybeate waters are also bottled and sent to distant places. 
They are often more effective if drunk upon the spot, but merely because, in that 
case, the general hygienic surroundings of the patient are better than they would 



PKOGKESSIVE PERNICIOUS ANMM1A 



be at home. The best-known and most popular ferruginous springs in Germany 
and Switzerland are situated at Cudowa, Rippoldsau, Elster, Schwalbach, Pyr- 
mont, Steben, Kohlgrub, Driburg, Liebenstein, and St. Moritz. " Steel-baths " are 
also much employed ; but the effect is due not to the iron contained in the water, 
but to the temperature of the water and the carbonic-acid gas it contains. Baths 
generally seem to be of decided service in chlorosis, and hence we often prescribe 
simple baths or salt-baths, giving a bath of fifteen or twenty minutes' duration, at 
a temperature of 90°-95° E., two or three times a week, adding five or six pounds 
of salt to the bath. 

Some other remedies besides iron are occasionally employed in chlorosis. Of 
these, the chief is arsenic. Its effects are often very beneficial, and it deserves a 
trial, especially in severe cases. It may be given alone or in combination with 
iron. We have repeatedly seen cases of chlorosis which showed no improvement 
after the use of iron, in which the combination of iron with small amounts of 
arsenic, a thirtieth to a fifteenth of a grain (gramme 0.002-0.004) three times a 
day, had a strikingly beneficial effect. Scholz and Striibing recommend the ad- 
ministration of sulphur in chlorosis — purified sulphur, ten parts; sugar of milk, 
twenty parts ; dose, as much as can be lifted on the point of a knife, three times a 
day. Other physicians extol manganese. ZSTo especial advantage, however, has 
been shown to pertain to these remedies. 

Although the constitutional treatment is always the main consideration, yet 
sometimes special symptoms demand attention. Violent headache may be re- 
lieved by antipyrine, or similar remedies; dyspeptic symptoms are to be treated 
chiefly by careful injunctions as to diet. The patient should avoid pressure from 
without upon the region of the stomach, and should have easily digested food. 
The internal administration of hydrochloric acid is proper only when the examina- 
tion of the gastric juice has shown that there is a diminution in hydrochloric acid; 
as a rule, there is an abundance of hydrochloric acid secreted (vide supra), and 
if so, alkalies are preferable. 

If there be constipation, it is desirable to remedy it rather by suitable diet than 
by laxatives. Thus we may prescribe fruit, Graham bread, and other foods which 
promote peristaltic action by the mechanical irritation which they exert; also 
gentle massage of the abdomen, and only when these fail, injections or mild 
laxatives. 



CHAPTER II 

PROGRESSIVE PERNICIOUS ANEMIA 

( Grave Form of Essential Ancemia) 

Definition and etiology. — We apply the term pernicious anaemia to a severe 
and rare form of anaemia which is usually fatal, and which develops as a primary 
disease, without demonstrable cause, in both men and women. We must hold 
fast to this conception of the disease, especially as the attempt has been repeatedly 
made of late to degrade pernicious ansemia from the rank of an idiopathic dis- 
ease, and regard it as merely a grave form of secondary anaemia which may result 
from any one of the most various causes. 

Of course, the diagnosis of primary anaemia may be wrongly made in cases 
where a more careful search will detect some special cause for the condition. 
Such a mistake may become evident at the autopsy. Thus, in repeated instances, 
cases which have been during life regarded as " pernicious anaemia " have been 
shown to be cancer of the stomach {vide page 448). In other cases, however, it is 



720 



CONSTITUTIONAL DISEASES 



more difficult to discover the primary cause of the anaemia. Thus the profound 
anaemia which attacked the men at work upon the St. Gothard Tunnel was 
at first regarded as idiopathic, but more careful investigation showed that the dis- 
ease was really due to anchylostoma (vide page 578), the ravages of which parasite 
have in other cases also been confounded with the symptoms of pernicious anae- 
mia. Reyher and Runeberg have lately called attention to the fact that the pres- 
ence of bothriocephalus latus in the intestine may produce an affection resem- 
bling severe and apparently primary anaemia. Of late there have been a number 
of cases reported where the post-mortem examination showed that the progressive 
marasmus and anaemia of the patient had resulted from an extensive atrophy of 
the coats of the stomach and — what is more important — of the intestine, associ- 
ated in some instances with well-marked lesions of the sympathetic plexus. These 
cases are very interesting, but have nothing whatever to do with pernicious anae- 
mia. Often the symptoms even during life differ not a 1 little from those of per- 
nicious anaemia, so that we can not think it right to establish what is called a 
" gastro-intestinal variety of pernicious anaemia." It is proper to group and 
classify the forms of secondary anaemia according to their various causes, but 
not the cases of primary idiopathic anaemia, which are all due to some trouble with 
the manufacture of the blood, or with the blood itself, and form a distinct clin- 
ical group. 

The credit of having been the first to study pernicious anaemia as a special 
form of disease belongs to Biermer (1868), although occasional instances of the 
disease had long before been noticed. Its occurrence during pregnancy was first 
pointed out by Gusserow. [The puerperal form of pernicious anaemia was de- 
scribed by Walter Channing in 1842.] 

With regard to the special aetiology of progressive pernicious anaemia, it must 
be confessed that we have as little definite information as about the aetiology of 
chlorosis. Often it has been thought that the disease might be infectious, but the 
discoveries thus far reported of specific micro-organisms in the blood — for instance, 
the so-called cercomonads of Klebs and Frankenhauser — lack confirmation. There 
do not usually seem to be any special exciting causes. It has been maintained 
that unfavorable hygienic surroundings and insufficient nourishment promote the 
development of the disease; and this would apply perhaps to some cases, but 
certainly it does not to all. We are inclined to regard it as characteristic of this 
disease, as well as of chlorosis, that the anaemia may develop despite the most 
favorable outward circumstances. There is, however, one factor which seems to 
have a decided influence, and that is the condition associated with pregnancy and 
childbirth. These are comparatively often the occasion of the development of the 
first symptoms of the disease in women. Still, pernicious anaemia has this essen- 
tial difference from chlorosis, that, as we have already said, it is not confined to 
women. Most cases occur in middle life, from about twenty-five to forty years of 
age. It is a very interesting but somewhat puzzling fact, that the disease may 
appear as a sequel to a great loss of blood, whether from one or several haemor- 
rhages. It seems as if the body were sometimes unable to recover from the effects 
of large haemorrhages of this sort, so that the acute merges into a chronic and 
progressive anaemia, which, despite nursing and treatment, advances to a fatal 
termination. It is quite doubtful, however, whether such cases should be classed 
as genuine pernicious anaemia. 

Pathology. — Pernicious anaemia so often terminates fatally that there has been 
abundant opportunity to make accurate anatomical investigations of the lesions 
it produces. We shall not here discuss the changes in the blood itself, inasmuch 
as they will more properly be described among the clinical phenomena. The 
changes in the internal organs are divisible into two groups: First, such as are 
secondary and the result of the anaemia; and, secondly, such as may perhaps be 



PROGRESSIVE PERNICIOUS AXiElEIA 



721 



primary and characteristic. All the internal organs are, of course, anaemic. An- 
other striking change is fatty degeneration. This is usually best marked in the 
heart, but it also affects the kidneys, the liver, and the walls of the stomach and 
intestines, as well as the intima of the blood-vessels. We have already pointed 
out that this fatty change is to be regarded as the direct result of the anaemia, 
probably because of the diminished supply of oxygen in the tissues. 

The second important lesion of pernicious anaemia is the haemorrhages, usually 
small, but occasionally large; these are usually numerous, and are found in all 
sorts of locations. The most important of these haemorrhages are into the retina, 
hecause they can be demonstrated by means of the ophthalmoscope during life. 
They are very frequent. We may also find minute haemorrhages in the serous 
membranes, such as the pleura or pericardium, in the brain and in the mucous 
membranes. Cutaneous ecchymoses are also occasionally found. We shall revert 
later to the aetiology of these haemorrhages. 

Still another secondary symptom is an abundant deposit of iron in the cells of 
many organs. This can usually be determined only by the aid of the microscope 
or micro-chemical tests. It is most abundant in the peripheral zone of the hepatic 
lobules, but it also occurs in the kidneys, pancreas, and other organs. Quincke 
has studied this point very carefully, and finds that the total amount of iron con- 
tained in the liver in pernicious anaemia is much larger than normal. The most 
natural and most probable interpretation of this fact is that the iron originates 
from the destruction of large numbers of red blood-corpuscles. 

The changes thus far described are undoubtedly the result of anaemia, and 
hence are the same in all severe anaemias, whatever their cause. On the other 
hand, search has been made for specific changes which could be regarded as the 
primary disease, and thus, of course, our attention has been especially directed to 
the organs engaged in the formation of the blood. The lymph-glands do not usu- 
ally present any special changes in pernicious anaemia. If they are much altered, 
it is probable that the disease is a different one, which we shall later have an oppor- 
tunity to study (vide pseudo-leukaemia). The spleen is in many cases normal. 
In exceptional instances, however, it is decidedly enlarged, although never enor- 
mous. Even when the organ is enlarged there are no important histological 
changes to be detected. Cases of pernicious anaemia with marked splenic tumor 
are often termed splenic anaemia (vide infra), but we do not ourselves see how 
such cases differ essentially from others in which the spleen is not enlarged. The 
changes in the bone-marrow are by far the most constant. This structure plays 
an important part in the formation of the blood. . C. Wood, and after him Cohn- 
heim, called attention to the fact that the bone-marrow is almost invariably 
affected in pernicious anaemia. Instead of its normal yellow color, it has a dark- 
red color, like raspberry jelly. This is due mainly to the fact that the numerous 
fat-cells of the marrow are all, or nearly all, destroyed. This is the more surpris- 
ing as the fatty tissues in other parts of the body are often very little affected in 
pernicious anaemia. The specific cellular elements of the marrow also exhibit cer- 
tain changes. There is a decided hyperplasia, and, as a rule, there are found large 
numbers of nucleated red blood-corpuscles. Cohnheim is inclined to regard the 
disease of the bone-marrow as specific and primary, but it must be confessed that 
there are many reasons which strongly oppose this view, and suggest the possibility 
of this change in the marrow being merely a secondary phenomenon, a sign of the 
extremely active formation and regeneration of the red blood-corpuscles. Neu- 
mann's investigations would lead to the belief that the nucleated red blood-cor- 
puscles are young blood-cells in the process of development. Furthermore, these 
vigorous processes of regeneration, and the corresponding changes in the bone- 
marrow, are often found in cases of profound anaemia which are beyond a doubt 
of secondary origin. 
46 



722 



CONSTITUTIONAL DISEASES 



We can not, therefore, feel certain that the lesion of the bone-marrow is the 
primary anatomical disturbance, and hence we are obliged to assume that essen- 
tial anaemia may be a disease of the blood itself — that is, some specific but un- 
known process which does direct injury to the red blood-corpuscles. 

Symptoms. — As already stated, the symptoms of pernicious anaemia usually 
beg-in, independently of any demonstrable cause, in individuals previously healthy, 
and develop so slowly and gradually that it is hardly ever possible to determine 
the precise date of the commencement of the disease. This is still more likely to 
be the case if the trouble occurs, as indeed it may, in individuals who were pre- 
viously feeble and pale without being actually ill. Occasionally a more acute 
onset is observed in pregnant women. 

The first symptoms are almost invariably traceable to the incipient anaemia. 
They include the subjective disturbances and the objective changes which are seen 
in any ordinary anaemia. The patient feels languid and is easily fatigued, is 
liable to headache, vertigo, palpitation, and tinnitus aurium; there are anorexia, 
frequent nausea, and, above all, a striking pallor of the skin and mucous mem- 
branes, but while these symptoms in ordinary anaemia and chlorosis are moderate, 
in the severe forms of essential anaemia they are extreme. 

In every well-marked case of pernicious anaemia the weakness of the patient 
is so great that he is permanently confined to bed, and standing or sitting for any 
length of time is impossible. Usually the patient lies upon his back, with his 
head rather low, and presents a countenance of waxy pallor. Very frequently a 
slight but distinct yellowish hue may be detected. Occasionally there are cutane- 
ous ecchymoses, but these are exceptional. The mucous membrane of the lips, 
the gums, and the conjunctivae are likewise pale and colorless. The intellect is 
unimpaired, but all answers to questions are slow, apathetic, and delivered in a 
low and feeble tone of voice. The patient is usually incapable of any great men- 
tal exertion. He is sleepy, and often yawns. If the body be moved, and especially 
if an upright position be substituted for a horizontal one, there is great liability 
to syncope c This may result from any slight physical exertion, and is often ac- 
companied by a peculiar spasmodic rigidity of the body. The main subjective 
symptoms are weakness, and more especially intense headache ; this often assumes 
a pulsating character, and is located mainly in the temples or forehead. There is 
also an annoying ringing in the ears, described as a singing, rushing, or roaring 
sound. There are certain other subjective sensations, namely, nausea, a sense of 
thoracic oppression, and pain in the bones, which will be considered later on. 

If we now proceed to a systematic physical examination, we are struck, in the 
first place, by the condition of the eyes. The pupils are often somewhat enlarged, 
but react in a normal manner. Vision is often disturbed by spots before the eyes. 
The anaemic amaurosis seen after a sudden large haemorrhage has not yet been 
observed in pernicious anaemia. The ophthalmoscopic examination of the fundus 
has very great diagnostic importance. We find in a majority of cases, although 
not in all, retinal haemorrhage. There may be either one or many haemorrhages. 
If they are extensive enough to involve the macula lutea or the disk, they may 
disturb vision greatly. Retinal haemorrhages invariably signify that the anaemia 
is profound, and are, with considerable justice, regarded as distinguishing perni- 
cious from simple anaemia. 

Respiratory Symptoms. — Breathing is usually accelerated, and, in the most 
advanced cases, is often remarkably deep and noisy (anaemic dyspnoea, vide supra). 
Sometimes there is a very annoying and almost painful sense of thoracic oppres- 
sion, which is evidently connected with the dyspnoea. There is a " hunger for air.' - ' 
Physical examination of the lungs gives negative results. Sometimes there is a 
little cough, and there may be sufficient haemorrhage into the mucous membrane 
of the air-passages to give rise to a slight haemoptysis. Even in this case no ana- 



PKOGKESSIVE PEKNICIOUS ANAEMIA 



723 



tomical changes can be detected during life. We may also mention in this con- 
nection that epistaxis is not very infrequent. 

Phenomena referable to the circulatory system are- of still greater clinical 
importance. The area of cardiac dullness is usually normal, although sometimes 
slightly increased. Upon palpation, we often find that the heart's action is exag- 
gerated, and that its beat is felt over a larger area than normal. The pulse is usu- 
ally decidedly rapid (100-120), but it is regular, and sometimes, but by no means 
invariably, small. It is often surprisingly strong. The loud " anaemic murmurs " 
are very characteristic. They can be appreciated at the apex of the heart, but are 
usually heard still better at its base. We generally hear a loud bruit de (Liable in 
the veins of the neck. 

Digestive Organs. — The tongue is usually pale, smooth, and dry. The appe- 
tite is often very poor. The most prominent disturbances, however, are not due 
directly to the condition of the stomach, but they result from the cerebral anaemia 
— that is, they are symptoms of the irritation of the nervous centers. We refer to 
eructations and vomiting, which may be very frequent and distressing. There is 
generally a tendency to constipation. Occasionally there is diarrhoea. 

The liver is usually normal; as is also the spleen in many instances, while in 
others it is shown by percussion and palpation to be enlarged. It is sometimes 
possible, as we can ourselves bear witness, to observe an enlargement of the spleen 
increasing as the anaemia grows more profound, and again decreasing if improve- 
ment occurs (vide infra). On ordinary examination, the urine does not usually 
differ essentially from normal. With few exceptions it is free from albumen, 
and it never contains sugar. As already set forth, however, accurate quantitative 
analysis often furnishes important evidence of changes in tissue-metamorphosis 
resultant upon the anaemia (cf. page 714). We will merely mention once more 
the comparative increase in the amount of urea excreted, and the occasional 
excess of uric acid. Sometimes the urine gives a vivid reaction for indican. 

In regard to what has already been said about the marrow of the bones, it is an 
interesting fact that they are very sensitive to pressure in many cases of perni- 
cious anaemia. The sternum in particular is painful upon light percussion ; and 
sometimes pressure will cause pain in the bones of the extremities. In rare in- 
stances swelling of the knee and other joints has been observed. A series of very 
interesting observations have been recently made by Lichtheim, Minnich, and 
others, which show that persons with primary or even secondary pernicious anaemia 
(e. g., anaemia due to the bothriocephalus) may quite suddenly develop well-marked 
nervous symptoms. These consist chiefly in paraesthesiae in the hands and legs, in 
slight disturbances of sensation, unsteadiness and ataxia of the legs, weakness or 
complete abolition of the tendon reflexes, etc. — in brief, a group of symptoms re- 
sembling tabes. The pupils have been observed to become irresponsive to light. 
Upon the post-mortem examination of such cases, there is found, particularly in 
the posterior columns of the spinal cord, a well-marked disease which consists for 
the most part in small scattered foci of degeneration, and in a more systemic (sec- 
ondary) degeneration of the columns of Goll. Sometimes small capillary haemor- 
rhages are also found. Slight changes of this sort may be observed in the spinal 
column, even when no special spinal symptoms had been present. Probably these 
conditions are due to toxic action. 

The blood has been made the subject of numerous and careful investigations ; 
nevertheless, no characteristic change has been discovered. The changes presented 
in pernicious anaemia likewise occur in cases of profound secondary anaemia. 
This seems the more readily intelligible to us because of the view which we have 
already expressed on page 710 with regard to the origin of secondary anaemia. 
To the naked eye the blood seems extremely pale and watery. The number of 
red blood-corpuscles is sometimes so diminished that it seems incredible that life 



724 CONSTITUTIONAL DISEASES 

should persist. It is not at all unusual, in the worst stages of the disease, to find 
only 500,000 to 1,000,000 red blood-corpuscles per cubic millimetre, or even 
250,000 — that is, even less than one tenth of the normal amount. The proportion 
of haemoglobine in the blood is consequently much diminished, but comparative 

determinations of the number of blood- 
corpuscles and the amount of haemoglo- 
bine seem to indicate that the individual 
blood-corpuscles have not lost any of 
their coloring matter. The red blood- 
corpuscles are found to present striking 
varieties in size and form (vide Fig. 79). 
While some corpuscles have a normal 
appearance, others may be of an unusu- 
ally large size (macrocytes). These 
" giant corpuscles " appear normal ex- 
cept in dimensions, and some observers 
(La ache) have thought that they were 
even possessed of an unusual amount of 
haemoglobine. It is therefore surmised 
that they represent an effort on the part 
of nature toward compensation. In con- 
trast with these large cells are found a 
varying number of minute red cells of a 
spherical shape : these were first de- 
scribed by Vanlair and Masius, and 
called microcytes. Finally, there are numerous red blood-corpuscles of abnormal 
shape. These Quincke was the first to notice. They present remarkable forms, 
being biscuit-shaped, hammer-shaped, or anvil-shaped, and so on, as illustrated in 
the accompanying cut. These " poikiiocytes " are found in perfectly fresh undi- 
luted blood, so that there is no reason to suppose that they are artificial products. 
Both the microcytes and the poikiiocytes are regarded as degenerative forms of 
the blood-corpuscles. They are the products of the division and constriction of old 
blood-corpuscles. Careful histological examination discloses several definite and 
histologically distinct forms of degeneration in the red blood-corpuscles. We have 
already pointed out that the microcytes and poikiiocytes are not essentially char- 
acteristic of pernicious anaemia, but occur in other severe forms of anaemia ; 
but besides these products of degeneration, we find in the blood, also, indications 
of an increase in the formation of new elements. We refer to the nucleated 
blood-corpuscles. Ehrlich, to whom we are indebted for the best investigations 
with regard to this matter, distinguishes the so-called normoblasts and megalo- 
blasts. The normoblasts are nucleated red blood-corpuscles of ordinary size, which 
correspond to the youthful forms of red blood-corpuscles normally present. The 
megaloblasts, on the other hand, are nucleated structures which exceed the ordi- 
nary red blood-disks in size, two to four fold. Megaloblasts are found normally in 
the embryo alone, so that Ehrlich conceives the appearance of megaloblasts to be 
a sort of reversion to the embryonic state. The appearance pf megaloblasts in the 
blood is very characteristic of pernicious anaemia. The white blood-corpuscles are 
not usually increased in number; in occasional instances, however, a temporary 
leucocytosis has been found. " Granule-masses " are often found in considerable 
abundance. Chemical examination of the blood has not as yet brought to light 
any facts of great importance. It has been already stated that there is a great 
diminution in the total amount of haemoglobine. The amount of albumen in the 
blood-serum remains nearly normal. 

We observe in pernicious anaemia the tendency to fever common to all varie- 



d d 




a b 

Fig. 79.— Changes in the red blood-corpuscles in 
pernicious anaemia. (From Quincke.) a. Nor- 
mal blood-corpuscles, b. Macrocytes. c. Mi- 
crocytes. d. Poikiiocytes. 



PEOGKESSIVE PERNICIOUS ANAEMIA 



725 



ties of profound anaemia. In many cases the evening temperature will for weeks 
reach 100°-101° (38°-38.5° C), or even higher. Previous to death, however, the 
temperature may become subnormal, falling to 86° (30° C), or even lower. 

As to the origin of all these symptoms we must, as we have said, regard the 
impairment of the blood, especially its poverty in red blood-corpuscles, as the 
essential morbid process. How this impairment is produced, whether by injury 
to the blood-corpuscles themselves or to the organs where they are formed, we do 
not know. A large part of the other morbid symptoms — the pallor of the skin, 
the weakness, the " anaemic cerebral symptoms," tinnitus, vertigo, nausea, faint- 
ness, etc., are due directly to the anaemia. In regard to certain other important 
symptoms, however, another factor is probably of great significance, namely, an 
auto-intoxication of the body with fibrine ferment or some similar substance. 

By the destruction of many red blood-corpuscles, probably a certain amount 
of haemoglobine is always set free, and enters the blood plasma. There is then 
a haemoglobinaemia. Erom many experiments, however (Dorpat school of Alex- 
ander Schmidt, Ponfick, Silbermann, etc.), we know that haemoglobine dissolved 
in the blood destroys the white blood-corpuscles, and in some way produces from 
them fibrine ferment. Chronic " ferment intoxication " of the body causes certain 
symptoms, which are almost never absent in pernicious anaemia — capillary haemor- 
rhages and fever. The haemorrhages are usually associated with embolism of the 
smaller vessels, seldom with local thrombi. Many severe nervous symptoms (vide 
supra) may perhaps also be referred to this intoxication. 

General Course, Duration, and Prognosis. — As the very name "pernicious" 
indicates, the disease generally terminates unfavorably. Death usually seems to 
be the direct result of the extreme anaemia ; special complications are exceptional. 
The disease often maintains a slow but gradual progress to the end. Its dura- 
tion, reckoning from the appearance of the first symptoms, may not exceed three 
to six months. It may even run its course in a still shorter time. It seldom lasts 
more than a year. Sometimes its course is interrupted; there may be an arrest 
of the process, or improvement, or even apparent recovery. Usually, however, 
there are fresh relapses. In a certain class of cases the disease lasts two or three 
years, and is marked by a number of " attacks of anaemia " so intense that the 
subsequent improvement of the patient seems simply marvelous. It is in cases 
of this sort that splenic tumor has been made out at the time the anaemia was at 
its height ; yet we do not perceive the necessity of establishing " splenic anaemia " 
as an affection essentially different from progressive pernicious anaemia. It is 
merely a clinical variety of the disease under discussion. Apparently, it likewise 
has an invariably fatal termination. 

Permanent recovery may occur in cases of idiopathic anaemia so profound that 
we are at first inclined to regard them as pernicious. These cases are unfortu- 
nately very rare, and even when there is a marked improvement the danger of a 
relapse is to be borne in mind. The prognosis is therefore always very grave, 
if not absolutely unfavorable. Of course, general hygienic surroundings and 
good care may exert some influence upon the course of the disease. It is note- 
worthy that if pregnancy be complicated by profound anaemia there is a great 
liability to premature delivery, after which there is often a rapid change for the 
worse. There are exceptions to this rule. 

Diagnosis. — It is seldom difficult to make out the existence of a profound 
anaemia, or to determine the degree of danger which the consequent symptoms 
indicate. We have, however, the same difficulty here as in chlorosis in proving 
that the anaemia is primary and idiopathic. The factors essential to this diagnosis 
have been already indicated. We should bear in mind the possibility of insidious 
tuberculosis, organic diseases of the stomach, or such parasites as the anchylos- 
toma and bothriocephalus. 



726 



CONSTITUTIONAL DISEASES 



Treatment. — Eor treating progressive pernicious anaemia we have only the 
same remedies as for the benign variety of anaemia. We must provide the patient 
with nourishing and digestible food, and regulate all other hygienic matters ; and 
in the way of medicine the greatest prospect of benefit lies in arsenic, while the 
efficiency of ferruginous preparations in pernicious anaemia is dubious. We may, 
however, try a combination of iron with arsenic. The best form in which to ad- 
minister the arsenic is pills, but subcutaneous injections, also, may be tried, in 
the manner which will be fully described in the following chapter. Besides 
arsenic, some physicians recommend phosphorus. 

If the case be not too far advanced, baths may prove useful adjuvants to the 
internal treatment. Salt baths or artificial carbonic-acid baths may be employed. 
Symptomatic treatment is often indicated: the dyspepsia may call for dilute 
hydrochloric acid, or the troublesome vomiting may require bits of ice, bromide 
of potassium, or opium. 

The transfusion of blood has been employed in pernicious anaemia. Some- 
times the effect seems to be favorable. Experience thus far, however, would not 
lead one to expect very great benefit from it. Von Ziemssen has lately recom- 
mended in all severe forms of anaemia the subcutaneous injection of blood. It is 
done by injecting under the skin, by thoroughly disinfected instruments, fifty 
cubic centimetres of defibrinated human blood, divided into two parts, twenty-five 
cubic centimetres being injected into each thigh. The point of injection is vigor- 
ously rubbed, and thus the injected blood is forced into the lymph-channels. In 
severe cases this procedure should be frequently repeated. Experience of this 
method has thus far been very favorable. Not only the subjective symptoms, but 
the objective condition of the blood, the number of red blood-corpuscles, some- 
times show a striking improvement after the injection. 

[In the experience of American and English clinicians, arsenic, long continued 
and in as large doses as are tolerated, is of far greater value than iron. 

The inhalation of oxygen is expensive, but seems to be of distinct service in 
some cases of grave anaemia of all forms.] 



CHAPTEE III 

LEUKAEMIA 

( Leucocythwmia) 

Definition and -ffitiology. — Virchow, in 1845, was the first to obtain an insight 
into the disease leukaemia ("white blood"). He detected the great increase of 
white corpuscles occasioned by it, and from this time these constituents of the 
blood were subjected to observation in all sorts of diseases. It was soon found 
that there may be a temporary increase of the white corpuscles in various primary 
diseases, and that in certain instances this increase may actually constitute the 
essential symptom. In this latter case the increase is due to 'a depraved condition 
of certain internal organs. In the temporary cases, in which the increase of white 
blood-corpuscles is usually not very great, we find one white corpuscle to one 
hundred red, or even one to fifty — the normal ratio being one to six hundred or 
more. This is usually termed leucocytosis, in distinction from leukaemia proper 
If we take for normal a count of about 6,000 to 10,000 leucocytes in a cubic milli- 
metre of blood, the term leucocytosis is applied to conditions in which the number 
of leucocytes rises to 15,000 or 20,000, or even still higher up to and beyond 
40,000. A leucocytosis of this sort is found, under normal conditions, at the time 



LEUKAEMIA 



727 



of digestion, also in pregnant women and in the new-born; under pathological 
conditions, chiefly in certain acute febrile diseases, particularly croupous pneu- 
monia, erysipelas, and sepsis. 

Genuine leukaemia is a rather rare disease. Its characteristics are well marked 
in most cases, but of its true nature we remain entirely ignorant. In a majority 
of the cases the change in the blood is associated with marked changes in the 
spleen and the bone-marrow, and often also in the lymph-glands. The organs 
just enumerated being concerned in the manufacture of the blood, and particularly 
of the white corpuscles, it is very reasonable to suppose that leukaemia is a disease 
which primarily affects these organs, and that the increase in white corpuscles re- 
sults from the disturbance thus occasioned. The cause of the disease in the organs 
mentioned is as yet unknown. Various authors have suggested that there may 
be some specific infection, but they have not been able thus far to produce 
any evidence of the truth of their surmise. In few cases can we discover even any 
exciting cause. The illness seems to develop spontaneously in perfectly healthy 
persons. In some cases, on the other hand, leukaemia does seem to be a sequel of 
some other disease. Thus it occasionally follows a tedious attack of intermittent 
fever. It has also been asserted that syphilis and other infectious diseases, such as 
typhoid fever, may give rise to leukaemia, but this is not very probable. Finally, 
trauma of the spleen or bones has in repeated instances been regarded as the occa- 
sion of the disease. The hygienic surroundings of the patient have also been re- 
garded as a cause of leukaemia. The disease is somewhat more frequent among 
the poorer classes than among the wealthy; but there are numerous exceptions to 
this rule. ^Etiological importance has also been ascribed to anxiety, trouble, and 
mental depression in general. Still, all these apparent exciting causes are 
scarcely ever of real importance, and in most cases of leukaemia there is, as we 
have said, no evidence of any of them. 

Leukaemia is most common in middle life, between thirty and forty-five years 
of age, but well-marked cases have been observed repeatedly even in childhood, 
as also, though less frequently, in old age. Men are somewhat more liable to 
the disease than women. It has been repeatedly stated that in female patients 
the disease is sometimes referable to sexual derangement, but apparently this was 
mistaking effect for cause. 

Pathological Anatomy. — The essential change in leukaemia is a great increase 
in the number of white blood-corpuscles. The characteristics of the blood can be 
studied during the life of the patient, and upon them the diagnosis is mainly 
hased. They will therefore be discussed under symptomatology, while we shall 
here confine ourselves to the lesions presented by the spleen, bone-marrow, and 
lymph-glands. 

Of the organs just enumerated, the spleen is the one most frequently affected 
(splenic leukaemia). It is often greatly increased in size, and may attain a weight 
•of six to eleven pounds (3-5 kilogrammes) and a length of a foot (30 centimetres). 
There is a true hyperplasia of the whole organ : all the histological constituents 
are increased. The cut surface is usually a rather vivid red in early cases, but 
later on it often has a lighter, yellowish color. The consistency is usually dimin- 
ished, but in the later stages it may be greater than normal. Upon microscopic 
examination, we find enlargement of the blood-vessels and a great increase in 
the cells of the pulp and of the follicles. Sometimes the hyperplasia of the folli- 
cles predominates, giving the spleen a spotted appearance, like marble. In such 
cases the pulp usually presents retrograde metamorphosis, with atrophy and fatty 
degeneration of its cells and deposits of pigment. In advanced cases a consider- 
able amount of firm connective tissue may be present. There are often haemor- 
Thagic infarctions, presenting the appearance of circumscribed spots, dark red, or 
in the later stages brownish yellow, in color. 



r 



728 CONSTITUTIONAL DISEASES 

Lesions of the bone-marrow are next in frequency to those of the spleen (med- 
ullary or myelogenous variety of leukaemia). Neumann and a few other au- 
thorities regard changes in the bone-marrow as an essential lesion, and hold that 
they can be demonstrated in every case of leukaemia. There would certainly 
seem to be exceptions to this last rule, but nevertheless in a majority of cases the 
marrow does present a peculiar yellowish or almost puriform appearance. By 
means of the microscope we can detect a great increase in the lymphoid cells of 
the marrow and the presence of a considerable number of nucleated red blood- 
corpuscles. 

In many cases the lymph-glands remain perfectly normal; but in others they 
become considerably enlarged, and form actual tumors in various parts of the 
body, such as the axilla, neck, and groin, and sometimes the internal lymph-glands. 
Such cases are examples of lymphatic leukaemia. Histologically, the change nere- 
is simple hyperplasia of the glandular tissue. 

These three forms of leukaemia — splenic, myelogenous, and lymphatic — can not 
be regarded as distinct diseases, inasmuch as cases occur which present all sorts of 
combinations of these different lesions. Purely myelogenous cases are very rare, if 
they occur at all; and we rarely meet with cases which are purely splenic or 
purely lymphatic. Most cases present lesions of the spleen and marrow con- 
jointly. In less frequent instances splenic disease is associated with that of the 
lymphatic glands. The fact that these combinations exist indicates that there i& 
one common cause for the disease, which assails sometimes one, sometimes two, or 
sometimes all three of the organs named. 

Just what the connection is between the changes in the blood and the lesions 
of these various organs is an unanswered question. The view which seems to us 
most plausible regards the disturbance in the spleen, marrow, or lymph-glands, 
as the case may be, as the primary one, and the alteration in the blood as a result 
of this primary disturbance ; there is an increase in the number of colorless cor- 
puscles formed, and a consequent increase in the number of them introduced into 
the circulatory fluid. It is true, however, that the number of red blood-corpuscles 
is usually diminished in leukaemia. This diminution in number might be ascribed 
either to scantiness of supply or to increase in the processes of destruction, but. 
which factor is in reality the important one must remain undetermined. 

Changes in Other Organs. — Leukaemia sometimes causes new growths of a. 
lymphatic character in certain organs other than those already mentioned. The 
growths may either be diffuse or circumscribed. They are observed in the tonsils, 
Peyer's patches, and the intestinal follicles. They are also found very frequently 
in the liver, kidneys, and retina, and more rarely in the lunges and the pleura. 
These various lesions may be regarded as in a certain sense analogous to the 
metastatic tumors of cancer or sarcoma, and suggest the possibility of the diffu- 
sion of the pathogenic poison throughout the whole body. In one or two cases 
a well-marked leukaemia has been found independent of any demonstrable organic 
lesions. It is impossible, at present, to explain such occurrences. Leube and 
Fleischer have reported a case of this sort, and are inclined to believe that the 
blood itself was diseased. 

There is little known as yet as to changes in the chemical composition of the 
blood and viscera in leukaemia. Glutine, xanthine, and hypoxanthine have been 
found in the blood, as have also lactic acid and formic acid. It is also interesting 
that nucleo-albumen is found in the blood serum of leukaemic patients, for this 
fact points directly to destruction of the blood-corpuscles (Matthes). 

It is noteworthy that octahedral crystals are often found after death in 
the blood, spleen, and marrow, and in other parts. These are known as Charcot's 
crystals, and have already been described as occurring in the sputum in bronchial 
asthma (see page 184). 



LEUKAEMIA 



729 



Symptoms. — The clinical phenomena of leukasmia are in many respects similar 
to those of progressive pernicious anaemia, • and need not be enumerated again 
here. In leukaemia, however, we have, in addition, symptoms referable to the 
spleen, lymph-glands or bone-marrow (as the case may be), and also the char- 
acteristic alterations in the blood. The blood-changes, being pathognomonic,, 
demand a full description. 

The pallor and watery character of the blood in leukaemia are noticeable even 
to the naked eye in advanced stages of the disease. They can not, however, be 
distinguished without the aid of the microscope from the changes present in grave 
anaemia (vide Fig. SO). In this way it is often possible to determine by the first 
glance that there is an enormous increase 
in the white corpuscles, their number 
seeming of more significance because the 
number of red globules is apt to be con- 
siderably diminished. If an accurate count 
is made we find in a cubic millimetre of 
blood about 2,500,000 to 3,500,000 of red 
blood-corpuscles and about 300,000 to 500,- 
000, or even 700,000 leucocytes. The 
proportion of white to red blood-corpus- 
cles is one to twelve, or even one to eight 
and one to seven. The earlier reports of 
ratios of one to two and one to one are 
probably clue to inaccurate counting. 
Still more interesting than these ratios 
are the special forms of leucocytes : even in 
the fresh unstained preparation it is easy 
to appreciate that there are decided dif- 
ferences in the size and character of the individual leucocytes ; but all these 
differences become far more distinct in the stained preparation* (Fig. 81). In 
this we see that a very large proportion of the leucocytes consists of the ordi- 
nary polynuclear cells, but we also find small mononuclear cells, called lympho- 
cytes, which probably originate in the lymph-glands, so that an increase in the 
number of them is regarded as especially characteristic of the lymphatic form of 
leukaemia. TTe also see in most cases numerous large mononuclear cells, almost 
twice as large as a white blood-corpuscle, so that they can be distinctly recog- 
nized even in the fresh unstained specimen. These cells are at present usually 
termed marrow-cells, or myelocytes, because they are found in large numbers in 
the bone-marrow, both in normal conditions and particularly also in leukaemic 
subjects, so that it is regarded as probable that the myelocytes which are present 
in leukaemic blood originate in the bone-marrow. Finally, we ordinarily find in 
every microscopic field several so-called eosinophilous cells — that is, cells whose 
marked granulation is noticeable even in the fresh specimen, but becomes still 
more striking when the granules are stained red with eosine. As to the origin 
(bone-marrow?) and the significance of eosinophiles, we have as yet no certain 
knowledge, nor can we make absolute statements as to the source of the lympho- 
cytes and myelocytes. Many investigators regard the mononuclear, small 
leucocytes, or lymphocytes, as merely the immature form of the polynuclear and 
large nucleated cells, into which they are supposed to develop. The red blood- 
corpuscles in leukaemia often undergo certain changes in size and shape (poikilo- 
cytosis\ but seldom to such a degree as in grave essential anaemia. We should 




Fig. 80. — Leukaemic blood. (From Funke. | 



* For particulars with regard to the various methods of staiuing the blood (which are chiefly due 
to P. Ehrlich >, the reader is referred to text-books on methods of clinical examination. 



730 



CONSTITUTIONAL DISEASES 




Fig. 81.— Mixed leukaemia (myelaemia). 
(From Rieder.) 



mention, however, that in leukaemia we almost invariably find nucleated red blood- 
corpuscles, and these are exclusively normoblasts (see the preceding chapter). 
Granular masses are usually present in leukaemic blood in large numbers. 

Splenic tumor is the most frequent and important of the organic lesions pro- 
duced by leukaemia. It is rarely possible to observe its development. In most 

instances the spleen is already large 
when the patient first comes under ob- 
servation. It projects from under the 
ribs as a firm, hard mass, the lower and 
anterior extremity of which often ex- 
tends to the median line of the body. 
The inner edge of the tumor is some- 
what characteristic; it is rather sharp, 
and presents one or two notches. At 
first there is little subjective disturb- 
ance or pain referred to the spleen. 
When the enlargement is very great, 
there is often an annoying or even dis- 
tressing feeling of distention and full- 
ness in the abdomen. Respiration may 
also be interfered with by the crowding 
up of the diaphragm. 

The lesion of the bone-marrow can 
be determined during life mainly if at 
all by the myelocytes (vide supra). 
The only direct symptom which renders its existence probable is pain in the bones, 
but even this is not an infallible symptom. There is seldom pain except upon 
pressure. It is usually brought out by percussion of the sternum, but there may 
be well-marked disease of the marrow without this " sternal pain." 

As already stated, the lymph-glands often remain perfectly normal. If they 
also are affected, the disturbance is betrayed by their increase in size. Not only 
may the glands in the neck, axilla, and groin be enlarged, but occasionally also 
those of the mesentery and retroperitoneum, as can be demonstrated upon palpa- 
tion of the abdomen. The enlarged lymph-glands rarely cause severe pain, if any 
at all. If the blood were found to contain large numbers of small mononuclear 
lymphocytes, this would suggest, as has already been said, involvement of the 
lymph-glands. Unfortunately, however, our knowledge as to the significance of 
all the various forms of leucocytes is too imperfect as yet to justify absolute diag- 
nostic conclusions. 

We have already referred to leukaemic new growths in other internal organs. 
These possess, for the most part, merely a scientific interest, as they cause no spe- 
cial symptoms. Sometimes hepatic enlargement occurs, as the result of a diffuse 
leukaemic infiltration. The changes in the retina associated with leukaemia are of 
importance, as they can be detected by means of the ophthalmoscope. The retina 
presents white spots or stripes running parallel with the blood-vessels. They are 
due to collections of lymphoid cells, or to actual lymphoid growths. These lesions 
have been inappropriately called leukaemic retinitis. Retinal haemorrhages occur 
also in leukaemia, as in grave cases of idiopathic anaemia. 

All the other clinical phenomena of leukaemia result from the abnormal con- 
dition of the blood, meaning thereby the anaemia. The ability of the blood to 
perform its normal functions is impaired mainly through the loss of red blood- 
corpuscles; the resulting symptoms are therefore precisely the same as in essen- 
tial anaemia, and we do not need to describe them again. They usually are the 
most prominent symptoms of the disease, and include noticeable pallor of the 



LEUKAEMIA 



731 



skin, equal to that seen in pernicious anaemia; anaemic murmurs over the heart 
and the veins of the neck ; general debility ; anorexia, and digestive disturbances ; 
palpitation and dyspnoea; and, finally, the whole group of the " cerebral symptoms 
of anaemia," that is, headache, vertigo, syncope, and tinnitus aurium. Sometimes 
there is a troublesome pruritus. Provided he has no great anaemia, the general 
condition of a leukaemic patient may be fairly good. A symptom that is observed 
remarkably often in men suffering from leukaemia is persistent priapism. This 
symptom may, as we ourselves have known, be the first one noticed by the patient. 
Its cause is to be sought not in conditions of nervous irritation, but in the forma- 
tion of white thrombi, rich in leucocytes, in the corpora cavernosa (Kast). — In a 
few cases paralysis of the cranial nerves has been observed, such as the facial, 
hypoglossal, and acoustic. This paralysis is due sometimes to small haemorrhages, 
and sometimes to degenerative changes in the medulla oblongata. 

We would also call attention once more to the frequent haemorrhages. These 
must be due to impaired nutrition of the vascular walls, and sometimes they 
justify our speaking of a " haemorrhagic diathesis." Obstinate epistaxis is par- 
ticularly frequent. Less often we have haemorrhage from the intestine, stomach, 
kidneys, or into the skin or muscles, etc. We may have cerebral haemorrhage, 
with hemiplegia, or sometimes immediate death, consequent upon it. Severe 
cases may present a slight oedema of the skin and serous effusions into the vari- 
ous cavities of the body. 

The urine in leukaemia is essentially like that excreted in pernicious anaemia. 
Fleischer and Penzoldt have shown that in leukaemia as well as in pernicious 
anaemia there is increased destruction of albuminoids, and a consequent relative 
increase in the excretion of nitrogen. There is often also a considerable increase 
of uric acid. These rules, however, do not seem to be without exceptions. 

The temperature is apt to undergo slight elevations, as in severe cases of anae- 
mia. In advanced stages there may be quite high fever of an intermittent char- 
acter, reaching 103°-104° (39.5°-40° C). The fever is sometimes accompanied 
by chills, and when the temperature falls there is often a profuse and debilitating 
perspiration. 

Complications are, on the whole, rare. Sometimes we observe pulmonary tu- 
berculosis, or some acute intercurrent disease such as pneumonia. We saw one 
case end in death from haemorrhagic angina and oedema of the glottis. 

Clinical History. — Leukaemia is almost always chronic in its course. The dis- 
ease begins insidiously and progresses gradually ; the patient grows pale, feels lan- 
guid, and has slight and apparently insignificant symptoms, which gradually 
give place to alarming phenomena. The patient may himself notice the organic 
lesions incident to the disease. If the leukaemia be of the lymphatic type, he is apt 
to be struck by the swelling of the lymph-glands, while in splenic leukaemia his 
attention is attracted by the feeling of tension and pressure in the abdomen, the 
increasing prominence of the left side, and the unusual sense of resistance present 
in that part of the abdomen. Sometimes it is obstinate epistaxis, or haemorrhage 
from some other source, which first attracts attention and leads to a careful exam- 
ination of the blood and spleen. 

The entire duration of the disease is usually one or two years or perhaps more. 
Many cases pursue a rather benign and slow course, while in others there is a more 
rapid advance of all the symptoms, even justifying the term of acute leukaemia. 
Attention has been particularly directed to such cases by Ebstein. In them the 
changes in the spleen and lymph-glands may be only moderate. Usually, however, 
there is a distinct splenic tumor. The lymph-glands are almost invariably in- 
volved, as is found at the autopsy, if not before. The constitutional symptoms are 
very severe and grow rapidly worse, and, in particular, there is apt to develop an 
acute haemorrhagic diathesis, with haemorrhages into the skin and the internal 



732 



CONSTITUTIONAL DISEASES 



organs, including the brain. Often the temperature rises to 104° (40° C). Al- 
though there may be many fluctuations in the course of the disease, it leads,, 
apparently invariably, in a few weeks to death. For diagnosis a microscopic 
examination of the blood is essential. It is characteristic of acute leukaemia, as 
A. Erankel has pointed out, that the leucocytes in the blood are, in an overwhelm- 
ing proportion, the small mononuclear lymphocytes (immature form, vide supra). 
These cases of acute leukaemia give one the decided impression of an acute infec- 
tious disease. 

In ordinary cases of leukaemia we see frequently an apparent arrest of the dis- 
ease, or temporary improvement, and fresh relapses. The final termination is, how- 
ever, almost invariably unfavorable. Recovery from leukaemia is not absolutely 
impossible ; still, it is very rare, and at the most can be hoped for only during the 
early period of the disease. In almost all the advanced cases the prognosis must 
be described as absolutely unfavorable. Death usually takes place with symptoms 
of profound anaemia, and progressive bodily weakness. Sometimes the end is 
hastened by the occurrence of dangerous haemorrhage from the nose or into the 
brain, or by some intercurrent disease. 

Diagnosis. — Leukaemia can be easily and unmistakably recognized by a micro- 
scopic examination of the blood. In a very early stage of the disease the increase 
of white blood-corpuscles may be so slight that a definite decision can not be made ; 
but the later developments will afford absolute certainty in any typical case. 

We can not fail to recognise a case of leukaemia if the blood be examined. 
Such an examination is therefore demanded in every case of obstinate anaemia,, 
and, above all, in such patients as have a chronic enlargement of the spleen, or 
swelling of the lymph-glands in various parts of the body. The enlarged lymph- 
glands are readily recognizable. The splenic tumor can usually be diagnosticated 
from its characteristic position and shape, and especially from its inner, rather 
sharp edge, usually notched. It may be simulated by hydronephrosis and other 
diseases causing enlargement of the kidneys, and in women by ovarian tumors. 
In cases of doubt the blood should be examined, and if the result be a positive one,, 
we may feel certain of our diagnosis. If there is a chronic enlargement of the 
spleen without a leukaemic change in the blood, we must consider all the possible 
causes of such an enlargement ; thus there may be a passive congestion of the 
spleen, with enlargement, as the result of hepatic disease, portal thrombosis, or 
disease of the heart, or a splenic tumor from malarial poisoning. Again, there are 
cases where we have the signs of a gradually progressive anaemia, apparently idio- 
pathic, and a chronic enlargement of the spleen, or still more frequently enlarge- 
ment of the lymph-glands in various parts of the body, without increase in the 
number of white blood-corpuscles. Such cases are termed pseudo-leukaemia, or 
splenic anaemia, and are described in the next chapter. 

Treatment. — Nearly the same remedies are employed in leukaemia as in idio- 
pathic anaemia. Of course the greatest attention should be paid to the general 
condition. The patient should be well nourished, and perhaps he may be sent into 
the country or to some health-resort. Of internal remedies, the preparations of 
iron have been mainly employed. They seldom produce any brilliant or permanent 
effects. We have much more confidence in the administration of arsenic, and this 
remedy should certainly be tried in large doses. It may be given either in the 
shape of pills, or, with still more advantage, subcutaneously. Ziemssen recom- 
mends that fifteen grains (gramme 1) of arsenious acid should be boiled with 
seventy- five minims (5 cubic centimetres) of a fifteen-per-cent. solution of sodic 
hydrate, and the solution then diluted to make three ounces and a third (grammes 
100). Of this one-per-cent. solution of arsenate of soda, at first one quarter, then 
one half, and, finally, an entire Pravaz's syringeful, is injected once or twice a 
day. [A Pravaz's syringe holds about thirteen minims. — V.] Of course, the only 



PSEUDO-LEUKEMIA 



733 



hope of permanent benefit from this treatment would be in incipient cases. We 
have seen repeatedly, however, most satisfactory although temporary improve- 
ment follow the persistent use of arsenic in leukaemia. 

What are called " splenic remedies " have been often employed, but they do not 
seem very effectual in leukaemia. Mosler obtained good results from the long- 
continued use of quinine (5-8 grains = 0.30-0.50 gramme, or more, in twenty-four 
hours). He also recommends a trial of piperine and oil of eucalyptus: 

I> Olei eucalypti gtt. 100 ; 

Piperini, 

Cerae albas aa oj (gramme 4.0) ; 

Pulv. altheae 3ij (gramme 7.5). 

M. et fiant pilulae no. c. 

S. Three to five pills three times a day. 

Local treatment of the spleen has been attempted. If an ice-bag be constantly 
kept on the splenic region, it will sometimes diminish the size of the tumor, and 
it may also relieve pain. Botkin has recommended faradization of the spleen, 
but we can scarcely expect any great benefit from such a procedure. Injections 
of quinine, arsenic, and other remedies, have been made into the substance of the 
spleen. We do not believe that this is advisable, because it may cause dangerous 
haemorrhage. The splenic tumor of leucaemia has actually been extirpated surgi- 
cally; but the proceeding is so ineffectual and so fatal that it is now universally 
abandoned. The transfusion of healthy human blood has also been tried, but 
without satisfactory results. Subcutaneous injections of blood (vide supra) have 
been tried in only a few cases, but they may, perhaps, have good results. In some 
recent cases inhalations of oxygen are said to have improved the symptoms. 



CHAPTEE IV 

PSEUDO-LEUKJEMIA 

(ModgMnPs Disease. Adenia. Malignant Lymphosarcoma. Pseudo-leucocythazmia) 

It was mentioned in the preceding chapter that there are cases in which the 
organic lesions are apparently the same as in genuine leukaemia, and yet there is 
little if any increase in the number of white corpuscles in the blood. There is 
generally, however, a diminution in the number of red corpuscles. These cases 
usually receive the name which Cohnheim gave them of pseudo-leukaemia. It is 
nevertheless doubtful, whether they are to be regarded as a special form of dis- 
ease, and there are various facts which indicate that they are at least very closely 
allied to genuine leukaemia. There is a great similarity in most of the symptoms 
of the two diseases and in their general course, as well as in the organic changes 
they produce. Furthermore, a case of pseudo-leukaemia may finally assume the 
character of genuine leukaemia, with its characteristic blood chang-es. 

The purely splenic type of pseudo-leukaemia is the least frequent one. As yet 
very few such cases have been reported. There is a gradually increasing anaemia 
with the usual symptoms, and associated with these increasing enlargement of 
the spleen. It is impossible to draw any sharp dividing line between such cases 
and cases of pernicious anaemia attended with moderate enlargement of the same 
organ (splenic anaemia). It may be said to be a matter of taste which name the 
physician shall give to a case of -this sort. The bone-marrow seems to present the 
same characteristics in splenic pseudo-leukaemia as in pernicious anaemia. 



734 



CONSTITUTIONAL DISEASES 



Pseudo-leukaemia Lymphatica, — Pseudo-leukaemia of a lymphatic type is a 
much more frequent and well-defined disease. It was first described in 1832 by the 
Englishman Hodgkin, and is sometimes called Hodgkin's disease. Wunderlich 
was the first in Germany to study the disease thoroughly ; he described it in 1858 
under the name of " progressive multiple hypertrophy of the lymph-glands " ; and 
later Billroth termed it " multiple malignant lymphoma." Trousseau gave it the 
name of " adenia." 

Little is known about the aetiology of lymphatic pseudo-leukaemia. The tend- 
ency of late is to assign adenia to the group of infectious tumors, although the 
reasons for this belief are as yet purely theoretical. Many cases seem to be directly 
referable to tuberculosis, in the form of tubercular adenitis without other tuber- 
cular disease. Whether this is true as regards all cases of pseudo-leukaemia is as 
yet very doubtful, but this point should receive especial attention in the future. 
Pseudo-leukaemia is most common in young and middle-aged persons, and is ap- 
parently rather more frequent in men than in women. 

Pathological Anatomy. — The hyperplasia of the lymph-glands may be very 
great, producing large tumors of varying consistency. These have been called 
lymphoma, lymphadenoma, and lymphosarcoma. On section, the tumors dis- 
play a white or grayish-red surface, and are seen to be made up of a number 
of swollen glands fused into nodular masses. Upon microscopic examination, we 
find a very abundant proliferation of lymph-cells, sufficient to obscure the reticu- 
lum of the gland completely. The new growth may even escape beyond the 
capsule of the gland and invade surrounding structures. Inflammatory adhesions 
often take place between the tumor and the overlying skin. There does not seem 
to be any essential difference between the harder and the softer varieties of these 
tumors. 

These changes in the lymph-glands are often, though not invariably, associated 
with a swelling of the spleen. Its increase in size is usually slight. Lymphomata 
may also develop in the tonsils, the intestinal lymphatics, liver, kidneys, and other 
organs. Whether there are changes in the bone-marrow has not yet been deter- 
mined. 

The symptoms are very gradually developed. It is almost invariably the 
swelling of the lymph-glands which first attracts the attention of the patient or 
his physician. The glands upon one or both sides of the neck are usually the 
first to be enlarged, and they may finally grow to tumors the size of the fist, or 
even larger, producing great disfigurement. To the changes in the neck succeed 
swelling of the axillary, inguinal, and perhaps also the internal lymph-glands. 
The changes are gradual, and vary in their rapidity and extent. 

At first the general health is hardly at all affected, but as the disease pro- 
gresses its constitutional effects become more and more marked. The patient 
grows pale and languid, and finally presents all the symptoms of profound anae- 
mia. We may also have certain symptoms due to mechanical compression occa- 
sioned by the growth of the lymphomata. The tumors in the neck may cause 
dysphagia, from compression of the pharynx and oesophagus; dyspnoea, from com- 
pression of the larynx and trachea ; and perhaps alarming cardiac disturbance, 
from interference with the vagus. Hypertrophy of the bronchial glands some- 
times occasions great difficulty in respiration; enlargement of the abdominal 
glands may produce ascites or jaundice; and enlargement of the glands in the 
groin may give rise to oedema in the lower extremities. In advanced stages we 
may have " cerebral symptoms of anaemia " precisely similar to those seen in 
genuine leucaemia or in pernicious anaemia. There may be a tendency to haemor- 
rhage, pruritus, and occasionally prurigo, and the urinary secretion and tempera- 
ture may be abnormal. For particulars the reader is referred to the preceding 
chapters on leucaemia and pernicious anaemia. 



PSEUDO-LEUKEMIA 



735 



Upon examination of the blood, there are usually found the changes charac- 
teristic of ordinary anaemia, without increase in the number of white blood-cor- 
puscles. Sometimes, however, there may be a slight leuco.cytosis ; and sometimes, 
as already said, lymphatic pseudo-leukaemia may merge into genuine leukaemia. 
The examination of the blood must therefore be repeated from time to time. The 
spleen should also be examined. It is usually somewhat enlarged, and in some 
cases the enlargement may be considerable. Such cases might be properly de- 
nominated splenic-lymphatic pseudo-leukaemia. We may also discover a tender- 
ness of the sternum or other bones. 

The disease often lasts but a few months ; it may, in rare instances, extend 
over two or three years or more. Recovery is not completely impossible in the 
early stages of the disease (vide infra), but at a later period the prognosis is abso- 
lutely unfavorable. The fatal termination results either from increasing debility 
and anaemia, or from the effects of mechanical compression, or from haemorrhage, 
or from some intercurrent disease. 

A peculiar form of pseudo-leukaemia has lately been described by Ebstein and 
Pel. In this there are, at intervals of about ten to fourteen days, periods of 
marked fever, which last, also, about the same length of time. The condition has 
received the name chronic relapsing fever. Death occurs with symptoms of anae- 
mia; and the autopsy shows firm swelling of the liver, spleen, and the retro- 
peritoneal, mesenteric, and bronchial lymph-glands. Less often the external 
lymph-glands also are swollen, so that they can be felt during the life of the 
patient. The character of the blood is not leukaemic, so that these cases must be 
provisionally regarded as pseudo-leukaemia. 

The diagnosis of pseudo-leukaemia is usually easy. It is to be based upon the 
objective signs and the condition of the blood. The disease is most apt to be 
confounded with swelling of the lymph-glands occasioned by tubercular infec- 
tion; but in this latter case the changes are seldom seen in so many parts of 
the body, and the patient usually presents other indubitable evidences of tubercu- 
losis. (See also under aetiology.) 

Treatment. — We possess only one remedy capable of promoting absorption of 
the lymphomata, namely, arsenic. We have ourselves, in common with a great 
number of observers, had the most convincing evidence of the favorable influence 
of arsenic. It must, however, be given in sufficient doses : for example, a pill con- 
taining one fifteenth of a grain (gramme 0.004), or even a larger amount of 
arsenious acid, three times a day; and its use must be persisted in for a long time. 
Still more efficient are subcutaneous injections of the solution of arseniate of soda 
which we have described quite fully in the preceding chapter. We have also seen 
apparent benefit from associating with the arsenic inunctions of iodoform (iodo- 
form one part, vaseline fifteen parts) over the tumors. 

In the early stages decided benefit may be expected from this mode of treat- 
ment. At a later period we may obtain a decrease in the size of the tumors, but 
we can hardly hope for any permanent improvement. Operative interference is 
out of the question, except at the very beginning of the disease. Later on, it 
would be perfectly useless, and it could seldom be carried out. 

Other suggestions with regard to treatment may be obtained from the chapters 
on anaemia and leukaemia. 



736 



CONSTITUTIONAL DISEASES 



CHAPTEE V 
H-ffiMOGLOBINJEMIA AND HEMOGLOBINURIA 

Definition and General ^Etiological Considerations. — If any cause produces a 
solution of the red blood-corpuscles in the blood-serum, hemoglobine is excreted 
through the kidneys. The hemoglobinemia — the presence of free hemoglobine 
in solution in the blood — excites hemoglobinuria, i. e., the excretion of hemo- 
globine in the urine. The causes of heinoglobinemia and its correlative herno- 
globinuria are manifold. In the first place, there is a whole series of poisons 
which, if introduced into the blood in sufficient amount, exercise a directly de- 
structive influence upon the red blood-corpuscles, and thus excite hemoglobinu- 
ria. To this list belong chlorate of potash (Marchand), pyrogallic acid and naph- 
thol (ISTeisser), sulphuric acid, glycerine, toluylendiamine, and many other sub- 
stances. Distilled water is also in this sense a poison. Bostrom has discovered a 
fact of practical importance which deserves mention in this connection. It is, 
that a certain kind of mushroom (Helvetia esculenta) , when fresh, contains a poi- 
son which is capable of producing intense hemoglobinuria, and such grave symp- 
toms as jaundice, delirium, drowsiness, and tetanic convulsions, with perhaps a 
fatal termination. This poison is, however, so evanescent and so readily soluble 
in hot water that the mushroom becomes perfectly harmless if thoroughly soaked 
and then boiled, or if it has been dried. 

Secondly, hemoglobinuria may be developed in connection with infectious 
•diseases. In this case, also, it is probably referable to the action of poisons cre- 
ated within the system. Thus hemoglobinuria has been observed in the course of 
a severe attack of scarlet fever or typhoid fever. Possibly malarial poisoning and 
syphilis may give rise to paroxysmal hemoglobinuria. This question will be dis- 
cussed later on. 

There is a third mode of origin which also possesses practical importance. If 
blood from one animal be injected into another of a different species, hasmoglo- 
binuria is almost sure to result. Not only do the injected blood-corpuscles undergo 
solution, but also the injected serum acts as a poison upon the original blood-cor- 
puscles, destroying and dissolving them. This transfusion-hemoglobinuria has 
been described by Prevost, Dumas, Ponfick, and Landois. It can be produced in 
human beings, as there was only too good opportunity to observe during the brief 
period when the transfusion of lamb's blood was in vogue. The practical deduc- 
tion is evident, that we should not use for injection into the circulatory system 
of a patient anything but an unirritating salt solution, or human blood. 

A fourth and very important etiological factor is exposure to extremes of 
temperature. Hemoglobinuria follows extensive burns. The blood-corpuscles in 
that region of the periphery exposed to the heat are destroyed. Cold is capable 
of producing precisely analogous results. This is particularly evident in the cases 
of so-called paroxysmal hemoglobinuria described by Wickham Legg, Lichtheim, 
Murri, and Kiissner. [Raynaud's disease (see page 900) and hemoglobinuria 
are associated in a sufficiently large proportion of cases to show -some relation- 
ship between the two.] 

Pathology and Symptoms of Hsemoglobingemia, particularly the Parox- 
ysmal Variety. — In most of the cases above enumerated, hemoglobinuria is the 
result of an obvious or easily demonstrable cause. There is, however, another 
variety which appears paroxysmally in individuals who are otherwise perfectly 
well. Its symptoms are extremely characteristic. Although not a very frequent 
disease, there has been abundant opportunity to study it. 

As just intimated, the disease is paroxysmal. Very often an attack is ushered 



H^HOGLOBIKZEMIA AND HEMOGLOBINURIA 



737 



in by frequent and persistent yawning. To this symptom are soon added pain in 
the limbs, headache, nausea, vomiting, and coolness of the periphery. The tem- 
perature speedily rises to 102° (39° C.) or more. With this is often associated a 
decided chill. Sometimes there is a violent pain in the hepatic region. There is 
a distinct enlargement of the spleen. Then the temperature falls again, perspira- 
tion appears, and the patient, although languid and depressed, soon recovers. 
A slight icteric hue can almost invariably be detected toward the end of the at- 
tack, the ordinary duration of which is from two to twelve hours. An eruption of 
urticaria has been repeatedly seen in connection with the attacks. 

The most interesting phenomenon of all remains to be described. We refer to 
the condition of the urine during and directly after the paroxysm. This secretion 
presents a dark brownish-red color resembling blood; it may even appear almost 
black. Its reaction is almost invariably acid; its specific gravity is usually 
rather low, say 1008-1012. On boiling the urine, the hsemoglobine is decomposed 
and a brown coagulum of albumen formed. If the fresh urine be examined 
through a spectroscope, we find the bands characteristic of hsemoglobine, and 
sometimes also the narrow bands indicative of methsemoglobine. It is therefore 
impossible to doubt the existence of hsemoglobine in the urine; and yet, upon 
microscopic examination, we find no red blood-corpuscles in the urine, or, in 
other words, no " hematuria." Frequently there are large numbers of opaque 
red granules in the urine, the shape of which is extremely irregular. These are, 
doubtless, granules of hsemoglobine. Some of them are free in the urine, some 
are attached to casts. Of the latter, we find hyaline and a few epithelial casts 
present. Sometimes masses of hsemoglobine assume the appearance of casts. The 
sediment may also contain a few cells of renal epithelium. The presence of this 
and of hyaline casts indicates that the kidneys have been slightly irritated by the 
excretion of hsemoglobine. Hence, we sometimes observe a persistence of slight 
albuminuria after the hemoglobinuria has ceased. In mild attacks, also, there 
may be merely albuminuria, without hemoglobinuria. 

If now we examine the blood during a paroxysm, we shall find that hemoglo- 
binemia is associated with hemoglobinuria of the paroxysmal type, as well as 
with that occasioned by the action of various poisons. Kiissner obtained blood 
from a patient during a paroxysm, and found that its serum had a ruby-red color, 
and contained hsemoglobine in solution. This proves that the destruction of blood- 
corpuscles takes place within the circulatory system. Indubitable tokens of this 
destructive process are to be seen upon microscopic examination of the blood 
during a paroxysm, especially when the paroxysm has been produced artificially 
in the manner described below. The red blood-corpuscles have little tendency to 
form rouleaux. They are pale, and many of them are irregular in shape (poikilo- 
cytes). Irregularly shaped flakes of hsemoglobine are also present, and often large 
numbers of decolorized red blood-corpuscles are to be seen. To these latter Pon- 
fick has given the name of " shadows." The exciting cause of the individual 
attacks of paroxysmal hemoglobinuria is, in most instances, catching cold. A 
paroxysm is usually due to being outdoors in a cold storm, and perhaps being wet 
through. In summer the attacks cease completely in patients of this sort ; still, 
as Eosenbach showed by experiment, an attack may even then be artificially ex- 
cited at any time by exposing the patient's skin on purpose to a decided chill — e. g., 
by causing the patient to take an ice-cold foot-bath, or the like. In order to show 
that there is merely a local action of cold in these cases, Ehrlich and Boas (each 
independently) arranged the experiment in the following manner : They tied an 
elastic ligature firmly around the finger of a subject, and had him immerse it for a 
quarter of an hour in ice-water. In every sample of blood taken from the finger 
the above-described changes could be most distinctly demonstrated, while blood 
taken from other parts of the patient's body showed scarcely any abnormality. 
47 



738 



CONSTITUTIONAL DISEASES 



The influence of cold is not the only exciting cause for such attacks, although 
it is the most frequent one. Paroxysms of hemoglobinuria have been seen after 
great bodily exertion, particularly after a rather long walk ; in women sometimes 
at the menstrual period; and also after mental excitement, and the like. No 
explanation has as yet been given why some few human beings have this remark- 
able sensitiveness of their red blood-corpuscles, while most persons undergo the 
same influences without similar consequences. In this regard should be noted 
the statement of Murri, that paroxysmal hsemoglobinuria is particularly apt to 
appear in persons who have a syphilitic taint. 

Finally, with regard to the origin of the other symptoms of the hemoglobin- 
uric attack, such as fever, at first it was thought that there was a sort of uremic 
condition, inasmuch as the urinary tubules are often so choked with granules of 
hemoglobine that the excretion of urine might well be hindered. Probably, 
however, another circumstance is still more important — viz., the toxic influence of 
the fibrine ferment which is formed because of the hemoglobinuria. The hsemo- 
globine, as it is set free, destroys numerous white blood-corpuscles, and in this 
way fibrine ferment is produced, as we have already mentioned (see page 725). 

Another important point is that it is not the kidneys alone which serve for 
the reception of the constituents of the disintegrated and dissolved blood-corpus- 
cles. Ponfick has been led by the result of certain experiments to believe that 
the spleen and liver are also affected. The spleen appropriates the undissolved 
remnants of the corpuscles, and, as a consequence, it may undergo considerable 
enlargement. The liver absorbs a large part of that portion of the hemoglobine 
which has undergone solution, and converts it into bile. As a result there seems 
to be an increased secretion of bile. Jaundice is probably due to local biliary 
stasis and biliary absorption in the liver itself (" hemo-hepatogenous jaundice " 
of Afanassiew). No proof has been furnished that a part of the haemoglobine dis- 
solved in the blood can be changed into bile pigment (true " hematogenous 
jaundice ")• 

Prognosis. — When hemoglobinuria is merely a symptom of other abnormal 
processes caused by poisoning or by some specific infection, the future of the 
patient depends entirely upon the severity of the primary disease. An attack of 
paroxysmal hemoglobinuria would not seem to involve any direct danger to life. 
Recurrence of the paroxysms is always to be feared if the patient be exposed to 
those influences which produce it. There are no certain means of decreasing the 
patient's liability to attacks. In a few cases, however, where there had been 
syphilis, the paroxysms are said to have been permanently banished by mercurial 
inunctions. Likewise, if we suspect malarial influences, quinine should be tried. 

No special treatment is required during the paroxysm itself. The patient 
must escape as soon as possible from the exciting cause ; it is then advisable for 
him to lie quietly in bed, and to drink a large amount of fluid, so as to wash out 
the masses of haemoglobin from the kidneys. 



CHAPTER YI 
SCUHVY 

{Scorbutus) 

Prefatory Remarks. — Scurvy is one of a group of diseases which may be 
termed " hemorrhagic." They all have one predominant symptom, namely, a 
decided hemorrhagic diathesis, respectively associated in the different diseases 



SCUKVY 



739 



with various other more or less pronounced disturbances. This tendency to spon- 
taneous haemorrhage is in many cases, particularly the milder ones, confined 
more or less exclusively to the skin, but in numerous other instances haemorrhage 
also takes place into the underlying tissues, such as the muscles or joints, as well 
as into the mucous membranes. 

The distinctions between these various diseases are founded upon the manner 
in which the haemorrhages occur and the symptoms which attend them. We 
may mention scorbutus, purpura simplex, purpura haemorrhagica, and peliosis. 
It should, however, be stated that, although it is possible to distinguish several 
varieties of disease, each one of which presents a tolerably characteristic picture, 
there are innumerable transitional forms. It may, indeed, be almost a matter of 
taste in any particular case what name shall be applied to it. The existence of so 
many intermediate forms renders it evident that the various members of this 
group of diseases are at least closely related if not actually identical. We shall 
even find, upon careful consideration, that certain other diseases not usually 
regarded as haemorrhagic are nearly akin to the group now under consideration. 
We refer to certain skin diseases, which are characterized mainly by inflamma- 
tory and exudative lesions of the skin. Chief among these should be mentioned 
erythema exsudativum multiforme, which not very infrequently exhibits some 
tendency to haemorrhages, and thus presents external appearances closely simu- 
lating the forms of purpura. In the last-mentioned forms of disease, however, 
there appears still another clinical relationship — viz., to the ordinary acute articu- 
lar rheumatism (q. v.). All of the haemorrhagic diseases are distinguished by 
a frequent involvement of the joints, while, on the other hand, acute articular 
rheumatism is sometimes associated with haemorrhagic lesions in the skin. 

In order to understand the underlying connection between these various dis- 
orders, a precise knowledge of their aetiology is requisite. Already considerable 
evidence has been gathered pointing to the importance of infectious influences in 
their production (vide infra), but no absolute proof has yet been obtained. Still, 
it must be said that various observations already made indicate that we are likely 
to find some aetiological relations between the haemorrhagic and the septic dis- 
eases. In the meanwhile, we must be guided mainly by the purely clinical phe- 
nomena. These, again, indicate that sharp distinctions between the various haem- 
orrhagic diseases would be purely artificial. In this and the following chapters we 
shall discuss the two main types of haemorrhagic disease. 

.^Etiology of Scurvy. — Scurvy is sometimes sporadic, and sometimes epidemic 
and endemic in its occurrence. There were formerly very extensive and fatal 
epidemics of the disease, at a time when the laws of health with regard to large 
aggregations of human beings were little regarded. The disease was prone to 
attack armies, or the inhabitants of besieged cities, or, especially, seamen. It 
was, and to a certain extent is still, one of the diseases most dreaded by the 
mariner. It has often swept away an entire ship's crew. To-day endemics of 
scurvy are by no means infrequent, although not so extensive as formerly. They 
are most apt to occur in prisons and similar institutions, and in barracks. 

These facts, under the light of our present views in regard to such matters, 
would almost force us to seek some organic infectious poison as the origin of the 
disease. Formerly men were inclined to direct their sole attention to such cir- 
cumstances as the character of the food, the dwelling, the climate, and similar 
conditions; nor can it indeed be denied that these hygienic factors do exert a 
decided influence upon the spread of the disease. It is, however, evident that they 
can not be its proper cause, for, beyond a doubt, scurvy may occur independently 
of any of the factors usually regarded as essential to its development. These 
causes must therefore be regarded as simply predisposing influences. 

Great aetiological importance has long been ascribed to certain errors in diet. 



CONSTITUTIONAL DISEASES 



These include the use of bad or insufficient food, the undue predominance of 
certain kinds of food, and in particular of the salt meats so much employed on 
shipboard; or, again, the deficiency of certain varieties of food, in particular the 
lack of vegetable food, and still more of fresh vegetables. Much industry and 
acuteness have been expended in defending the theory that the lack of vegetable 
food is injurious because of the deficient supply of potassium salts under such 
circumstances (Garrod). Nevertheless, this view does not reach the heart of the 
matter, for in numerous epidemics of scurvy there has been no such lack of vege- 
table nourishment; and in some instances the diet employed has contained an 
unusual abundance of potassium compounds. 

A like predisposing but not specific influence is exerted by the other factors to 
which serological importance has been assigned. They are indeed often present 
in epidemic as well as in sporadic cases, but, as previously stated, they may not 
exist at all. To this class belong damp and unfavorable quarters, cold, moisture, 
persistent heat, and excessive muscular exertion. 

Age and sex exert no great influence upon the disease. Weakly persons seem 
to be somewhat more liable to be attacked than are the vigorous. The possibil- 
ity of contagion has been maintained repeatedly, but contagion has not been 
proved to exist, and unprejudiced observation would incline one strongly to doubt 
its existence. 

[It seems probable that the dietetic causes of scurvy lie rather in a want of 
variety in the food than in the absence of any one class or order of foods. Wales 
says (Pepper, System of Medicine) : ""No single natural order contains plants 
that supply all the elements essential to the nutrition of the body and the right 
composition of the blood. The graminaceous and leguminous articles of food, for 
instance, are numerous but not various; they all afford the same or analogous 
albuminous elements, which have about the same nutrient value as the corre- 
sponding substances in animal food, and hence health and vigor can not be sus- 
tained on a diet of flesh combined with wheat, rice, and oatmeal, or with beans 
and peas, or with all of them together. Outbreaks of scurvy have occurred on 
shipboard where the ration is made up principally of these articles — as in Anson's 
ship when supplied with an abundance of fresh animal, farinaceous, and legumi- 
nous foods. It is clear, therefore, that, in order to obtain a variety of materials 
required in nutrition, we must resort to several of the natural groups, those par- 
ticularly which comprise the succulent vegetables and fruits." 

It is certain that scurvy is a disease which we can produce artificially, and that 
it is preventable in the vast majority of cases. It is now as rare among seamen as 
it was formerly common — a change which is the result chiefly of care to vary the 
diet, especially on long voyages. The United States law requires that lime- or 
lemon-juice, sugar, and vinegar shall be carried by all sailing vessels bound on 
ocean voyages or engaged in the fisheries, specifies the circumstances and mini- 
mum doses under which the antiscorbutics are to be given, and provides penalties 
for violation or neglect.] 

Clinical History. — The disease does not usually begin suddenly. There is a 
gradual onset, marked by certain constitutional symptoms. The chief of these 
are languor and debility, a sense of thoracic oppression, palpitation, and usually 
a " rheumatic, dragging pain " in the loins and extremities, especially in the lower 
extremities. The patient is obliged to take to his bed if the case be at all severe ; 
he is very sensitive to cold, and often is drowsy and apathetic. These somewhat 
indefinite premonitory symptoms last for a few days or a week, when other and 
more characteristic phenomena appear. 

Among these new appearances are spontaneous haemorrhages, occurring chiefly 
in the lower extremities. There are cutaneous haemorrhages, producing dark-red 
macules of varying size, most of them with a hair-follicle in their center, and 



SCUKVY 



there are almost invariably haemorrhages into the deeper tissues also. The sub- 
cutaneous connective tissue and muscles, and sometimes the periosteum, are 
affected, These deeper extravasations are a peculiarity of scurvy. They can 
sometimes be felt as hard, painful swellings in the parts affected, and are some- 
times discernible from the discoloration of the skin, which soon results from the 
solution and diffusion of the blood-pigment. The patches present a diffuse bluish 
color, merging into greenish or yellowish at the periphery, and they are often 
quite large. They have a precisely similar appearance to " black-and-blue " spots 
resulting from injury. Of course, the more abundant and the more superficial 
the extravasation, the more extensive and darker is the macule. Similar appear- 
ances may sometimes be observed in the upper extremities and trunk, mainly in 
severe cases. The face and scalp rarely present ecchymoses. 

Sometimes a haemorrhage results in the necrosis and sloughing away of a por- 
tion of the skin. The necrosis i£ succeeded by ulceration ("scorbutic ulcers"). 
Under unfavorable hygienic influences this process may assume a grave signifi- 
cance. It should also be stated that we may observe other cutaneous disturbances, 
such as erythema, wheals, vesicles (the contents of which may be tinged with 
blood — " scorbutic pemphigus "), papules, and pustules. These eruptions are more 
frequent in some epidemics than in others; they may either be associated with or 
replace the cutaneous ecchymoses. 

In the ordinary sporadic cases of scurvy which occur among us, haemorrhages 
into the mucous membrane, except of the gums, are very rarely seen. The same 
is true of haemorrhages from the stomach and other internal organs. In severe 
cases, during epidemics and under bad hygienic surroundings, it is otherwise; 
haemorrhage may take place from the nose, stomach, intestines, bronchi, and kid- 
neys, and blood may be effused into the serous membranes. 

Next in importance to haemorrhage is another peculiar symptom, presented by 
the mucous membrane of the mouth, and particularly that of the gums. In order 
to establish a diagnosis of scurvy in sporadic cases, we must demonstrate the 
existence of these two main symptoms — namely, the haemorrhage into the skin 
or muscles, and the changes in the gums now to be described. 

The scorbutic changes in the gums usually appear quite early in the course of 
the disease, being in many cases simultaneous with the haemorrhages, although 
they may either precede or follow the latter. The gums assume a bluish hue, 
become swollen and spongy, are painful, and have a tendency to bleed. The 
changes are usually most pronounced in the salient parts of the gums between 
the teeth. It is a remarkable fact that they are hardly visible at all at places 
where there are no teeth; and the gums of very young children and of aged 
patients remain almost intact. In severe cases the gums are not only swollen but 
necrosed; the change is at first a superficial one, but it may extend inward and 
produce dirty-looking ulcers. Other parts of the mouth are liable to become 
involved in the ulceration, producing a diffuse ulcerative stomatitis, and giving 
the breath a most offensive odor. 

Certain other local and constitutional phenomena are not infrequent, though 
less characteristic than the haemorrhages and the alterations in the gums. Chief 
among the general disturbances is scorbutic anaemia. This is often referable in 
part to the unfavorable hygienic influences surrounding the patient, but the dis- 
ease itself seems to impair the general nutrition. The patient looks pale, has a 
dry skin, and loses flesh rapidly. The temperature is often normal. Sometimes 
there may be an occasional rise of temperature, either in the beginning or in the 
further course of the disease. If complications occur, they are not infrequently 
accompanied by considerable fever. 

Among more localized symptoms should be mentioned the premonitory sore 
throat which sometimes occurs. It is usually of the ordinary catarrhal variety, 



742 



CONSTITUTIONAL DISEASES 



but it may assume a hemorrhagic character. Bronchitis also may occur. Lobular 
pneumonia and genuine lobar pneumonia have been repeatedly seen in severe 
cases. Pleurisy, pericarditis, and inflammations of other serous membranes occa- 
sionally complicate the disease. They may likewise display a hemorrhagic tend- 
ency in the exudations to which they give rise. Disturbances in the joints are 
sometimes seen, and are characterized by an effusion of liquid into the articular 
cavities, which effusion may be either serous or hemorrhagic. This is a favor- 
able opportunity to call attention to a peculiarity common to all the hemorrhagic 
diseases and allied affections (vide supra) — they are apt to be associated with 
articular swelling. 

The pulse may be somewhat accelerated, or may be slower than normal. It is 
usually small and compressible. Endocarditis may occur, but it is very excep- 
tional. The blood does not present any constant and characteristic alterations in 
scurvy. The spleen may be decidedly enlarged, particularly in severe cases. 
Albuminuria has been repeatedly observed, but it is almost wholly confined to 
severe cases, in which, indeed, a typical acute nephritis may be developed. 

Course of the Disease. Varieties of Scurvy. Prognosis. — The sporadic cases 
usually met with in this region almost invariably pursue a favorable course. The 
symptoms are confined mainly to constitutional disturbance, ecchymoses in 
the lower extremities, and the affection of the gums, the grave complications 
above mentioned being rarely met with. The average duration of the disease is, 
nevertheless, some weeks. Recovery is deferred in proportion as the hygienic 
surroundings are bad, but even then the termination is almost sure to be 
favorable. Scurvy has, however, a noteworthy tendency to relapse, so that the 
course of the disease may be very much prolonged. Even when the illness has 
terminated in recovery, there remains behind a certain liability to fresh attacks 
of scurvy, just as acute articular rheumatism is apt to recur. We are acquainted 
with a patient who has been severely ill with scurvy some five or six times within 
the last few years, and this without any demonstrable cause. 

The prognosis in grave cases, occurring under unfavorable hygienic influences, 
and aggravated by the lack of proper food and attention, is far otherwise. Here 
death is not infrequent, sometimes as a result of progressive cachexia, some- 
times because of pneumonia, pericarditis, cerebral hemorrhage, or a similar 
intercurrent disease. 

Anomalous or rudimentary cases of scorbutus may occur. They are most apt 
to be seen when the disease is epidemic or endemic. As a rule, the symptoms are 
mild. We find, for example, a scorbutic gingivitis and stomatitis without hem- 
orrhage, or, on the other hand, hemorrhages into the skin and mucous membranes 
unattended by alteration in the gums. There have even been cases reported of 
simple scorbutic anemia without any local symptoms. 

[The experience of army surgeons during our civil war deserves mention 
in this connection. Hammond, Woodward, and others state that many cases 
classed in the sick reports as " general debility " were cases of incipient or imper- 
fectly developed scurvy, hemorrhage from mucous membranes or into the skin 
being absent.] 

Diagnosis. — The diagnosis of scorbutus is almost self-evident when the two 
chief symptoms of hemorrhage and alteration in the gums are both present. If. 
however, one or the other of these symptoms is suppressed or imperfectly devel- 
oped, it may be difficult to determine what disease we have before us, or to exclude 
ordinary stomatitis, rheumatic peliosis, and similar diseases. One characteristic 
sign should be emphasized again in this connection. The hemorrhage of scurvy 
is scarcely ever confined to the skin, but almost invariably there are large extrava- 
sations deeper in, in the muscles and fascie. These occasion, secondarily, the 
characteristic bruise-like bluish-yellow spots seen through the skin. 



BARLOW'S DISEASE 



743 



Treatment. — The essential requisites in the treatment of scurvy are proper 
hygiene and diet. Eresh air, suitable nourishment, and good nursing, if promptly 
supplied, are usually of themselves sufficient to induce recovery, while the physi- 
cian possesses no remedies which compensate for their absence. 

The belief that a main cause of scurvy lies in a deficiency of fresh vegetables 
has given rise to a practice, still in vogue, of prescribing a great abundance of 
fresh vegetables, such as lettuce, spinach, and sorrel, fruit, lemonade, and other 
drinks prepared from fruit syrups. There is no reason to deviate from a course 
to which experience has given its sanction, although we have repeatedly had 
opportunity to see that the administration of fresh vegetables is by no means 
essential to rapid recovery. Patients supplied with any other proper nourishment 
thrive equally well. Certain varieties of plants have attained a special reputa- 
tion as "antiscorbutics," such as the spoonwort (CocMearia officinalis), so fre- 
quently mentioned in accounts of early polar expeditions. None of these plants, 
however, possess the specific properties assigned to them. The administration 
of vegetable acids and the salts of potassium (bitartrate and nitrate of potas- 
sium), in a chemically pure form, has also been repeatedly tried, but it has not 
gained popularity. 

The drugs most employed are the bitters and tonics. They have no specific 
value, but are perhaps as good remedies to prescribe as any. We may give a 
decoction of cinchona, to which may be added a small amount of dilute sulphuric 
acid and syrup, or some preparation of gentian or a similar bitter. It was once 
believed that the internal administration of the mineral acids exerted a specially 
favorable influence upon the hemorrhagic diathesis ; but this is very doubtful. 

Certain symptoms may demand attention; in particular, the affection of the 
mouth and gums. It is of great importance to cleanse the mouth frequently with 
disinfectants and mild astringents, such as chlorate of potassium or sage tea. It 
is also advisable to paint the inflamed and spongy gums at short intervals with 
tincture of myrrh or tincture of rhatany. The absorption of the ecchymoses in 
the lower extremities will be promoted by cautious massage. Inunctions of lini- 
mentum chloroformi and the like give relief from the pain caused by the extrava- 
sations into the deeper tissues. In severe cases stimulants are often demanded, 
such as camphor, ether, and alcohol. Such complications as appear may also 
demand special treatment. 

Convalescence is promoted by continued attention to diet, bathing, and the 
administration of iron and quinine. 



APPENDIX 

barlow's disease 

In this connection we desire to mention briefly a peculiar symptom-complex 
which has been associated with scurvy, in regard tc the real nature of which we 
do not yet possess any definite knowledge. The disease is, therefore, usually 
named after the person who discovered it (1883), as Barlow's disease. 

The disease has been seen thus far in children alone, and most often between 
the ages of six and eighteen months; almost all the children had previously 
shown definite signs of rickets. There is little, if any, fever, but an extremely 
painful swelling of the bones, particularly of the epiphyses of the long bones, 
though the lower jaw, cranium, and other parts may be involved. The epiphyses 
may become loosened, but the joints themselves are not affected. Upon careful 
examination it is found that the swelling is due to subperiosteal haemorrhages. 
In association with these there may be other indications of a hsemorrhagic diath- 



CONSTITUTIONAL DISEASES 



esis, such as hemorrhage into the skin, and into the serous membranes, and 
hematuria. In mild cases the hemorrhages along the bones are absorbed and do 
not recur. In severe cases, however, the hemorrhages are constantly repeated, 
and the child may finally die of exhaustion. 

The prognosis is consequently to be expressed with some reserve. Treatment 
consists chiefly in suitable regulation of the diet. If the hemorrhages are quite 
large it is advantageous to make a surgical incision, and allow the blood to escape. 



CHAPTER VII 
PURPURA. MORBUS MACULOSUS WERLHOFIX. PELIQSIS 

As already stated in the preceding chapter, the various "hemorrhagic dis- 
eases " are so intimately related to one another that it is quite impossible to make 
a rigid categorical division of them. The numerous names which have been 
introduced into the literature of this subject certainly contribute more to obscure 
than to elucidate the attendant phenomena. 

Erom a clinical standpoint this fact is the all-important one — namely, that 
there are cases in which the foremost symptom is the spontaneous occurrence of 
hemorrhage. There are cutaneous ecchymoses, and there may be at the same 
time hemorrhages in the internal organs and into the mucous membranes. In 
the milder cases of this sort these hemorrhages constitute almost the only symp- 
tom of disease; but they may be associated with considerable general disturb- 
ance, indicated by fever and weakness, or with certain local complications. The 
true cause of these diseases has not yet been discovered. There is seldom any 
evidence of an exciting cause, and the disorder may attack either the well-nour- 
ished or the poorly nourished, the old or the young, men or women. There is, 
however, an indisputable relationship between these diseases and certain others — 
namely, scurvy, erythema exsudativum, and perhaps acute rheumatism and endo- 
carditis. This similarity indicates that the process is of an infectious, or toxic, 
character. Such an assumption promotes greatly a proper understanding of the 
phenomena under consideration. It is also said that subcutaneous injections of 
blood from patients with morbus maculosus may cause a like affection in rabbits 
(Petrone and others). In some few cases the weight of evidence would seem, 
however, to point to an antecedent impairment of nutrition in the walls of the 
blood-vessels. A good example of this is seen where cutaneous ecchymoses occur 
in old and marantic individuals (peliosis senilis). There is some doubt whether 
these exceptional cases belong with the others. 

The mildest forms of the diseases under discussion are termed purpura. The 
hemorrhages are seen mainly in the skin of the lower extremities, and are apt to 
take place in the follicles. There may also be ecchymoses upon the trunk and 
upper extremities, but the mucous membranes and the deeper tissues remain 
intact. A means of distinguishing purpura from scorbutus lies in the fact that in 
purpura there are no hemorrhages into the muscles and no lesions of the gums, 
although it should be confessed that transitional forms between the two occur. 
The disorder is called purpura simplex if the cutaneous ecchymoses constitute 
the only symptom, or, at any rate, the only important one. These cases almost 
invariably terminate in recovery, and are over at the end of ten days or three 
weeks. Sometimes elevations of the skin are formed resembling wheals, and 
hemorrhages take place here and there into them. This subvariety has been 
called by some purpura urticans. It forms a connecting link between purpura 



PURPURA. MORBUS MACULOSUS WERLHOFII. PELIOSIS 745 



simplex and those cases of erythema exsudativum which are associated with haem- 
orrhage. Further particulars may be found in special works upon dermatology. 

Quite often the haemorrhages are attended by " dragging rheumatic pains " ; 
such cases are termed purpura rheumatica or rheumatic peliosis (Scbonlein). 
There may also be constitutional disturbance, slight fever, anorexia, and indis- 
position to either bodily or mental exertion. There may sometimes be actual 
arthritis, with an inflammatory effusion into the joints. The knee and other 
joints of the lower extremities are most apt to suffer in this way. The gums are 
usually normal; nor is there, as a rule, haemorrhage into the mucous membranes 
or the viscera. These cases may last but two or three weeks. Often, however, 
they are more tedious, being marked by the recurrence of the ecchymoses and 
articular pain. Most of them get well at last. 

ISTo sharp dividing line can be drawn between the forms of purpura thus far 
described and certain graver cases. These latter are most of them grouped under 
the name of purpura hcemorrhagica, or its preferable because more distinctive 
synonym — every purpura being hemorrhagic — morbus maculosus Werlhofii. 
The cutaneous ecchymoses in this class of cases are usually extensive ; and, fur- 
thermore, we have haemorrhages into the mucous membranes of the nose, mouth, 
soft palate, stomach, and intestinal canal, as well as into internal organs (the 
brain and kidneys), and also into the serous membranes. The constitutional 
disturbance is apt to be severe. The condition may be distinctly " typhoidal." 
Fever may be entirely absent, even in grave cases, although sometimes there is 
a considerable rise in temperature. 

There are usually no local symptoms beyond those already mentioned. In 
typical cases the gums remain intact. Swelling of one or more joints has been 
repeatedly observed, as have also endocarditis and acute haemorrhagic nephritis. 
If marked cerebral symptoms are developed, suggesting an apoplectic shock, we 
may surmise that a cerebral haemorrhage has taken place. It should also be stated 
that marked gastro-intestinal disturbance may occur. Cases of this sort have 
been observed by Henoch in children. They may also occur in adults. In rare in- 
stances there may be intestinal ulceration, with perforation and consequent peri- 
tonitis. The spleen may undergo acute enlargement. 

All the .symptoms which have been enumerated render distinct the similarity 
of the clinical picture, in severe cases of morbus maculosus Werlhofii, to that of 
severe septic infection. In fact, it is not impossible that continued investigation 
will deprive morbus maculosus of its individuality as a specific form of disease, 
and show that it is merely a special form of profound sepsis. 

The prognosis in purpura hemorrhagica should always be a guarded one ; the 
patient is in danger both from the general depression and anaemia, and from 
certain special lesions. Even a severe case may, however, recover. The disease 
sometimes proves very tedious ; it may occupy several months. 

Treatment. — The general regimen to be prescribed is similar to that directed 
in scurvy. The physician must strive to support his patient's strength by 
proper nourishment. A great many internal remedies have been recommended, 
most of them on purely theoretic grounds. It is difficult to say whether they 
actually exert a favorable influence upon the course of the disease. The follow- 
ing drugs are chiefly employed: Ergotine, perchloride of iron, dilute sulphuric 
acid, and cinchona. If there be swelling of the joints or endocarditis, we should 
advise a trial of salicylic acid or antipyrine. Such special symptoms as demand 
attention, particularly heart-failure, should be treated according to general 
principles. 



•746 



CONSTITUTIONAL DISEASES 



CHAPTEE VIII 
HAEMOPHILIA 

Definition and ^Etiology. — Haemophilia is the term used to denote a peculiar 
constitutional anomaly, exhibited in a remarkable tendency to spontaneous and 
traumatic haemorrhage. The condition is probably in every instance congenital, 
and is usually hereditary; the existence of families of " bleeders " has long been 
known. Generation after generation displays frequent cases of haemophilia, both 
among the direct descendants and the lateral branches. Bleeders are very apt to 
have a numerous progeny. Not all of the children, however, fall victims to the 
disease. Grandidier has pointed out two facts which are of interest in this 
connection, as they might aid in deciding as to the marriageability of certain 
persons. 

If a man belonging to a family of bleeders marries a healthy woman, neither a 
bleeder herself nor inheriting a predisposition to haemophilia, his children are 
almost certain to be healthy, even though the father himself be a bleeder. On the 
other hand, a woman belonging to a family of bleeders, even though she herself 
be healthy, will almost always have some children who are subject to haemophilia. 
In other words, hereditary predisposition is transmitted much oftener through 
the female than through the male members of the family. Haemophilia itself is, 
on the contrary, much more frequent in the male sex than in the female; at least 
this is true of the pronounced cases. Hossli, who has lately published a very 
careful family tree of bleeders of Tenna (Canton Graubunden), comes to the fol- 
lowing conclusions : " The inheritance of haemophilia is often from the father, 
through the daughter, to the grandson, also from the mother, through the daugh- 
ter, to the grandson, and most rarely directly from the father to the son." It is 
doubtful whether race and place of residence are of aetiological importance. So 
far as is known, haemophilia appears to occur in all countries, although it is for- 
tunately rare everywhere. 

[A similar transmission through the females, who themselves usually escape, 
is seen in color-blindness and in pseudo-hypertrophic paralysis.] 

The real causes of haemophilia are entirely unknown to us. We can make one 
or two steps toward finding the source of the haemorrhage, but we are unable to 
proceed further. It would seem that the bleeding must depend, in the first place, 
upon an abnormal delicacy of the walls of the vessels predisposing them to rup- 
ture, and, secondly, upon deficient coagulability of the blood. This latter abnor- 
mality is evident from the fact that in haemophilia it is difficult to check even the 
most insignificant haemorrhage. Thus far all attempts to discover any anatom- 
ical or chemical explanation of this imperfect coagulability have been vain. It has 
not been possible to detect any variation in the saline constituents of the blood, 
or in the amount of albuminoids, such as fibrinogen, that it contains, or in its 
morphological elements. And likewise no anatomical change in the vascular walls 
or the heart has yet been reported which throws light upon the character of the 
disease. Various authorities have laid stress upon the small diameter of the 
arteries and the thinness of the intima, but these conditions may occur independ- 
ently of haemophilia. Eatty degeneration of the intima is, to be sure, often found 
in connection with this disease, but it is doubtless rather a result of the coinci- 
dent anaemia than the cause of the haemophilia. The observations with regard to 
the heart are very contradictory; sometimes it is found to be very small, some- 
times of normal size, and again actually hypertrophied. 

The subjects of haemophilia do not present any distinctive constitutional pe- 
culiarities. It has been stated that they are very apt to be blondes with a delicate 



HAEMOPHILIA 



747 



white skin, and superficial and abnormally distended cutaneous veins; but the 
exceptions to this rule are not a few. 

Clinical History, — Haemophilia does not display equal malignity in all cases. 
If we have opportunity to obtain thorough information with regard to families of 
bleeders, we shall find that quite often rudimentary varieties occur side by side 
with typical and severe cases. There is, to be sure, a striking tendency to haemor- 
rhage even in them; but the haemorrhage never assumes threatening proportions. 
By perseverance and industry it is possible to collect an almost unbroken series 
of cases, varying in degree from extreme mildness to extreme severity. The fol- 
lowing sketch applies mainly to typical and severe cases. 

That haemophilia is a hereditary constitutional disease is shown by the fact 
that it sometimes appears in earliest infancy. Many cases of umbilical haemor- 
rhage in the new-born are referable to haemophilia. Of course this does not 
apply to all cases. In Jewish children the disease may betray itself for the first 
time when the rite of circumcision is performed. In many cases the disease is 
not recognized at so early a period; but this is no proof that the disease is not 
already developed, inasmuch as the young child is not much exposed to trauma- 
tism and other causes which naturally occasion haemorrhage. 

The most striking symptom in a fully developed case of haemophilia is the 
occurrence of severe haemorrhage as a result of the most insignificant causes. A 
slight blow produces a " black-and-blue spot " such as is ordinarily seen only after 
a very violent injury. The prick of a pin, a slight cut on the finger, or the extrac- 
tion of a tooth, may give rise in haemophilia to an obstinate and alarming haemor- 
rhage. Epistaxis may be caused by blowing the nose, haemorrhage from the 
gums by brushing the teeth,, and so on. Whether there is ever a perfectly spon- 
taneous haemorrhage is uncertain. It is true that in severe cases haemorrhages 
take place independently of any visible cause. This may be seen in the skin and 
mucous membranes (nose and gums) ; and in rare instances we may even have 
free haemorrhage from the stomach, intestines, or urinary passages. Yet it may 
be doubted whether these occurrences are not the result of comparatively insig- 
nificant mechanical injuries which escape our notice. At any rate, we scarcely 
ever find haemorrhage taking place into the parenchyma of the viscera, in places 
where injury from external sources is entirely out of the question. This fact con- 
stitutes an important point of distinction between haemophilia and the acquired 
hemorrhagic diathesis. 

The second important symptom of haemophilia has been already referred to : 
it is extremely difficult, and may even be impossible, to check by artificial means 
any free haemorrhage which may occur. It is this which makes the disease so 
dangerous, and prevents most patients from reaching old age. It has frequently 
happened that an apparently trifling wound of the skin, some insignificant 
operation, or a leech-bite, or in women childbirth, has started up a haemorrhage, 
which eventually became fatal. In other cases the haemorrhage is finally checked, 
but not until it has caused profound anaemia. Bleeders are apt to recover with 
remarkable rapidity from the effects of excessive haemorrhage; yet continually 
repeated haemorrhages may lead to a persistent and profound anaemia, attended 
by all the symptoms described in the preceding chapters. 

We see, therefore, that the general condition in haemophilia varies with the 
severity of the individual case, and with the more or less fortuitous circumstances 
which develop its dormant characteristics. If no special accident occurs, the 
patient may maintain the appearance of perfect health for years. In the worst 
cases, however, such a state is very temporary, if it exists at all, because the haem- 
orrhages can be so easily excited. As a consequence, the skin almost always pre- 
sents a greater or less number of ecchymoses, while haemorrhages from the inter- 
nal organs contribute from time to time to the general debility and anaemia. 



748 



CONSTITUTIONAL DISEASES 



Certain complications may occur in hemophilia, but they are little characteristic. 
There is a noticeable tendency to " rheumatic " inflammation of the muscles and 
swelling of the joints, wherein is seen a striking analogy to the " hemorrhagic 
diseases." Often there is an actual effusion of blood into the joints. This may 
cause considerable functional disturbance of the joints, and eventuate in anchy- 
losis. Various writers have also called attention to the comparative frequency of 
neuralgia, especially in the trigeminus. 

Prognosis. — In only too many instances the victims of hemophilia die in 
childhood; in other cases the patient attains an advanced age. A fact of great 
practical importance is that often, although not invariably, hemophilia grows 
gradually milder with advancing years. If, therefore, the patient have survived 
the period of adolescence, we may believe that his prospects are gradually improv- 
ing. The prognosis of hemophilia is obvious. The amount of danger at any 
given time depends upon the severity of the hemorrhage and the consequent 
anemia. The comparative severity of the case must be judged from its previous 
history; as has just been said, the prognosis grows more favorable as the patient 
grows older. 

Treatment. — Prophylaxis assumes a very important place in the treatment of 
hemophilia. First, children who inherit a tendency to the disease, or who have 
given evidence of its existence, should be treated with a view to improve their 
general constitutional condition, so as to check the development of the disease as 
far as possible. The means to this end need not be described at length. They 
comprise good nourishment, fresh air, cautious endeavors to harden the system, 
baths, and tonics. Secondly, when hemophilia already exists, the patient should 
be guarded as much as possible from any mechanical injury, such as might excite 
hemorrhage. Thus caution is demanded in performing vaccination and other 
apparently trifling operations. 

As regards direct treatment of the disease, no effectual remedy is known. The 
general tonic treatment already referred to should not be neglected; but the 
administration of ergotine, acetate of lead, and similar drugs is indicated, if at 
all, only when hemorrhage is actually taking place, and even then it is very apt to 
fail. The only way to stop the hemorrhage is by surgical methods, and these 
need not be described here. They do not differ essentially from those employed 
when hemorrhage occurs independently of hemophilia. If mechanical efforts 
to check the bleeding fail, we can expect nothing- from the remedies above men- 
tioned, nor from sulphate of sodium and the other laxatives which have been 
recommended. Eor the symptomatic treatment of the anemia and of its results, 
we may refer to the first chapter of this section. 



CHAPTER IX 
DIABETES MELLITITS 

Definition and etiology. — Under normal circumstances the blood always con- 
tains a slight amount of sugar ; but this ingredient does not usually pass over in 
appreciable quantities into the urinary excretion. If, however, the amount of 
sugar in the blood exceeds certain limits — that is, if there exists an abnormal 
" glycemia " — then sugar is excreted in the urine, and we have glycosuria. This 
is seen as a more or less temporary phenomenon under the most varied conditions. 
The amount of sugar in the urine is usually comparatively slight, and it soon dis- 
appears again. Its presence does not imply any persistent abnormal condition. 



DIABETES MELLITUS 



749 



This phenomenon has been termed glycosuria or melituria, in contrast with the 
peculiar disease which has for its chief symptom a persistence of sugar in the 
urine, and has therefore received the name of diabetes mellitus. It is not neces- 
sary in this connection to enumerate all the causes of glycosuria, i. e., of a tem- 
porary appearance of sugar in the urine. It may be briefly mentioned, however, 
that glycosuria is observed even in healthy persons after excessive indulgence in 
sugar. If a healthy person takes at one time about seven ounces (grammes 200) 
or more of grape-sugar dissolved in water, there will probably be after an hour or 
two a demonstrable, although not a very great, amount of sugar in the urine. 
This is the so-called alimentary glycosuria. In this case the blood is so over- 
burdened with sugar that the sugar can not be oxygenated fast enough. A 
portion of the sugar, therefore, escapes change and is excreted with the urine. 
If the same amount of sugar is given in divided doses at intervals, there will be 
no glycosuria. If glycosuria appears upon the administration of small amounts 
of sugar (two to three ounces, grammes 50-100) we are justified in speaking of a 
morbid alimentary glycosuria, the power of the body to assimilate sugar being 
subnormal. An abnormal glycosuria of this sort is observed, for example, not in- 
frequently in obese beer-drinkers, and in patients with severe traumatic neuroses, 
or with exophthalmic goitre. Temporary glycosuria is also observed not infre- 
quently in certain kinds of poisoning, particularly after severe poisoning with car- 
bonic oxide, morphine, hydrocyanic acid, mercury, nitrite of amyl, and curare. Von 
Mehring has lately discovered in phloridzine, a glucoside in the bark of the roots 
of apple and cherry trees, a substance which causes a very large amount of sugar 
in the urine if given to dogs, rabbits, etc. A marked glycosuria may be produced 
in man also by giving phloridzine, without other disturbances of the general con- 
dition. It is not improbable that the phloridzine-glycosuria is different from the 
other toxic glycosurias, in that it depends upon a change in the renal epithelium, 
as a consequence of which the cells become permeable to the sugar which is cir- 
culating in the blood. Temporary glycosuria has also been seen occasionally in 
connection with the acute infectious diseases — for example, malignant pustule, 
cholera, typhus or typhoid fever, scarlet fever, diphtheria, and malarial poison- 
ing. A far more frequent cause is disturbance of the nervous system. Thus, 
glycosuria may result from severe concussion of the brain, fracture of the skull, 
cerebral haemorrhage, cerebro-spinal meningitis, and after epileptic fits. It is 
especially apt to occur when there is disease of the medulla ; and we need hardly 
point out how close is the connection between this clinical fact and the famous 
discovery of Claude Bernard, who found by experiment that, when certain in- 
juries are inflicted upon the floor of the fourth ventricle, glycosuria inevitably 
follows. This glycosuria is explained by assuming that, as a result of nervous 
influences, the liver discharges its supply of glycogen into the blood in the form 
of grape sugar. The blood is overwhelmed with the sugar, and a portion escapes 
into the urine. 

In some other oganic diseases, also, there may be a temporary and symp- 
tomatic glycosuria. Formerly, special attention in this regard was directed to 
hepatic diseases, but it is to be noted that, as a rule, even when there is extensive 
disease of the liver — for example, in hepatic cirrhosis — no glycosuria is observed, 
even if the patient is given large amounts of sugar in his dietary. On the other 
hand, the combination of persistent diabetes mellitus and hepatic cirrhosis is not 
very exceptional. As we shall point out again later on, we regard both diseases in 
these cases as co-ordinate effects of the same cause, chronic alcoholism. We shall 
likewise refer again to the relation between diabetes and renal disease. Espe- 
cially great interest attaches to the question of the relation between glycosuria 
and diseases of the pancreas, since Minkowski and Von Mehring made the impor- 
tant discovery that we can excite severe diabetes in dogs by extirpation of the 



750 



CONSTITUTIONAL DISEASES 



pancreas. The ligation of the excretory duct of the gland, or the diversion of the 
pancreatic juice into a fistula leading to the surface of the body, does not excite 
diabetes, nor does the diabetes occur if the pancreas is partially and not wholly 
extirpated. Pancreatic diabetes, therefore, implies a disturbance of a special 
function of the pancreas, of which we have as yet no intimate knowledge, but the 
abolition of which prevents the complete splitting up or oxidation of sugar in the 
normal organism. Diseases of the pancreas in man (carcinoma; pancreatic cal- 
culi, with secondary atrophy of the gland) occasion glycosuria sometimes, but by 
no means invariably. The atrophy of the pancreas observed in many cases of 
genuine diabetes will be discussed later on. We should mention in this connec- 
tion, also, the glycosuria which sometimes appears in association with exoph- 
thalmic goitre, and finally the interesting and frequent combination of acro- 
megaly (q. v.), and the persistent excretion of sugar in the urine. 

In contrast with the temporary phenomenon of glycosuria, we apply the name 
diabetes mellitus to a chronic morbid state, in which a permanent disturbance in 
the metabolism of the carbohydrates is indicated by a persistent excretion of 
sugar in the urine, and in which this anomaly of metabolism is the main symptom 
of the disease. If the excretion of sugar in this disease is not absolutely per- 
sistent, at least it is sure to occur under certain conditions of nutrition. It is 
doubtful whether diabetes mellitus is to be regarded from an ^etiological stand- 
point as a single, distinct disease. With regard to most of the " pure " cases, par- 
ticularly the severe form of diabetes which usually occurs in youthful individuals 
without any demonstrable cause and also without any primary organic lesion, 
there is great probability in the assumption that the morbid process is a single 
and definite one, although we are as yet entirely unacquainted with its real 
nature. On the other hand, with regard to the so-called milder forms of diabetes 
mellitus, particularly those which occur in middle and advanced life, there are 
probably various causes which may excite the disease. Still, it must be emphat- 
ically stated that no sharp dividing line can be drawn between the " severe " 
and the " milder " forms of diabetes. The physician is, therefore, bound in every 
individual case to search for certain causative factors and harmful influences, 
which sometimes, at least, play a part in the development of the disease. These 
causative factors are the following : First, heredity : diabetes has been repeatedly 
observed to occur in several generations of the same family, or in several brothers 
and sisters. It is noteworthy that the disease may also occur in families where 
there is a hereditary predisposition to nervous diseases. Eor example, we ob- 
served once in the same patient the remarkable combination of diabetes and 
progressive muscular atrophy of spinal origin. Second, improper mode of life: 
by this is meant chiefly unsuitable diet, especially the persistent overindulgence 
in starchy foods and sugar ; sedentary habits are also considered harmful, espe- 
cially if associated with overeating. This is said to be the reason why diabetes is 
more frequent among the wealthy classes, and why it is comparatively common 
in corpulent persons (vide infra). Our personal observations lead us to ascribe 
to long-continued and excessive beer-drinking (four or five litres and more per 
day) an influence upon the development of diabetes. In such cases it may be that 
we have a combined action of the excessive ingestion of carbohydrates in a state 
of solution, and of chronic alcoholism. It can, in our opinion, be no mere coin- 
cidence that diabetes so often attacks brewers, inn-keepers, and the like, in Ba- 
varia. Furthermore, the complication of diabetes with other results of chronic 
alcoholism, such as hepatic cirrhosis, chronic nephritis, and alcoholic neuritis, 
is an argument for the correctness of our supposition. The " diabetes of obes- 
ity " has been long recognized, but in many cases it is really a " beer diabetes." 
Third, taking cold and getting wet are said, in occasional rare instances, to deter- 
mine the appearance of diabetes. The author has never seen a clear case of this 



DIABETES MELLITUS 



751 



sort. Fourth, emotional disturbances, excessive mental exertion, anxiety, and 
passion, are sometimes thought to occasion the disease; and apparently with 
some reason. Fifth, it is very remarkable that sometimes the same factors which 
we have already seen to be possible causes of temporary glycosuria, may also occa- 
sion a chronic diabetes mellitus; thus, cases of diabetes have been known to 
follow injuries to the head, and such acute infectious diseases as typhus, typhoid, 
and scarlet fevers, cholera, and malarial poisoning. Sixth, a few authors (Schmitz 
and others) have hinted at the possibility of the disease being transferred by con- 
tagion — for example, in the case of married people. This interpretation of the 
scattered instances which have been reported is, however, at least open to doubt. 
Seventh, a very important matter is the occurrence of diabetes in association 
with, or as a sequel to, certain other constitutional diseases. In this category be- 
long the above-mentioned diabetes of the obese ; also the simultaneous appearance 
of diabetes and genuine gout (q. v.) ; and finally, the extremely important com- 
bination of diabetes with general arterio-sclerosis. That all these combinations do 
frequently occur can not be doubted, but it is very difficult to explain the connec- 
tion between them; often both conditions may be the simultaneous effect of the 
same cause — for instance, congenital anomalies of constitution, unhygienic modes 
of life, and alcoholism. 

If we survey all the facts thus far known with regard to the setiology of 
diabetes, we feel obliged to conclude just as in almost all other constitutional 
diseases, that in regard to the development of diabetes we must distinguish 
endogenous and exogenous factors. The endogenous relate to the constitutional 
tendencies which the patient possesses, perhaps by inheritance; and the exoge- 
nous to harmful influences from without, such as trauma, infection, and intoxi- 
cation. The severe cases of diabetes which seem to occur absolutely spontane- 
ously in young persons, are mainly of an endogenous character; while in the 
milder forms of later years the above-mentioned exogenous influences often play 
an important part, although even in them the endogenous factor can not be 
entirely disregarded, for the same noxious influence does not produce, by any 
means, the same effect upon all persons. 

Diabetes occurs everywhere, but certain countries and districts seem to be 
particularly liable to it — for example, India, Ceylon, and Italy. In Germany, 
Wiirtemberg and Thiiringen are said to present the largest relative number of 
cases. Jews are very liable to the disease. Most cases occur in patients between 
thirty-five and fifty years of age. Next in liability to the disease come younger 
individuals, under thirty-five and over twenty years old. After the fiftieth year 
diabetes is not exceptional, but, in the other direction, children under ten are 
very seldom attacked by it, although they are not absolutely exempt. With 
regard to sex, males are much more often attacked than females. 

Clinical History. — With few exceptions, the symptoms of diabetes mellitus 
come on slowly and gradually. Sometimes the symptoms are merely general and 
indefinite, such as languor, emaciation, weakness, and deficient endurance. 
Sometimes we have mild nervous disturbances, including headache, mental de- 
pression, wakefulness, and neuralgia, and in still other cases gastro-intestinal 
symptoms, including nausea, eructations, and irregularity of the bowels. At last 
the patient's attention is called to the altered character of the urine, and particu- 
larly to its increased amount. He also notices that he is very thirsty, and that, 
in spite of his enormous appetite, he is constantly growing weaker. Sometimes 
quite different symptoms first arouse suspicion of the existence of diabetes ; these 
will be mentioned later. In order to make a diagnosis of diabetes mellitus, a 
knowledge of the abnormal character of the urine is indispensable, so that it is 
proper to begin our consideration of the symptoms of diabetes with a description 
of diabetic urine. 



T52 



CONSTITUTIONAL DISEASES 



1. Character of the Urixe. Demonstration of Sugar. — Usually the first 
point that attracts attention is the increased amount of urine. There are often a 
hundred to a hundred and fifty ounces (three to five quarts, 3,000-5,000 cubic 
centimetres) excreted in twenty-four hours, and sometimes the amount equals or 
exceeds ten or twelve quarts (8,000-12,000 cubic centimetres). Under suitable 
treatment and with proper diet the amount may, of course, be much smaller. 
In not very exceptional cases, mostly of the milder varieties (vide infra), there 
is slight, if any, increase in the amount of urine (diabetes decipiens) ; and in 
severe cases with initial polyuria we may often observe that during intercurrent 
diseases, and likewise in the last days before the fatal termination of the disease, 
the daily amount of urine diminishes. 

In color the urine is light yellow, corresponding to its amount. It often has 
something of a greenish hue, but a small quantity of it may seem almost as color- 
less as water. Ordinarily the urine is clear and without sediment; but after it 
has stood for some time it may become cloudy, usually as a result of the abundant 
development of fermentation spores. 

The odor may be somewhat aromatic, suggesting acetone (vide infra). Its 
taste is said sometimes to be distinctly sweetish. The reaction is acid, and the 
acidity of the urine may increase on standing, because of the alcoholic and lactic- 
acid fermentation processes which the sugar undergoes. 

The specific gravity is almost invariably greatly increased, as a result of the 
large amount of sugar. If a pale urine is found to have a specific gravity of more 
than 1025, we may feel almost certain that it contains sugar. Specimens often 
have a specific gravity of 1030-1045, and even higher. In exceptional instances 
the specific gravity may fall below 1020. A specific gravity below 1020 is excep- 
tional, but one should never be kept from making an examination for sugar 
because of the low specific gravity of the specimen. We have ourselves demon- 
strated sugar by means of the fermentation test in urine which had a specific 
gravity of 1007. 

The diagnosis requires that sugar be detected in the urine. The sugar found 
in both the blood and the urine of diabetic patients is grape-sugar (glucose, dex- 
trose). The amount of sugar secreted in twenty-four hours often reaches half a 
pound to a pound (grammes 200-500). Of course the amount varies greatly ac- 
cording to the diet, mode of life, and treatment of the patient. The greatest 
amount ever known to be produced in twenty-four hours was more than two and 
one fifth pounds (grammes 1,000). The percentage of sugar in the urine varies 
between 0.5-1 per cent, at the lowest extreme, and 8-10 per cent, as the maxi- 
mum ; usually it is about 2-4 per cent. It is noteworthy that in the last weeks, 
or just before death, the sugar in the urine may become greatly diminished in 
amount, or may absolutely disappear. 

The most important tests for sugar in the urine are : First, Trommer's test : To 
urine in a test-tube sufficient potassic or sodic hydrate is added (say one part to 
three or four of urine) to make the reaction strongly alkaline ; then a solution of 
sulphate of copper (about one part of the salt to ten of water) is added, drop by 
drop. If the urine contain sugar, the hydrated cupric oxide, which is at first 
formed, is largely dissolved, and usually the fluid assumes a beautiful deep-blue 
color. \Ye ought, properly, to go on adding the sulphate of copper until the 
hydrated cupric oxide ceases to be dissolved. The urine is then heated, where- 
upon the cupric oxide is reduced and a yellow, or reddish-yellow, precipitate of 
cuprous oxide, or hydrated cuprous oxide, is formed. The application of heat 
should not be continued long after the precipitation begins to take place, lest 
the test be obscured; the reduction will go on even without heat. If the urine 
contains more than 0.5-1 per cent., this test is perfectly reliable. If the reaction 
be a doubtful one — that is, if there be no precipitate of cuprous oxide, although 



DIABETES MELLITUS 



753 



the urine becomes yellow; or if cuprous oxide be finally precipitated when the 
urine cools — we should be cautious in making a diagnosis, as the urine may con- 
tain substances other than sugar capable of reducing the copper, such as uric 
acid, kreatinine, mucine, etc. Second, the bismuth test (Bottger's) : Sodic 
hydrate or sodic carbonate is added to the urine, and then a small pinch of sub- 
nitrate of bismuth. Upon boiling, the urine, if it contains sugar, quickly assumes 
a perfectly black color, the oxide being reduced to the metallic state. It is much 
more convenient, and consequently universally customary at present, to make the 
bismuth test by adding to the urine about one tenth of its volume of the follow- 
ing solution (jSTylander) : two parts subnitrate of bismuth, four parts Rochelle 
salts, one hundred parts of an eight-per-cent. solution of sodic hydrate. After 
one or two minutes' boiling the fluid turns black. Errors with this test are most 
apt to occur if the patient has taken certain drugs, such as antipyrine, salicylic 
acid, or rhubarb. Third, the potassium test (Moore's) : Potassic hydrate is added 
to the urine in the test-tube and the uppermost layer cautiously heated ; if it con- 
tains sugar, the urine quickly assumes a deep-brown color, as a result of the 
action of the potassium on the sugar; and this upper dark-colored layer contrasts 
strongly with the clear urine below. 

[Fehling's test is justly a favorite in this country, and has the advantage of 
being applicable to the quantitative as well as to the qualitative analysis. The 
difficulty of its not keeping well can be met by having separate bottles for the 
copper and tartrate solutions, and making the mixture at the time of using the 
test. The Fehling's-test pellets put up by chemists are convenient for the quali- 
tative analysis, but, on the whole, they are inferior to the solution.] 

If the above-described tests leave us still in doubt, there can be only a small 
amount of sugar, if any, present. We may, however, attain certainty by employ- 
ing the fermentation test (which causes a decomposition of the sugar into alcohol 
and carbonic dioxide), or circumpolarization (deflection of the plane of polariza- 
tion to the right by the grape-sugar). Certainly in no doubtful case should we 
omit to perform the fermentation test, for it is easy and gives absolutely unam- 
biguous results. Further particulars in regard to these and other tests, and also 
in regard to the quantitative estimation of sugar, may be found in works on 
medical chemistry. 

Diabetic urine sometimes contains other varieties of sugar in small amounts 
— namely, levulose, which deflects the plane of polarization toward the left, and 
inosite ; these are, however, of no practical importance. 

The amount of urea is usually somewhat increased (vide infra). In the main, 
this is doubtless connected with the increased ingestion of albumen, but in severe 
cases it may be that the carbohydrates are so imperfectly appropriated that the 
albumen of the body is broken up and consequently contributes to an increase in 
the excretion of nitrogen. Uric acid is usually excreted in approximately nor- 
mal amounts. In exceptional cases it also seems to be excreted in excess. The 
amount of kreatinine is apt to be increased (Senator). The amount of phos- 
phoric acid and sulphuric acid usually corresponds to the amount of urea, or, in 
other words, to the decomposition of albuminoids. Occasionally, according to 
Teissier, the amount of phosphates is surprisingly great, and it may either corre- 
spond with the amount of sugar simultaneously excreted, or replace the sugar in 
the urine. This subject has not yet been fully investigated. The amount of sodic 
chloride excreted depends, as in health, merely upon the amount ingested. 

Hallervorden has discovered an important fact in regard to the excretion of 
ammonia. In many cases of diabetes, although not in all, it is much increased : 
forty-five to ninety grains (grammes 3-6), or even more, may be excreted in 
twenty-four hours. Despite this, diabetic urine has an acid reaction; and, as 
Stadelmann has shown, the basic elements are considerably out of proportion to 
48 



754: 



CONSTITUTIONAL DISEASES 



the acids known to us. It is, therefore, evident that diabetic urine, since it 
contains a large amount of ammonium and yet has an acid reaction, must have 
among its constituents some unusual acid. The later investigations of Minkow- 
sky and Kiilz have shown that the acid is mainly oxybutyric acid, or, more accu- 
rately, beta-oxybutyric, although sometimes still other acids are found in the 
urine, particularly volatile fatty acids and lactic acid (Rumpf). The oxybutyric 
acid is often excreted in large amounts, up to two or three ounces (grammes 50- 
100) daily. It is traced to the destruction of albumen, and usually does not 
appear in the urine until the patient is obliged, because of the imperfect appro- 
priation of carbohydrates, to use the albumen of the body instead to satisfy the 
needs of the economy. The appearance of oxybutyric acid in the urine is, there- 
fore, unfavorable from a prognostic point of view, and in particular it indicates 
that there is danger of diabetic coma (vide infra). 

Oxybutyric acid is probably the substance from which are derived two other 
organic bodies which are not infrequently found in the urine of diabetes — viz., 
acetone and acet-acetic acid. These substances also arise from the destruction of 
albumen — that is, the body albumen — so that they are seen especially in severe 
cases with impaired nutrition (Van Noorden). Acetone is probably developed 
from acet-acetic acid. The latter is the cause of the reaction which was first 
demonstrated by Gerhardt, which consists in the appearance of a Burgundy-red 
color on the addition of chloride of iron, and which is not infrequently to be 
observed in diabetic urine. Acetone is shown by Legal's test : a few drops of 
fresh solution of nitro-prusside of sodium are mixed with the urine, and then 
sodic hydrate is added. If acetone is present a purple-red color appears, [and 
persists, even if acetic acid is added (excluding kreatinine). — V.]. 

The not infrequent occurrence of albumen in diabetic urine will be mentioned 
below, when considering the renal complications. 

2. Metabolism in Diabetes. Sources of the Sugar and Variations in its 
Amount occasioned by External Influences. — Inasmuch as the presence of sugar 
in the urine is the most prominent symptom in diabetes, the question of its 
origin is all-important. One fact is indubitable — namely, that the secretion of 
sugar depends in large part upon the amount of potential sugar ingested — that is, 
upon the proportion of starches in the food. The amount of sugar excreted with 
the urine increases and diminishes with the amount of starchy food eaten. If 
a diabetic patient abstains totally for any length of time from such articles of 
food as contain starch, sugar will, in many instances, entirely disappear from the 
urine. In other words, the system of a diabetic patient is almost, if not quite, 
incapable of oxidizing sugar into carbonic-dioxide gas and water. Although, 
therefore, in a diabetic patient the absorption of oxygen from the atmosphere 
goes on as usual, yet there always remains a deficit in the excretion of carbonic- 
dioxide gas and water, corresponding to that portion of the ingested carbo- 
hydrates which is not oxidized. 

The oxidation of sugar is not absolutely nil in diabetes. Kiilz has proved by 
numerous experiments that not all the starch is excreted in the form of sugar. 
In severe cases of diabetes the largest part of the ingested sugar is excreted as 
such, unoxidized, with the urine, but in mild cases only a small portion is thus 
excreted. It is, therefore, necessary to determine the degree of tolerance for 
carbohydrates in every individual case of diabetes ; even in the same patient this 
tolerance is not the same at all times. Another very interesting fact was dem- 
onstrated by Kiilz. The diabetic patient has lost only the power of oxidizing 
that kind of sugar which turns the plane of polarization toward the right. The 
sugar which turns it toward the left (levulose), inuline, and also certain other 
carbohydrates, such as mannite and inosite, are broken up even in diabetic 
patients in very large part, if not completely, so that the amount of sugar ex- 



DIABETES MELLITUS 



755 



creted in the urine is but little, if any, increased by the ingestion of these sub- 
stances. 

Yet the carbohydrates are not the only source of the sugar excreted by dia- 
betic patients. In many cases, although not in all, sugar persists in the urine 
even when the patient receives a dietary absolutely free from carbohydrates. 
In such instances, there can be no doubt that the glycogen, or the sugar which 
is formed out of it, is referable to the albumen of the food. In general, we may 
say that it is always a sign of a severe variety of diabetes to have a part of the 
sugar which is formed out of albumen, when carbohydrates are absolutely ex- 
cluded from the diet, excreted unoxidized ; while it is a proof that the variety is a 
milder one, to have the sugar vanish from the urine when the patient is put upon 
a diet which contains little, if any, carbohydrates. 

Muscular exertion is one of the external influences which modify the excre- 
tion of sugar in diabetes. According to our present views, muscular activity 
consumes mainly non-nitrogenous substances, and, accordingly, we find in dia- 
betes that an increase of muscular exertion, other things being equal, diminishes 
the amount of sugar excreted. 

Emotional excitement is said to increase the amount of sugar excreted. 

Intercurrent acute febrile diseases may cause a great diminution in the' 
amount of sugar, but sometimes there is no essential change. Probably the 
altered diet of the patient plays an important part in this connection, although^ 
the modifications of metabolism occasioned by the high temperature or by the dis- 
ease itself also exert some influence. Just before death the urine may become 
entirely free of sugar. 

3. Constitutional Symptoms in Diabetes Mellitus. — In many of the milder 
cases there is for a long time little apparent disturbance of the general health; 
The patient is well nourished, and suffers little discomfort, except that he is 
rather easily fatigued, and somewhat inconvenienced by the polyuria and the 
polydipsia. In severer cases the system is deeply affected by the drain upon it. 
The patient becomes emaciated, weak, and easily exhausted, and at length there 
may be profound marasmus. Mentally, the patient is apt to be depressed and 
irritable. The intellectual powers are not impaired, but there is indisposition to 
mental effort. The temperature is normal or subnormal. Eever invariably indi- 
cates some complication. 

4. Symptoms referable to the Digestive Organs. — We have already men- 
tioned the excessive thirst experienced in diabetes. This may be a source of great 
discomfort, obliging the patient to drink at short intervals, even through the 
night. The interdependence of polyuria and polydipsia is not yet fully under- 
stood. The most natural view seems to be that the increased excretion of water 
by the kidneys is the primary factor, and the increased thirst secondary thereto. 
One cause of the polyuria is the excretion of sugar, in order to dissolve which a 
large amount of water is necessary, but certain nervous factors would also seem 
to be implicated. That they exert some influence is rendered probable by the fact 
that the amount of urine does not always correspond to the amount of sugar 
excreted. A very large amount of urine may be excreted containing little or no 
sugar ; and, on the other hand, there are genuine cases of diabetes mellitus where 
the amount of urine is normal, and the patient feels no unusual thirst (diabetes 
decipiens). It has also been suggested that the sugar may irritate the nerves of 
the mouth and throat, and thus cause thirst. According to this idea, the polyuria 
would be partly the result of the excessive ingestion of liquids. The abnor- 
mally great appetite in diabetes seems to be due to defective assimilation of the 
food. Many patients are never able to eat enough. They have a longing, in 
many cases, for carbohydrates. Occasionally the hunger becomes ravenous, and 
is associated with headache and a general sense of weakness, all these symptoms 



756 



CONSTITUTIONAL DISEASES 



being alleviated when food is taken. This rule has rare exceptions in which the 
appetite is not unusually great, even though the case be severe. 

The tongue is frequently dry ; it is broad and thick, with an irregular and fis- 
sured surface, sometimes coated and sometimes red. The gums may be spongy, 
and may exhibit a tendency to bleed. A very characteristic condition is necrosis 
along the free borders of the gums, probably due to an enfeeblement of the resist- 
ing power of the tissues. This is particularly apt to lead to a gradual loosening 
of the incisors, so that at last they drop out. The teeth frequently decay rapidly. 
The saliva is invariably found to give an acid reaction. This is true of the isolated 
secretion of the parotid gland also, and is said to be due to the presence of lactic 
acid. It is only in exceptional instances that sugar can be demonstrated in the 
saliva. In severe cases thrush sometimes forms upon the soft palate. 

Special gastric symptoms are usually absent. There may be a dilatation of 
the stomach, due to the great quantity of food ingested, but this has no practical 
importance. If disease of the stomach does develop (e. g., chronic gastritis) the 
complication is an unfavorable one. There is usually constipation, but some- 
times there is a severe, though temporary, diarrhoea. The liver and spleen are 
seldom much affected; the liver rarely is somewhat enlarged. Jaundice is fre- 
quently observed, but it is always referable to some complication. As a rule, 
the secretion of the bile goes on as in health. After death, we may find, atrophy 
of the pancreas (vide infra). 

5. Symptoms referable to the Eespiratory Organs. — In many cases the or- 
gans of respiration are unimpaired for a long while. It may be mentioned that 
often patients have a decidedly fruity odor to the breath (acetone odor). In the 
later stages of the disease pulmonary complications are very frequent. First in 
importance is tuberculosis of the lungs. This is particularly apt to occur in the 
severe forms of diabetes in youth, and it may pursue a rapid and fatal course. 
The diagnosis can be settled by the discovery of tubercle bacilli in the sputum. 
Next in point of frequency is pulmonary gangrene. Sometimes there is a diffuse 
gangrenous process, and sometimes there are isolated foci of necrosis, which be- 
come liquid, and have an acid reaction, but they often have comparatively little 
odor. The expectoration in these cases may be odorless. Croupous pneumonia 
may also occur. It often terminates unfavorably, and may, as we have ourselves 
observed, result in gangrene. 

6. Symptoms referable to the Circulatory System. — In many instances the 
circulatory apparatus presents no special lesions. The pulse is either of a nor- 
mal rate or a trifle slow. It is usually soft, although exceptionally it may exhibit 
increased tension. There is often distinct evidence of cardiac weakness 
(Schmitz); the pulse is small, intermittent, sometimes very slow (50 or even 40 
beats per minute), and sometimes accelerated (100 to 120 beats per minute). 
There are shortness of breath, faintness, nausea, and the like. Sometimes sudden 
and profound cardiac disturbance occurs, and this may occasion speedy death 
(vide infra, coma). Not infrequently, diabetes is combined with general arterio- 
sclerosis (vide infra). 

7. Genito-urinary Symptoms. — Despite the great demands made upon them, 
the kidneys often maintain a normal condition. As we shall see when we come 
to the pathological anatomy of diabetes, the kidneys are often very large. Some- 
times a chronic nephritis is developed as a complication, usually in the later 
stages of the disease. The urine contains albumen, and there are oedema and 
other symptoms of renal disorder. The cause of albuminuria in diabetes does not 
seem to be the same in every case ; sometimes it is due to changes in the kidneys 
resulting from the persistent excretion of abnormal urinary constituents. In 
this connection we must think, not only of the sugar, but also of the other sub- 
stances — such as acetone, diacetic acid, and oxybutyric acid — which, as they 



DIABETES MELLITUS 



traverse the kidneys, damage the renal epithelium. In other cases, diabetes and 
nephritis seem to be simultaneous and co-ordinate results of the same cause, such 
as arterio-sclerosis or alcoholism. Finally, it must not be forgotten that other 
complications of diabetes — e. g., pulmonary tuberculosis — may promote the devel- 
opment of nephritis. It is an interesting fact that in diabetes, glycosuria and 
albuminuria may to a certain extent alternate with each other. If the amount 
of albumen in the urine becomes considerable, the excretion of sugar usually 
undergoes marked diminution. Many physicians therefore consider the transi- 
tion of diabetes into chronic renal disease (contracted kidney) as a comparatively 
favorable symptom. 

Saccharine urine is apt, as it decomposes, to cause irritation of the skin (de- 
velopment of fungi). This is the explanation of the troublesome pruritus pudendi, 
which is especially marked in women. It may, indeed, be this symptom which 
first directs attention to the disease. Sometimes the external genitals are at- 
tacked by eczema or furunculosis. Men often suffer from balanitis, with inflam- 
matory phimosis, or paraphimosis. A frequent and important symptom in men is 
impotence. This sometimes occurs very early in the disease, but it may afterward 
undergo improvement. The origin of it is probably referable to degenerative 
changes in the nervous system (vide infra). Some authorities state that diabetes 
is apt to occasion atrophy of the testicles. 

8. Disturbances of the Organs of Special Sense. — An important and not 
infrequent result of diabetes is cataract. This may occasion almost total blind- 
ness. The cause of cataract in diabetes is not known. It was formerly supposed 
that the sugar in the blood absorbed water from the crystalline lens, and thus 
occasioned its opacity; but this has not been confirmed. Diabetic patients are 
subject to disturbances of accommodation. Retinitis and atrophy of the optic 
nerve may occur, but they are very rare. Purulent choroiditis, if it develops, 
is probably merely a chance complication. 

JNTone of the other special senses is peculiarly affected in diabetes. 

9. Cutaneous Affections. — In most cases the skin is remarkably dry and 
rough. There may, however, be abundant perspiration. Several authorities claim 
to have found sugar in the perspiration, but this statement has not been confirmed 
by later investigators. Sometimes there is a troublesome pruritus. We often see 
a rapid loss of hair and a shedding of the nails. In many cases there is a great 
tendency to furunculosis. This may be the first symptom to suggest the existence 
of diabetes. In the later stages there are sometimes extensive carbuncles, and 
multiple phlegmonous abscesses in the subcutaneous cellular tissue, which may 
prove fatal. Bacteriological examinations of all these processes have not yet been 
made, so far as we know. Probably they are complications, like the frequent 
occurrence of pulmonary tuberculosis in diabetes. Occasionally we have seen 
a pemphigus-like eruption on the skin. This, in one case, developed into a local- 
ized gangrene. Gangrenous processes have been repeatedly observed, in par- 
ticular necrosis of one or more toes, which may take the form of perforating 
ulcer (mal perforant), or rarely of an entire extremity. This gangrene often 
seems to be due to arterial sclerosis; in other cases its cause is obscure. The 
gangrene of the toes may be apparently the first symptom of the disease, and it 
may be very slight. It is not until all therapeutic and operative procedures prove 
unavailing that suspicion is aroused, leading to the discovery of diabetes. We 
have often seen cases of this sort, which usually turn out badly, in obese drinkers. 

(Edema of the subcutaneous cellular tissue may occur independently of nephri- 
tis. It is then probably occasioned by the cardiac weakness. 

10. Symptoms referable to the Nervous System. — It has already been men- 
tioned that there is frequently in diabetes a moderate disturbance of the whole 
nervous system, as indicated by headache, physical and mental hebetude, and 



758 



CONSTITUTIONAL DISEASES 



depression of spirits. There are, besides, a number of nervous complications which 
are probably referable to the irritative or degenerative effects upon certain nerve 
areas of the abnormal products of metabolism formed in diabetes. This is the 
explanation of the comparatively frequent appearance of neuralgia, most often 
in the form of sciatica. This is probably due to neuritis of the nerve. Bilateral 
sciatica may be one of the first symptoms of the disease, and a very obstinate one. 
We also meet with occipital neuralgia, facial neuralgia, and pain resembling 
hemicrania. Sometimes, also, we observe localized anaesthesia of the skin and pe- 
ripheral palsies. These are probably due to degenerative changes in the peripheral 
nerves. We have ourselves seen, in one case, paralysis of the peroneal nerve, due 
to peripheral neuritis. Another symptom which should be grouped with those 
just considered, is one which was first pointed out by Bouchardat — viz., the com- 
paratively frequent abolition of the patellar reflex in diabetes. It should be said, 
however, that we have repeatedly seen cases, of the most severe form, in which the 
knee-jerk remained perfectly normal. If the reader will imagine a case in which 
absence of the knee-jerk is associated with neuritic pains in the legs, he will 
understand the reason for the term " diabetic pseudo-tabes." The pathological 
basis of the symptoms just enumerated has been repeatedly shown to be neuritic 
degeneration. In some few cases there may even be slight changes in the poste- 
rior columns of the spinal c£»rd, perhaps of toxic origin. 

The most important nervous symptom of all is a peculiar disturbance which 
occurs in a considerable proportion of all cases with more or less suddenness, and 
usually terminates in a surprisingly speedy death. This strange phenomenon 
was first thoroughly investigated by Kussmaul, although known long before. It 
is termed diabetic coma. The condition sometimes develops without any evident 
cause. In other instances it is apparently brought on by violent muscular exer- 
tion, mental excitement, or some trifling illness, such as gastric catarrh, bron- 
chitis, or sore throat. 

Frequently certain mild prodromata herald its onset. There may be nausea, 
headache, a sense of thoracic oppression, and general uneasiness. Soon the con- 
dition becomes aggravated. The patient is seized with a feeling of great anxiety, 
and becomes delirious, sometimes jumping out of bed and growing uncontrol- 
lable. Gradually, however, the excitement gives place to an ever-increasing 
drowsiness, usually terminating in the most profound coma. One of the most 
frequent and striking symptoms attending this condition is the peculiar alteration 
in respiration. The breathing becomes remarkably deep and noisy. Its rate may 
remain nearly normal; or it may be considerably increased, so as to justify the 
term " diabetic dyspnoea." The patient is sometimes cyanotic. The pulse is usu- 
ally very rapid and small. The temperature gradually sinks, and has in repeated 
instances fallen to 86° (30° C), or even lower. In most instances, also, the 
breath has a very noticeable odor, resembling fruit or chloroform, which may be 
perceived on entering the room. Even the urine may have this same odor; and 
it almost invariably becomes dark red on the addition of ferric chloride, and 
gives a distinct acetone reaction (vide supra). 

Diabetic coma does not pursue the same course in all cases; sometimes the 
patient lingers on for several days before death, while in 'other instances the 
change is extremely rapid and death speedy. The early stage of excitement 
may be wanting. The patient becomes somnolent and then speedily comatose, 
and never regains consciousness. Temporary improvement, and even complete 
cessation of the threatening symptoms, are not impossible, but they are very 
exceptional. 

As to the cause of diabetic coma, the results of recent investigations are in- 
teresting, although they do not explain everything. Of course the cases where 
an autopsy discloses some marked organic lesion, such as cerebral haemorrhage, 



DIABETES MELLITUS 



759 



capable of producing the nervous symptoms, are not true diabetic coma. Nor 
do the cases of sudden death reported by Frerichs deserve to be classed as diabetic 
coma, where death occurred with the symptoms of acute cardiac failure — namely, 
collapse, coolness of the extremities, small and rapid pulse, and unconsciousness. 
Besides, these patients never have the acetone odor, the exaggerated respiration, 
nor the ferric-chloride reaction, and usually the myocardium is found to be in 
an advanced state of degeneration. 

In genuine diabetic coma, on the other hand, everything seems to indicate 
that the system has been poisoned by some noxious product of abnormal metabo- 
lism. Great effort has been made to discover what this product is, but with im- 
perfect success. Kussmaul regarded acetone as the injurious substance, and 
therefore called diabetic coma " acetonemia." Other investigators believe that 
acet-acetic acid (Jaksch) is the cause of the phenomenon in question, or at least 
regard the coma as a result of poisoning from some of the unusual acids present 
in diabetes (Stadelmann, vide supra). No one view has obtained general accept- 
ance, nor has it been possible to produce diabetic coma in animals by the employ- 
ment of acetone, acet-acetic acid, crotonic acid, or similar substances (Brieger 
and others). It is, nevertheless, extremely probable that these substances do have 
some close connection with " diabetic intoxication " (Frerichs). Far more proba- 
bility attaches to the theory which was advocated first by Stadelmann and then by 
Minkowsky, according to which diabetic coma is the result of an " acid intoxi- 
cation." There is no doubt that, as we have already stated, in diabetes there 
is a formation of abnormal acids, particularly oxybutyria acid. If these acids 
accumulate in the blood, they neutralize its alkalies, so that it loses its capacity 
of combining with the carbonic acid formed in the tissues, and carrying it away. 
Certainly the symptoms of diabetic coma bear a great resemblance to the phe- 
nomena which have been observed in animals when poisoned by acids — viz., 
stupor, dyspnoea, diminution of the amount of carbonic dioxide in the blood, and 
increase in the excretion of ammonium in the urine {vide supra). The blood of 
patients who die in diabetic coma contains large amounts of oxybutyria and 
sarcolactic acids. 

11. Changes in the Lymph-glands. — There may be extensive and distinct 
swelling of the lymph-glands, particularly in severe cases of diabetes. The glands 
are hard and insensitive. 

Pathological Anatomy and Histochemistry of Diabetes Mellitus. — If we ex- 
clude the organic diseases, such as pulmonary tuberculosis and nephritis, which 
are merely complications, the pathological changes in diabetes are trifling. Ber- 
nard's discovery, that an injury inflicted in a certain spot on the floor of the 
fourth ventricle produces glycosuria in animals, has directed the attention of in- 
vestigators to the condition of the nervous system in this disease. In some in- 
stances, tumors, sclerosis, or similar troubles have been found in the medulla and 
cerebellum ; but in these cases there was evidently a symptomatic glycosuria and 
not an idiopathic diabetes {vide supra). In idiopathic cases the central nervous 
system presents no striking macroscopic changes. By means of the microscope, 
Frerichs has found lesions of the medulla oblongata in frequent instances. The 
minute blood-vessels are widely dilated; there are small capillary haemorrhages, 
some of a more recent and others of a more remote date ; and occasionally there 
are microscopic foci of myelitis. The nervous elements proper, the nerve-fibers 
and ganglion cells, betray no alteration ; and as the changes enumerated are not 
invariably present, their significance is dubious. 

The stomach and intestines present no constant alterations of importance. 

The liver has naturally been the object of repeated and careful examinations, 
because of its well-known part in the manufacture of glycogen. Yet this organ 
seldom presents any special abnormality. It is usually of the natural size, and 



760 



CONSTITUTIONAL DISEASES 



it may contain either considerable or very little blood. The amount of glycogen in 
the hepatic cells can be demonstrated with iodine by a micro-chemical reaction. 
It appears that, other things being equal, there is less glycogen present than 
normal. It is usually found only in the cells situated upon the periphery of the 
lobules, and in small quantities. In an extremely advanced case of diabetes 
Ehrlich obtained, by means of a hollow needle, small amounts of the hepatic 
parenchyma for examination during life, and found that glycogen was almost 
completely absent. In other cases the liver has been examined as early as possi- 
ble after death, and, with rare exceptions, has presented no trace of glycogen. 

The spleen is usually of normal size. Occasionally it is atrophied, or, on the 
other hand, slightly enlarged. No other changes in it have been observed. 

Not a few cases have presented a striking atrophy of the pancreas (Bouchar- 
dat), a fact which has acquired great significance from Minkowsky's discovery, 
already mentioned, that glycosuria may come on after extirpation of the pancreas. 
It is uncertain whether the coeliac plexus may also sometimes share in the 
atrophy of the pancreas. We must also state, however, that atrophy of the pan- 
creas is not at all a constant lesion in diabetes, so that it is not proper to regard 
the disease of the pancreas as the special cause of diabetes in all cases. Lately in 
repeated instances the pancreas has been found perfectly normal, even upon the 
most careful microscopic examination. 

The kidneys are usually enlarged, from functional hypertrophy. Ehrlich dis- 
covered in them a glycogenic degeneration of the loops of Henle. The epithelial 
cells in the loops are enlarged, and the protoplasm in these cells, although appar- 
ently homogeneous, is found, by the addition of a solution of iodine in mucilage, 
to contain glycogen, in flakes and clumps of varying size. How important this 
glycogenic degeneration of the kidneys may be has not yet been determined. 
Perhaps the glycogen represents sugar which has been absorbed by the cells. 
That chronic nephritis may complicate diabetes has already been mentioned. 

No thorough investigation of the chemical composition of the blood in diabetes 
has yet been made. One fundamental and constant characteristic is the greatly 
increased proportion of sugar in the blood. There is usually somewhere between 
0.2 and 0.45 per cent, of sugar, while in health the blood rarely contains over 0.1 
per cent. The lymph, and such serous effusions as are found, contain sugar, but 
the saliva, perspiration, bile, gastric juice, and other secretions rarely furnish evi- 
dence of its existence. 

Varieties, Course, and Prognosis of the Disease. — The study of a large num- 
ber of cases of diabetes will show great variations in the course and duration of 
the disease. As already stated, we may in practice distinguish between mild 
and severe forms of diabetes. Following Seegen's suggestion, this division is 
usually based upon the relation between the sugar excreted and the character 
and amount of the food eaten. Those cases are regarded as belonging to the mild 
form in which the sugar disappears from the urine when the patient takes food 
containing no carbohydrates. Some patients with this milder form may ingest 
small amounts of the amylacea, particularly if they take a proper amount of 
physical exercise (vide infra), without bringing on glycosuria. In the severe 
form of diabetes, on the other hand, the excretion of sugar in the urine persists 
even on a purely meat diet, and if any carbohydrates are taken, there will be a 
corresponding and large increase in the amount of sugar in the urine, as soon as 
half an hour to an hour thereafter. Of almost greater practical importance are 
the clinical signs which sometimes indicate, at the first glance, that an individual 
suffers from the mild or the severe form, as the case may be. The severe cases 
usually attack youthful individuals; the patient loses flesh rapidly, his face 
becomes narrow, and is apt to assume a peculiar expression of quiet melancholy; 
he is languid and feeble, and the urine presents all the indications of diabetes in 



DIABETES MELLITUS 



761 



an extreme degree. The milder cases, on the other hand, are more apt to occnr in 
later life, the patient has only moderate discomfort, and usually retains consid- 
erable strength and energy; he is but little, if at all, emaciated, and even the 
changes in the urine are so slight that they are not recognized until the attention 
is especially directed to them. It must be noted, however, that an apparently 
mild case of diabetes may become severe. Sometimes, also, the behavior of the 
case as to the excretion of sugar remains like that of the mild variety, and still, 
fatal complications occur at last, such as coma, necrotic processes, and pulmonary 
tuberculosis. 

In general, the clinical course of diabetes presents great variations. In a few- 
instances the disease occupies only a few weeks, and it may almost be termed 
" acute diabetes." Other cases last one or two years, and still others ten or 
twenty years. The patient's condition may vary from time to time. We have 
repeatedly seen the sugar disappear temporarily from the urine, and the patient 
apparently completely recover; but sooner or later the disease breaks out again. 
These cases, which are commoner in old people, have been called " intermittent 
diabetes." The relapse is often brought about by emotional excitement or some 
grave error in diet. Again, the disease may become apparently stationary and 
the patient enjoy comparative comfort for years. 

Different cases also differ in the relative severity of particular symptoms. 
Thus, the clinical picture presented by diabetes may be modified by the general 
constitution of the patient — for instance, his corpulence or emaciation; by such 
complications as diseases of the lungs, kidneys, or brain, or syphilis and gout; 
and by many other conditions. In practice, especially in practice among the 
better classes, it is very important to have a knowledge of the milder forms of 
diabetes, in which sugar is present in the urine only at times, and not in very 
large amount. The more we are accustomed to examine every urine for sugar 
the oftener we find such cases, as to the significance of which our knowledge is 
still very slight. The glycosuria of the corpulent is worthy of special considera- 
tion. It is, as we have said, particularly apt to occur in obese beer-drinkers, and 
it is not uncommon in patients who have formerly suffered from true gout. The 
tendency to the formation of furuncles and cataract is noteworthy. We must also 
mention the cases of diabetes in neurasthenics — that is, cases where there is 
sugar in the urine, and where the chief complaint is of general nervous symptoms, 
pressure in the head, anxiety, a dull feeling, incapacity for mental work, neural- 
gic pains, etc. In such cases glycosuria has not at all the serious significance that 
it has in genuine and severe diabetes. Finally, we would point out an especial 
clinical form of diabetes, in which glycosuria occurs in patients with severe gen- 
eral arterio-sclerosis; usually the patients are men in middle or advanced life. 
Not infrequently the condition seems referable to long-continued mental excite- 
ment or exertion. The amount of sugar in the urine is not large, and the sugar 
usually entirely disappears with appropriate diet; still, this form can not be un- 
qualifiedly regarded as mild, for we must bear in mind, also, the serious results of 
arterio-sclerosis. There are particularly apt to be cardiac symptoms referable to 
arterio-sclerosis of the coronary arteries. In all these " mild " varieties of dia- 
betes there may be no polyuria or thirst, so that an error in diagnosis is easy 
unless a careful examination of the urine is made. 

We should also mention the interesting fact, of which Frerichs reports some 
striking examples, that diabetes mellitus in a few exceptional cases may gradu- 
ally change into diabetes insipidus (see the following chapter). The reverse 
change is also said to occur. 

The usual termination of diabetes is death. We have already seen how great 
a difference there may be in the length of time preceding the fatal termination, 
and in what various ways it may be brought about. The most frequent immediate 



762 



CONSTITUTIONAL DISEASES 



causes of death are marasmus, diabetic coma, pulmonary consumption, nephritis, 
furunculosis, or the development of carbuncles. 

There is no doubt that complete recovery may occur ; but this is rare, and is 
possible only in the milder cases. It should also be borne in mind that, as we 
have said, apparent recovery does not exclude the possibility of a fresh outbreak 
of the disease. 

Theoretical Discussion of the Nature of Diabetes. — We have endeavored to 
give an approximately complete summary of the facts pertaining to diabetes. We 
trust we shall be excused from detailing all the theories and hypotheses which 
have been devised to explain the peculiar phenomena of the disease, particularly 
the glycosuria. It is a better way simply to confess that the true nature of dia- 
betes mellitus as yet remains very obscure. We shall confine ourselves to a few 
remarks upon the present state of the question. 

The essential fact which demands explanation is the excess of sugar in the 
blood. The blood of a healthy man does not contain over 0.15 per cent, of sugar, 
while that of a diabetic has 0.22-0.44 per cent. The source of this sugar is prob- 
ably the same as of the sugar normally contained in the blood. The largest part 
of the sugar probably comes from the carbohydrates ingested as food. These 
are, for the most part, converted in the primse viae, into sugar, which sugar 
thereupon enters the portal system. It may also be assumed that glycogen, so 
widely diffused throughout the system, is another source of sugar. The liver is 
the main seat of the manufacture of glycogen; but it is produced in other parts 
as well, and in particular in the muscles. The question next arises, From what 
is the glycogen formed? A part of it is manufactured from the carbohydrates 
contained in the food, but another part is certainly due to the ingested albu- 
minoids. Thus, Von Mehring found that in fasting animals, who have no 
more glycogen stored up in the body, diabetes may be produced by giving phlorid- 
zine (vide supra). The sugar excreted can therefore come only from the de- 
struction of albumen in the body. Again, the transformation of glycogen into 
sugar is not confined to the liver, but it may take place wherever glycogen is pro- 
duced. How it takes place is unknown. It is usually assumed that there is some 
" saccharine ferment." 

It would seem, therefore, that the sources of sugar are the same in diabetes as 
in health. We have next to seek for the reason of its excessive accumulation in 
the blood. Under normal circumstances, the sugar present in that fluid rapidly 
undergoes decomposition into other substances. In health there is no great 
excess of sugar in the blood, even upon a diet extremely rich in starch; and it is 
possible to eat large amounts of sugar without any glycosuria. That changes in 
the secretory action of the kidneys are not the cause of the excretion of the sugar, 
is evident from the fact that in diabetes insipidus no glycosuria occurs even if a 
large amount of sugar is ingested (Ererichs). We see, therefore, that diabetes 
can not be explained by assuming that there is an increased production of sugar, 
nor in fact is there such an increase, except as corresponds to the increased 
amount of ingesta. On the other hand, everything points toward the conclusion 
that in diabetes the ordinary processes effecting the decomposition and destruction 
of sugar are suspended. The sugar is excreted by the kidneys unaltered, for the 
reason that it is not destroyed. It is difficult to conjecture what the circum- 
stances may be which thus interfere with the decomposition of the sugar. Per- 
haps it is some special nervous influence, or perhaps some ferment may be want- 
ing in diabetes which in health promotes the metamorphosis of the sugar. This 
latter supposition is rendered the more probable by the above-mentioned experi- 
ments of Von Mehring and Minkowsky. Lepine also, having repeated these ex- 
periments, has reached the conclusion that the blood, under normal conditions, 
receives directly from the pancreas a " glycolytic " ferment which decomposes 



DIABETES MELLITUS 



763 



sugar. In a diabetic subject this glycolytic function of the blood is supposed to be 
much impaired, because the blood is deprived of this ferment, and as a conse- 
quence sugar is excreted unchanged; but this explanation has been disputed, 
so that really the question as to the true cause of diabetes remains absolutely 
unsettled. 

Diagnosis. — For the diagnosis of diabetes mellitus it is indispensable that 
sugar should be demonstrated in the urine. We have also to decide whether the 
condition be a temporary or a permanent one, or, in other words, whether we 
have to deal with mere glycosuria (vide supra) or genuine diabetes mellitus. 
This point is to be determined by means of the symptoms and general course of 
the disease. 

Diabetes often exists for some time unsuspected even by the physician. It 
may therefore be well to name over the symptoms which may be the first to 
attract the patient's attention, and which should therefore always suggest to a 
physician the possibility of the existence of diabetes. They are : 1, languor and 
debility; 2, furunculosis ; 3, pruritus pudendi in women, balanitis in men; 4, 
cataract ; 5, sciatica, especially if bilateral ; 6, impotence. We should be in the 
habit of examining the urine for sugar in all cases when complaint is made of 
indefinite symptoms, which can not be explained without further evidence, espe- 
cially if the patient is fat or nervous, and also if he is elderly and shows signs of 
arterio-sclerosis. 

If symptoms similar to those just enumerated lead to an examination of the 
urine, and the result of this is ambiguous, it is advisable to have the patient par- 
take of a meal rich in starchy elements, and to examine the urine thereafter, pref- 
erably by means of the fermentation test. If even then no sugar is found, dia- 
betes does not exist. 

Treatment. — Medical science does not possess the power to cure the disease, 
but it can greatly benefit the patient, both by alleviating his symptoms and by 
shielding him, at least for the time, from many of the secondary effects. 

The first requisite is to institute a proper regimen. All the hygienic circum- 
stances of the patient should be regulated. This is more important than any sort 
of medicinal treatment. We must consider that the increased amount of sugar 
in the blood is not without influence upon the tissues of the body, that as a con- 
sequence of the imperfect conversion of the carbohydrates there may be other 
injurious substances formed in the blood, and that the presence of sugar in the 
urine may lead to certain disagreeable symptoms (pruritus, balanitis) ; and con- 
sequently we must aim by our dietetic treatment to prevent any excessive accu- 
mulation of sugar in the blood, and at the same time to furnish the body with a 
substitute for the carbohydrates which can no longer be employed as food. 

It would be erroneous to conclude that this last point is the only essential one, 
and that we accomplish our whole duty by reducing the amount of sugar con- 
tained in the urine to a minimum. The general condition of the patient should 
invariably be considered. There can be no doubt that a diabetic patient whose 
strength is well maintained is better off, even if there is considerable sugar in his 
urine, than one whose urine contains less sugar, but who yet is daily growing 
weaker. In managing the dietary of a diabetic patient, we must first determine 
what tolerance for carbohydrates there may be in each particular case. The prin- 
ciple of dietetic treatment of diabetes does not consist in the simple withdrawal 
of all carbohydrates, but rather in allowing each patient as much of such sub- 
stances as his body is in a condition to appropriate. This amount varies greatly 
in different cases, and also in the same patient at different times. We must first 
determine whether the case belongs to the severe or the mild type, as above de- 
fined — that is, whether sugar entirely disappears from the urine if no carbo- 
hydrates whatever are allowed. If it does — that is, if we are dealing with the 



764 



CONSTITUTIONAL DISEASES 



milder form of diabetes — we then proceed, after the urine has been freed from 
sugar, to give gradually increasing amounts of carbohydrates, at the same time 
examining the urine every day in order to see whether the starch ingested is com- 
pletely oxidized in the blood. The more carbohydrates that can be allowed with- 
out the appearance of sugar in the urine, the more favorable the case. When we 
have in this manner measured the ability of the system to utilize carbohydrates, 
the patient is kept for a considerable time upon such food as his system can 
manage completely to appropriate. The experience of physicians has shown that 
this sort of limitation of the carbohydrates may have a permanent beneficial in- 
fluence, inasmuch as after the patient has adhered for a considerable time to a 
diet which keeps the urine free from sugar, the tolerance of the system for carbo- 
hydrates increases. TVe may, therefore, try gradually to make some increase in 
the amount of carbohydrates, and we shall not infrequently rind that after per- 
sistence in such a diet for a considerable time, the patient will bear more car- 
bohydrates without the return of glycosuria. Thus, guided by constant examina- 
tions of the urine, we can easily prescribe the correct diet for the individual 
patient. 

If we are dealing with the severe form of diabetes — that is, if sugar is still 
excreted in the urine, even when the diet consists exclusively of meat and fat — 
we may try the effect of withdrawing all carbohydrates completely for a consid- 
erable time. Many physicians (Cantani, Naunyn, and others) have observed that 
an absolutely strict diet of this sort, excluding all carbohydrates, may have a very 
favorable therapeutic effect, so that finally the patient will regain a certain tol- 
erance for carbohydrates ; but it is precisely in these severe cases that, in our 
opinion, it is improper to be guided too much by general rules. TTe should con- 
sider not only the character of the urine, but the condition of the individual in 
other respects — his subjective sensations, his weight, and his strength. Many of 
these severe cases undoubtedly feel better when they are allowed a moderate 
amount of carbohydrates than when they are on a purely nitrogenous and fatty 
diet, despite the somewhat greater amount of sugar excreted. Particularly when 
the appearance of acetone, acet-acetic acid, butyric acid, and the like in the urine, 
suggests a considerable destruction of the albuminoids of the body, and perhaps 
an impending diabetic coma, practical experience has shown that we should not 
insist too strictly upon a purely nitrogenous diet, but should try. by the cautious 
administration of carbohydrates, to improve the general condition and avert the 
danger of coma. 

As we have already mentioned, it is decidedly advantageous to make up for the 
diminution in carbohydrates by giving other food which does not contain nitrogen. 
The most natural thing, certainly, is to allow an abundance of fat as a substitute 
for the carbohydrates; and practical experience is, as regards this matter, in 
entire unison with theory. Fat is well borne by most diabetics, and it may be 
allowed in the form of butter, cream, salad oil, and the like. It should be particu- 
larly recommended to emaciated patients, if they can digest it. Sometimes cod- 
liver oil may be prescribed for a time. Beside the fats, the use of alcohol as a 
preventive of waste might be considered; in small amounts brandy and claret 
may be allowed to some patients. We would earnestly advise against the use of 
larger amounts, for the toxic effect of alcohol might injure the vitality of the 
cells (vide supra). 

With a view of aiding the physician in preparing a bill of fare for his indi- 
vidual cases, we append a list of the separate foods which are available for the 
nourishment of diabetic patients : 1. A diet which contains almost no carbo- 
hydrates would be as follows: On waking, tea or coffee with cream, but no sugar; 
for breakfast, eggs, ham, cold meat : at noon, broth, not thickened, fish with 
butter, meat with greens or salad; for supper, tea, eggs, cold meat, cheese; in 



DIABETES MELLITTJS 



765 



addition the patient may drink water or a moderate amount of claret. The fol- 
lowing articles are almost absolutely devoid of carbohydrates : all sorts of meat, 
ham, smoked meat, tongue, all sorts of fish, crabs, caviare, oysters, sardines, eggs, 
green-colored vegetables, lettuce, endives, cress, asparagus, cauliflower, spinach, 
cucumbers, red and white cabbage, string beans when young, sorrel. Of course, 
if these are boiled, only butter can be added, or meat, but no cereal. Other arti- 
cles of this class are all sorts of cheese ; such fatty foods as butter, olive-oil, and 
cream; meat broths, artificial meat-peptone, meat extract, somatose, mineral 
waters, and lig\ht claret. 2. Articles which contain a small amount of carbo- 
hydrates, and which, therefore, may be allowed in moderate amounts if there is 
a certain degree of tolerance for carbohydrates (vide supra) : rusks, rye bread, 
milk, cocoa, turnips, kohl rabi, radishes, nuts, sour fruits — such as apples, cur- 
rants, and cherries. 3. Articles which contain a large amount of carbohydrates, 
and are therefore to be prohibited or allowed sparingly, according to individual 
circumstances : all sweet dishes, cake, honey, potatoes, oatmeal, rice, peas, beans, 
lentils, sago, sweet fruits, sweet wines, and beer. 

The hardest thing for diabetics to do without is bread. Every physician who 
has had much experience with diabetic patients can relate experiences of the cun- 
ning of patients in satisfying- their unconquerable longing for this forbidden 
article by the employment of underhand means. Hence, many attempts have 
been made to furnish special sorts of bread for diabetic patients, containing a 
minimum proportion of carbohydrates. Most of these preparations, however, 
the patients do not like. Chiefly to be recommended are gluten bread and aleu- 
ronat bread. Finally, it is well to employ saccharine to sweeten food and drink, 
particularly tea and coffee, provided the saccharine does not produce, dyspepsia 
and also proves agreeable to the patient. 

[The dietetic treatment of diabetes is so important that it is desirable to go 
more into detail. 

There is some discrepancy between the authorities on this point, a more strict 
diet being laid down by some than by others. Ralfe's list is as rigid as any, and 
is as follows : 

To avoid: Milk (except very small quantities for cooking purposes). The liver 
of all animals (as the liver of oysters and all mollusca is large, and abounds in 
glycogen, these animals must be forbidden), so also the interior of crabs, lobsters, 
etc. Bread, biscuits, rusks, toast, farinaceous vegetables, such as potatoes, Jeru- 
salem artichokes, rice, oatmeal, corn-flour, sago, tapioca, arrowroot, etc. Saccha- 
rine vegetables, turnips, carrots, parsnips, green peas, French beans, beet-root, 
asparagus, tomatoes. Blanched vegetables of every sort, as celery, sea-kale, 
endive, radishes ; also the stalks and white parts of such vegetables as cabbage, 
lettuce, broccoli, etc. Fruits of all kinds. Jams, syrups, sugars. Certain condi- 
ments, such as chutney and sweet pickles, cocoa, chocolate, liqueurs, sweet wines. 

May take : Meat, fish, poultry, game, bacon, ham, eggs. Bread and biscuits 
made with prepared gluten, bran, or almond-flour. Green vegetables, summer 
cabbage, turnip-tops, spinach, broccoli-tops, water-cresses, mustard and cress, 
laver, sauerkraut, the green parts of lettuce, sorrel, mushrooms. !Nuts of various 
kinds (except chestnuts). Cheese. 

Flint's list is more lenient, allowing oysters and a much larger choice of vege- 
tables, such as asparagus, string beans, artichokes, cauliflower, tomatoes, etc. 
("Journal of the American Medical Association," July 12, 1884; also "Peppers 
System of Medicine," vol. ii, page 221). 

Donkin's treatment by skim milk exclusively is highly approved by Tyson. 

Bhenish and similar wines, moderate quantities of spirits, or a malt liquor in 
which the sugar has been entirely converted into carbonic acid and alcohol (Bass's 
ale, for instance), are permitted. 



766 



CONSTITUTIONAL DISEASES 



In the opinion of the writer, it is always well to begin treatment with a very 
stringent dietary, which may be relaxed gradually as circumstances dictate. The 
severity of the case is to be regarded rather than the name of the disease. The 
gluten and other diabetic flours are unreliable; and I agree with Flint that, if 
bread be allowed, it is better to give the crust of a French roll, the ingredients of 
which are known. Saccharine may be used to sweeten tea and coffee, jellies, ice 
cream, and the like.] 

Certain other general directions are important. The patient should take suffi- 
cient exercise. Kiilz has determined by means of accurate experiments that, 
other things being equal, the assimilation of sugar is increased by muscular 
activity, with a consequent diminution in the excretion of sugar. Practical 
experience also shows that regular exercise is extremely beneficial. A proper 
discretion should be employed, however; nothing would be more injudicious than 
to force a feeble patient to exhausting efforts ; but if the patient be vigorous and 
well nourished, he should be strongly urged to take a walking-trip in the moun- 
tains, or to try horseback riding and the like. Methodical massage of the muscles 
sometimes has a good effect. 

Proper care of the skin is indispensable. Baths, cold sponging, and douching 
may be employed. Strict attention should also be given to the teeth, lest they be- 
come carious. Thorough ventilation should be maintained, both day and night. 

Of internal remedies, opium should be named first. One good effect of this 
drug is that it lessens the annoying thirst. It sometimes also causes decided 
diminution in the amount of urine and sugar excreted. It is further indicated 
when there is general restlessness or sleeplessness. It is often well borne by 
diabetic patients, even in large doses. A patient sometimes can take four to 
eight grains (gramme 0.25-0.5), or even more, of opium in twenty-four hours 
without any bad effects. We have repeatedly administered to patients with a 
severe form of diabetes, for weeks at a time, from sixty to one hundred drops of 
laudanum, divided into three doses daily, with apparently the best results. It 
should be especially noted that the bowels were not at all disturbed by the drug. 
It is deserving of mention that the alkaloids of opium, such as morphine and 
codeine, possess much less value than opium itself. 

[The inhalation of oxygen is worthy of mention as a remedial measure. 

Purdy seems to show that diabetes attains its highest mortality in those 
States which combine relatively high altitudes with low temperature. A resi- 
dence in the Gulf States or Southern California may therefore be curative or pro- 
long life.] 

The alkalies, and still more the alkaline mineral waters, enjoy a reputation 
second only to that of opium. Hundreds of patients visit Carlsbad, Neuenahr, 
and Vichy every year, to return much benefited. Of course it must not be for- 
gotten that it is not merely the waters which produce these beneficial changes. 
Other factors are also important, in particular the strict diet, exercise, fresh air, 
and freedom from the cares of the household and business. Why the alkalies 
should act favorably we do not know. Perhaps it is because they neutralize the 
abnormal acids in the organism. Griesinger, and later Kiilz, as well as others, 
have made careful comparisons of the amounts of sugar excreted under like cir- 
cumstances, with and without the ingestion of bicarbonate of soda or of Carlsbad 
water and similar substances, and for the most part have not been able to per- 
ceive any benefit from these remedies. Practical experience, however, shows the 
value of these alkaline waters ; and their use is to be recommended, provided the 
patient is comparatively vigorous and fit for travel, although his expectations 
should not be raised to too high a pitch. 

From a theoretical point of view, there is interest in the fact that certain 
remedies which are antagonistic to fermentation have been shown by Ebstein and 



DIABETES INSIPIDUS 



767 



Miiller to diminish the excretion of sugar in many cases of diabetes. Chief 
among these are carbolic acid and salicylate of sodium. Carbolic acid is 
given in the amount of ten to twenty grains (gramme 0.5-1.5) per diem. The 
amount of salicylate of sodium is one to two and a half drachms (grammes 5-10) 
daily. There is no doubt that these drugs possess the property ascribed to them ; 
but they are not advantageous to the patient, inasmuch as the general condition 
is seldom improved by their use. On the contrary, very unpleasant effects are 
sometimes observed. 

We need not enumerate all the remedies which have been recommended in 
diabetes. We have already mentioned those that possess any extended repu- 
tation. We may therefore merely refer to certain drugs which have been lately 
introduced. 

Cantani has suggested the employment of lactic acid in the amount of one to 
two and a half drachms (grammes 5-10) per diem, dissolved in half a pint of 
water. This drug may perhaps serve as a physiological substitute for sugar, as 
glycerine is supposed to do (vide supra), but it has no specific virtues. Cer- 
tain salts of ammonia, such as the carbonate and acetate, are said to diminish 
the excretion of sugar, and have therefore long been employed in diabetes. 
Good results can not, however, be claimed for them, nor for iodoform (3-7 grains, 
gramme 0.2-0.4, daily), nor for the lately much-lauded jambul. The trials of 
pancreatic juice, also, have led to no definite results. 

It is evident, in brief, that the best mode of treating diabetes, at least accord- 
ing to our present knowledge, is by regulating the diet, and that it is well, in 
addition, to recommend the employment for a time of the above-mentioned min- 
eral waters, with opium and other internal remedies to combat special symptoms. 
The treatment of such complications as phthisis or cutaneous eruptions need not 
be described here. 

In diabetic coma, camphor or ether, subcutaneously, should be employed, 
together with lukewarm baths and douching. In consideration of the possibility 
that diabetic coma is connected with an acid intoxication (vide supra), we should 
always try the administration of large doses of carbonate of soda, either by the 
mouth or in an enema, or by the subcutaneous or intravenous injection of a three- 
to five-per-cent. solution. The results thus far, it must be confessed, are not very 
favorable ; still, sometimes this mode of treatment has been decidedly beneficial. 
A more important matter seems to be, as ISTaunyn pointed out, the administra- 
tion of two to five drachms (grammes 10-20) of the bicarbonate of soda, daily, 
for a long time, to any diabetic patient whose urine gives a positive ferric chlo- 
ride reaction (vide supra), thus justifying' suspicion that an acid intoxication is 
beginning. « 



CHAPTER X 
DIABETES INSIPIDUS 

Definition and etiology. — In the preceding chapter a distinction was drawn 
between diabetes mellitus and the symptomatic condition termed glycosuria. 
There is a similar distinction to be made between diabetes insipidus and polyuria. 
Polyuria is an increase in the volume of urine, and mainly in the amount of 
water excreted by the kidneys. It is a symptom which may be produced in many 
different ways. In the first place, it is a natural consequence of the ingestion of 
large amounts of water, or of the absorption of serous effusions ; it also occurs in 
certain diseases of the nervous system, especially of the medulla and cerebellum ; 



768 



CONSTITUTIONAL DISEASES 



it is occasionally seen, as we have had opportunity to observe, in chronic 
hydrocephalus, and is a not very infrequent phenomenon in hysteria. Large 
amounts of urine are also secreted in certain renal diseases (interstitial ne- 
phritis and amyloid degeneration), and often during convalescence from acute 
diseases, such as typhoid fever, or after the ingestion of certain drugs, called 
diuretics. 

Diabetes insipidus, on the other hand, is a disease which may develop idio- 
pathically in persons otherwise perfectly healthy. Its aetiology is unknown. It 
occasionally seems to be excited by emotional disturbance, concussion or other 
injury of the brain, or some previous acute disease, such as typhoid or typhus 
fever, malarial poisoning, and cerebro-spinal meningitis. The disease sometimes 
appears in the syphilitic, and it may, therefore, in many instances, be due to syphi- 
lis. Patients frequently state that their symptoms began immediately after 
drinking a very large amount of some fluid, as on a very hot day or after a long 
march. Einally, there are cases in which the disease appears to be hereditary, or 
to attack members of the same family. A distinction should be made between 
genuine diabetes insipidus and those cases in which the primary symptom is not 
polyuria, but an abnormal thirst, polydipsia, so that the polyuria is merely a 
result of drinking so much water. In many of these cases the polydipsia is un- 
doubtedly a hysterical symptom (see the chapter on hysteria). 

The true nature of diabetes insipidus is entirely unknown to us. The 
view which seems most probable of any is, that some nervous disturbance is 
its direct cause. In support of this, we have the appearance of a " symptomatic 
diabetes insipidus " in connection with organic disease of the brain (vide supra), 
and the fact that polyuria may be artificially excited by injury to a definite spot 
in the floor of the fourth ventricle or by section of the vagus nerve. Diabetes 
insipidus presents a most striking analogy with diabetes mellitus. This is shown 
both by the similarity in aetiology and symptomatology, and still more by the fact 
that occasionally one disease merges into the other. 

Diabetes insipidus is a disease of very infrequent occurrence, and is decidedly 
less often seen than diabetes mellitus. Most patients are youthful or middle- 
aged. Genuine diabetes insipidus has also been observed in children, perhaps in 
connection with hereditary syphilis. The male sex is somewhat more liable to 
the disease than the female. 

Clinical History. — Diabetes insipidus may be developed gradually or with con- 
siderable abruptness; the latter case is especially frequent when there is some 
definite cause, such as the ingestion of a large amount of liquid, or traumatism. 

The essential and characteristic symptom is an increase in the volume of 
urine. This is usually very considerable. Often eight or ten quarts (8,000 to 
10,000 cubic centimetres) are excreted in twenty-four hours, and cases have even 
been reported where the amount reached the almost incredible volume of thirty 
to forty quarts (litres). If a healthy person and a sufferer from diabetes insipidus 
are each given the same amount of water in food and drink, the sick man will 
excrete more urine than the healthy. In color the urine is very pale, and some- 
times almost like water. The specific gravity is very low, being usually 1004 to 
1002, or even 1001. The reaction is slightly acid, sometimes, almost neutral. 

The percentage of solid constituents in the urine is, of course, trifling. The 
total amount of solids, however, corresponds perfectly with the ingesta, or indeed 
is even somewhat above normal. The amount of urea, in particular, seems to be 
increased, but it has also been stated that other constituents of the urine have 
been excreted in abnormally large amounts — namely, phosphoric acid, sulphuric 
acid, lime, and kreatinine. Inosite has been found in the urine by Strauss and 
other observers, so that it has even been proposed to give diabetes insipidus the 
name of "diabetes inositus," in distinction from diabetes mellitus. Inosite is 



DIABETES INSIPIDUS 



769 



not invariably present, however, in the urine of diabetes insipidus. In cases of 
true diabetes insipidus, albuminuria is extremely exceptional. 

Another important symptom is the excessive thirst. To make up for the 
loss of water by way of the kidneys the patient is obliged to drink great quantities 
of liquid, and, indeed, it is always found that the amount of water ingested, in the 
way of drink and solid «food, somewhat exceeds the total volume of urine excreted. 
Despite this, the tongue is usually dry, as is also the skin, the insensible perspira- 
tion being considerably below the normal amount. The furunculosis seen in dia- 
betes mellitus is exceptional in diabetes insipidus. The same is true of pruritus, 
balanitis, etc. Occasionally profuse salivation has been associated with the 
•disease. 

Symptoms referable to the various internal organs are few. Cataract has been 
occasionally observed, but it is much less frequent than in diabetes mellitus. The 
same may be said of pulmonary tuberculosis. In most cases the appetite is not 
excessive. The bowels are regular or slightly constipated. There is seldom much 
gastro-intestinal disturbance, unless from some chance complication. The sexual 
functions are usually unimpaired. 

The general health is considerably affected in cases of any severity. The 
patient becomes emaciated, languid, and feeble, and has no inclination to mental 
or physical exertion. Sleep is often disturbed, the mind depressed. The tempera- 
ture is normal, or even a trifle below normal, probably as a result of the large 
amount of cold water drunk. 

Diabetes insipidus is a very chronic disease. If there is no serious complica- 
tion it may last for decades, yet there are cases that run a more rapid and unfa- 
vorable course. Sometimes there are considerable vicissitudes in the condition of 
the patient, in part dependent upon external circumstances and in part appar- 
ently spontaneous. In case some intercurrent acute disease develops there may 
be, during its continuance, a considerable diminution in the amount of urine 
■excreted. 

The termination is usually unfavorable. Recovery is extremely rare. In the 
more fortunate cases the condition finally becomes stationary, and the patient 
attains to advanced years. Sometimes, however, death occurs more prematurely, 
being usually hastened by phthisis or some similar complication. 

Weil has lately contributed to our knowledge of this disease the results of an 
accurate study of its hereditary and apparently congenital variety. Weil narrates 
the history of a family in which marked polyuria and corresponding polydipsia 
appeared in numerous members for several generations. These persons all en- 
joyed excellent health, with this exception; and most of them attained old age. 
We hardly need to emphasize the fact that this form of the disease is radically 
•different from the ordinary acquired variety. Perhaps its true cause is an abnor- 
mal congenital permeability of the glomeruli, but we have no certain information 
in regard to it. 

Post-mortem Appearances. — Such lesions as have been found in diabetes in- 
sipidus are usually the result of fortuitous complications, such as tuberculosis, 
carcinoma, and pneumonia. There are but very few changes referable directly to 
the disease itself : among these are enlargement of the kidneys and dilatation of 
the ureters. In rare instances a possible cause for the symptoms has been found 
in some lesion of the central nervous system, but these were cases of symptomatic 
polyuria and not of genuine diabetes insipidus. Instances of this sort are seen in 
connection with tumors or inflammatory changes in the medulla or cerebellum, 
and exostoses at the base of the skull. 

Diagnosis. — The characteristic urinary phenomena usually render the diagno- 
sis of diabetes insipidus an easy matter. It is of course necessary to exclude such 
diseases as might occasion symptomatic polyuria (vide supra) ; but this is seldom 
49 



770 



CONSTITUTIONAL DISEASES 



difficult if we make a careful physical examination and duly consider all the 
attendant symptoms. The differential diagnosis between diabetes insipidus and 
diabetes mellitus can almost invariably be made by means of the urinometer. If 
the specific gravity is below normal, it is scarcely necessary to test for sugar, 
although in doubtful cases this is the sole criterion.* [The early stage of con- 
tracted kidney has repeatedly been mistaken for diabetes insipidus. — V.] 

Treatment. — No special injunctions with regard to diet are required. It 
would of course be a mistake to forbid the patient to assuage his excessive thirst ; 
but we may possibly lessen the amount of water drunk by prescribing bits of ice, 
or lemonade and other acid drinks. Opium sometimes lessens both the thirst and 
the amount of urine excreted. Rather large doses should be prescribed, say 
fifteen to twenty drops of laudanum, several times a day. It is also important that 
the skin should be well cared for by means of baths and friction, and every effort 
should be made to promote the general vigor of the patient. He should have 
nourishing food and good air. 

There have been a great number of internal remedies recommended as spe- 
cifics, but, in general, we can expect no great results from them. Most employed 
are valerian, of which one to one and a half drachms (grammes 5-10) are given 
daily in powder, or infusion ; and ergotine, of which one and a half to eight grains 
(gramme 0.1-0.5) are given several times a day. Other remedies which are said 
to have been sometimes tried with benefit are carbolic acid, atropine, and the 
bromides ; also, galvanization of the cervical cord. 

Occasionally we may find an apparent cause for the disease and endeavor to 
remove it. If there is a suspicion of syphilis, mercurial inunctions should be 
tried, perhaps in combination with iodide of potassium or sodium. Sometimes, 
as we can confirm by our own experience, they have an excellent effect. Of course, 
where there is symptomatic polyuria, the primary disease, such as hysteria, de- 
mands treatment. [Da Costa and others report very good results as following the 
administration of ergot.] 



CHAPTER XI 

GOUT 

(Podagra) 

Etiology. — Thomas Sydenham was the first to write a careful clinical descrip- 
tion of gout. He himself suffered from the disease for about forty years, and he 
has given a detailed description of his own case in the treatise which he published 
in 1683, under the title " Tractatus de podagra et hydrope." It was, however, Wol- 
laston who, in 1797, threw the first light upon the peculiar anomaly of metabolism 
which exists in this disease. He demonstrated that the gouty deposits found in 
the joints and other parts of the body are mainly uric acid. Erom his time an all- 
important point with regard to the nature of the disease has been the relation 
between the symptoms of gout and disturbances in the manufacture and excretion 
of uric acid. In 1848 Garrod showed that in gout the blood contains an excess 
of uric acid, and that the excretion of uric acid by the kidneys is diminished. 
He was thus in a position to frame a theory consistent with all the clinical facts. 
Numerous investigations have been undertaken since his day; but we still re- 
main with regard to gout in a position analogous to that which we hold toward 
diabetes. We are, it is true, in the possession of a considerable number of well- 



* [Compare, however, the author's statements on page 752. — Trans.] 



GOUT 



771 



established facts relating- to it, but we do not know why the normal chemical pro- 
cesses are disturbed, and we are unable to explain the' connection between the 
various phenomena observed. 

• Clinical experience has taught us certain remote causes of gout, first of which 
comes heredity. About fifty per cent, of all cases occur in patients whose families 
have already suffered from the disease, or have given other indications of the 
uric-acid diathesis — such as renal calculi; and it is sometimes possible to trace 
this transmitted taint through many generations. It is decidedly more apt to 
pass down through the male members of the family than through the female. 

isext in importance to hereditary influences is the mode of life. From time 
immemorial this has been regarded as an exciting cause of the disease. It has 
been a matter of universal belief that over-feeding, and especially the ingestion of 
too large a quantity of albuminoids, is strongly provocative of the disease. The 
same opinion has been held with regard to persistent over-indulgence in alco- 
holic beverages. Seneca relates that at the time of the decay of the Roman 
Empire women practiced such excesses that they were as subject to gout as the 
men, and an old verse runs : " Wine is the father of gout, feasting is its mother, 
and Venus is the midwife." That this old view of gout as a rich man's disease 
has much truth in it can not be denied. The not infrequent cases of genuine 
gout which we observe every year in Erlangen attack mainly great beer drinkers, 
who for years have imbibed three or four litres of beer a day; but, on the 
other hand, it would be going too far to refer all cases of genuine gout to an im- 
proper mode of life, and excessive indulgence in alcohol. Sometimes genuine 
gouty arthritis is seen in individuals who have always lived moderately, or who 
have even been in needy circumstances. 

Besides alcohol, there is another well-known poison which is capable, by its 
chronic action, of producing that change in metabolism which forms the founda- 
tion of gout ; we refer to lead. We are absolutely certain that persons who have 
much to do with lead, such as compositors and house-painters, suffer with com- 
parative frequency from genuine gout, with deposits of uric acid in the joints. 
We have repeatedly seen cases of this sort in Leipsic and Erlangen. In a sur- 
prising number of patients lead-poisoning is associated with contracted kidney. 
We have repeatedly observed that the combination of chronic alcoholism and 
chronic lead-poisoning is especially provocative of gout. 

With regard to all other alleged setiological factors, confirmatory evidence is 
lacking. Possibly, however, when the foundation for the disease is already laid, 
an attack may be excited by certain determining causes — namely, trauma, taking 
cold, errors in diet, or mental emotion. 

The geographical distribution of gout is remarkably unequal. The disease is 
more frequent in England than in Germany, although in the latter country 
certain regions appear to be more affected by it than others. In Leipsic gout 
seemed to us to be rather rare, but in Bavaria it is more common. 

Gout is rarely seen in childhood and youth. It is a disease of middle or 
advanced life. Men are much more often attacked than women. 

Clinical History. — Gout may produce symptoms in many different organs ; 
but its effect upon the joints is so characteristic that the arthritic disturbance 
has long been termed " normal or regular gout," in contradistinction from " atypi- 
cal, internal gout." This distinction is of course an artificial one, for the various 
phenomena of gout present the most manifold gradations and transitions. It will, 
however, be advantageous, in attempting to gain a practical insight into the vari- 
ous symptoms of the disease, if we first discuss the so-called " typical attack of 
gout," subsequently appending a description of the other manifestations of the 
disease. Eurthermore, the regular attack of gout is, in at least a majority of 
cases (vide infra), the first and earliest symptom of the disease. 



772 



CONSTITUTIONAL DISEASES 



1. The typical attack of gout (primary articular gout) is sometimes abrupt ; 
but it is often preceded for a longer or shorter period by certain premonitory 
symptoms, the meaning of which, though not evident to one who is about to suffer 
from his first attack, is sufficiently clear to more experienced patients, particu- 
larly as each individual case is apt to present a marked similarity in the prodrom- 
ata of the separate paroxysms. These premonitory symptoms vary in different 
individuals. Sometimes they consist of dyspeptic disturbances; sometimes of a 
feeling of languor and mental depression; very often of dragging, muscular 
pains or cramps in the calves of the legs; or again of slight feverishness, with 
chilliness, sense of heat, and perspiration. These prodromes occur a longer or 
shorter time before the true attack of gout. On the other hand, it must be con- 
fessed that a patient may feel unusually well just before an attack. 

The attack is noticeably apt to begin in the night-time, or very early in the 
morning. The patient is awakened by a sudden and very violent pain in the 
metatarso-phalangeal joint of one of the great toes ("podagra"). The joint 
becomes swollen, the skin over it red, hot, and tense, the veins in the neighbor- 
hood distended. At the same time there is chilliness and moderate fever (101°- 
102°; 38.5°-39° C). This condition persists till morning. Then the pain is 
almost sure to abate, the fever to remit at the same time that sweating begins, 
and the patient to feel tolerably well during the day. The joint, however, re- 
mains swollen, with inflammation and oedema. The next night the pain begins 
again, and there is a fresh fever ; and these alternations are repeated, as a rule, 
for three to seven days. Usually there are not many other symptoms present ; 
the appetite is impaired, but ordinarily there are no marked gastric disturbances, 
such as eructations and vomiting, or intestinal symptoms. There may be a 
slight bronchitis. Even when the attack is more persistent than this, the pain 
is usually much less severe after the first two or three nights. After that time 
it gradually abates ; and it is commonly said that an attack is brief in propor- 
tion to the violence of its first symptoms. When the pain ceases, swelling soon 
disappears, the skin undergoes a slight desquamation and resumes its normal 
appearance, the general health of the patient rapidly improves, and he is often 
found to be better after an attack than he was before. 

For theoretical purposes (vide infra) it would be very advantageous to possess 
a more accurate knowledge of the condition of the urine, and in particular of the 
excretion of uric acid during the attack and at other times. As yet, however, 
there have been but few careful investigations made, and these have led to some- 
what contradictory conclusions. Garrod has made a very important observation ; 
it is, that the amount of uric acid excreted diminishes several days before the 
commencement of an attack, and remains diminished during the attack. Subse- 
quently to the attack the excretion of uric acid is said to be above normal. In 
contrast with the excretion of uric acid in the urine, the amount of uric acid in 
the blood is increased during the attack. This is an important fact which was 
discovered by Garrod, and which has been confirmed by others, including Salo- 
mon, Klemperer, and others. 

If there has been one attack of gout, there are almost sure to be others. They 
come sooner or later, at regular or irregular intervals, and separated by weeks, 
months, or even years. The attacks recur at long intervals in mild cases, more 
frequently and at gradually diminishing intervals in the severe. Spring and 
autumn are regarded as the time when attacks of gout are most apt to occur. In 
these subsequent attacks the great toe still remains the part most constantly and 
severely affected; but other joints may also suffer — for example, the wrist, the 
small joints of the fingers (see Fig. 82), the knee, or the shoulder. In all these 
joints there appears an acute and very painful inflammation, with considerable 
swelling of the affected parts. Sometimes traumatism apparently determines the 



GOUT 



773 



localization of the gouty disturbance. In each attack, the trouble is usually con- 
fined to a single joint. It is only in exceptional or advanced cases that several 
joints are simultaneously invaded. 

The longer the disease has lasted, the less typical are the separate attacks. 
There may now be less suffering at the time of an attack; but the articular 




Fig. 82.— Acute attack of gout in the joints of the fingers. (Personal observation.) 

changes are more persistent. The joints gradually become deformed. There are 
symptoms referable to other parts of the body; and the gout gradually passes into 
its second chronic stage. Occasionally the disease is irregular and atypical from 
its incipiency; and the first manifestations may not be arthritic, but referable 
to the kidneys (vide infra) or other organs. 

2. Chronic Gout and the Gouty Diseases of Various Organs. — As a rule, the 
most striking results of chronic gout are the changes in the joints. There is a 
gradual development of marked deformity, particularly in the small joints of the 
fingers, the joints of the great toe, and less often the other joints. The fingers 
(see Fig. 83) are deflected toward the ulnar side, at the metacarpophalangeal 
joints, as in arthritis deformans, and at the same time the fingers, as a whole, are 
thickened, particularly at the joints. Almost always the small finger-joints early 
undergo firm anchylosis. The great toes are often bent out of shape. "Not infre- 
quently there are formed around some of the joints which are often attacked, 
particularly the metatarso-phalangeal joint of the great toe, soft fluctuating 
masses, which are very painful. If these burst spontaneously, or if they are in- 



774 CONSTITUTIONAL DISEASES 

cised, they are found to contain little, if any, pus, but much detritus, and numer- 
ous crystals of uric-acid salts, mainly the urates of sodium and calcium. When 
these nodes break open they may develop into tedious ulcers ; similar gouty nodes 
(arthritic tophi) may develop in other portions of the skin, particularly in the 
lobe of the ear, and sometimes also in the tendons and muscles. 




Fig. 83.— Changes in the joints of the fingers in genuine chronic gout. (Pei'sonal observation.) 



Gout may affect the mucous membranes. A gouty dyspepsia is very frequent. 
Its symptoms are more or less severe. The gouty are also subject to intestinal 
catarrh of varying severity, and to bronchitis and conjunctivitis, as well as to 
catarrh of the urinary organs. Ebstein regards " gouty gonorrhoea " as essen- 
tially a catarrh of the excretory ducts of the prostate gland. It is not an easy 
matter to explain why these various forms of catarrh should occur in gout. 
Some of them may be complications. In other cases they are doubtless the 
result of passive congestion, due to cardiac failure (vide infra) ; but in still other 
instances it must be confessed that they are apparently due to the toxic influence 
of the accumulated uric acid or other noxious products of abnormal metabolism. 

[My experience, though far more limited than that of Draper, nevertheless 
leads me to believe, as he does, that the irregular forms of gout are by no means 
uncommon in women as an inheritance from a previous generation. The mani- 
festations in some of these cases are so ill-defined that a diagnosis may be diffi- 
cult without a knowledge of the family history; in other cases, more or less de- 
formity of the smaller joints, or slight recurrent swellings of those parts, throw 
much light on the condition underlying the symptoms.] 

Inflammation of serous membranes — for example, of the pleura— also occurs ; 



GOUT 



775 



and there may be pneumonia. The skin not infrequently suffers from acute or 
chronic eczema, which sometimes appears to be referable directly to the gout. 
Keratitis, iritis, and other inflammatory disturbances of the eye are also said to 
be caused directly by gout. Cirrhosis of the liver has been repeatedly found, and 
is probably to be referred chiefly, in our opinion, to chronic alcoholism. 

By far the most important of all these gouty manifestations are referable to 
the kidneys and to the circulatory system. The disorder of the latter is some- 
times symptomatic of the renal trouble, but in other instances it occurs inde- 
pendently of it. There may be severe gouty arthritis for years without any lesion 
of the kidneys ; but this is exceptional. In severe cases of gout it is the rule that, 
-sooner or later, symptoms of renal disorder present themselves. The so-called 
" gouty kidney " is a form of chronic interstitial nephritis. However important 
this complication, its symptoms do not need to be discussed here, as they are pre- 
cisely similar to those seen in ordinary cases of contracted kidney (vide page 628 
et seq.). The distinctive symptom of this disturbance is albuminuria; and the 
gradually developing secondary hypertrophy of the left ventricle is the pivot on 
which turns the whole future course of the disease. So long as the heart remains 
capable of performing its functions, the condition of the patient will probably 
remain endurable if not actually comfortable. Finally, however, compensation 
is sure to become impaired; and then appear oedema, dyspnoea, debility, and 
emaciation — in short, all the familiar symptoms of cardiac failure. A speedy 
end may be brought about by uraemia, cerebral embolism, or cerebral haemorrhage ; 
but in other cases the patient suffers for years, both from the heart disease and 
from fresh arthritic attacks. 

The cardiac hypertrophy just mentioned is the result of the contracted kidney. 
Other disturbances of the circulatory system appear to be referable directly to the 
gout itself. Among these are chronic endocarditis or myocarditis, and perhaps 
certain "functional" symptoms, such as palpitation and angina. An important 
symptom. is chronic endarteritis or arterio-sclerosis. This is often seen in gouty 
subjects, and in many instances seems to be connected with the gout. Some- 
times, also, there are gouty lesions of the veins, such as varicosities or throm- 
hosis. Of course, these changes in the blood-vessels may, in their turn, give rise 
to various disorders. 

In a few very rare instances gout seems to attack the brain and. spinal cord. 
Usually, however, the nervous disturbances seen in gout are, as already stated, 
symptoms of uraemia, or of circulatory disturbance, arterio-sclerosis of the cere- 
bral arteries, and the like. The patient may also have certain functional nervous 
troubles, such as neuralgia or migraine. The direct cause of these is seldom 
evident. 

Complications of Gout. — Apart from chance complications there are several 
morbid conditions which undoubtedly may stand in close relation to gout. 
Among these is, first, the formation of renal calculi, or gravel (q. v.). This 
has often been observed in gouty persons. Another not very infrequent combina- 
tion is gout and diabetes mellitus; ordinarily, attacks of gout appear first, and 
later glycosuria develops. Often gout and diabetes seem to alternate. The con- 
nection between the two affections seems to us to be that both diseases result 
from the same cause (chronic alcoholism, less often heredity), so that they de- 
velop together, or one after the other. Equally obvious is the explanation of the 
frequent association of gout with obesity, arterio-sclerosis, etc. 

Anatomical Changes in Gout. Theory of its Nature. — The essential ana- 
tomical lesion in gout consists in an abundant deposit of crystalline urates in the 
tissues. This is most evident in the affected joints, the cartilaginous surfaces of 
which are often completely covered with white, chalk-like material. In severe 
<cases the same appearance may also be presented by the articular ligaments, ten- 



776 



CONSTITUTIONAL DISEASES 



dons, and bursas, while there are at the same time numerous concretions of urates 
here and there beneath the skin. These deposits are composed mainly of acid 
sodic urate, with traces of calcic urate, calcic phosphate, and sodic chloride. 
However certain it is that these abnormal deposits of uric acid should be regarded 
as the pathognomonic sign of gout, we are absolutely without knowledge as to 
their origin and intrinsic importance. One question in particular remains un- 
solved — whether the deposits of uric acid excite the inflammatory symptoms, or 
whether, conversely, the deposits of uric acid are secondary and are formed in tis- 
sues already attacked by the disease. Ebstein believes that the process of the pre- 
cipitation of uric acid is invariably preceded by a tissue necrosis. The uric acid 
while still in solution acts as a chemical irritant upon the cartilage here and there, 
and thus produces necrosis, whereupon the urates are crystallized out and depos- 
ited ; but this view has not escaped contradiction, and possibly the primary damage 
in gout is due not to the uric acid itself, but to some other noxious substance. 

The nephritis of gout corresponds in its pathological appearances to that of the 
true contracted kidney, with one exception; the organs usually present deposits- 
of uric acid or urates, in stripes, both in the lumen of the urinary tubules and also 
in the epithelial cells and the interstitial tissue. In the connective tissue it is 
probable that some lesion precedes the deposit. 

The lesions presented by the heart, blood-vessels, and remaining parts of the 
body are not especially characteristic of the disease. The blood of gouty subjects, 
as Garrod demonstrated, contains an excess of uric acid. 

With regard to the true nature of gout our knowledge is still more limited and 
unreliable than in the case of diabetes. The earlier view was that in gout an 
excessive formation of uric acid took place because of the incomplete oxidation 
of uric acid into urea. This view has been losing ground, because of late it is 
assumed that uric acid is not at all an end-product of the ordinary metamorphosis 
of albumen, but that it is the specific product of the metamorphosis of nucleine, 
which is the special form of albumen contained in the cell nuclei; thus uric acid 
resembles the alloxur bases — that is, xanthine, hypoxanthine, etc. Upon the in- 
gestion of ordinary albumen the uric acid is not increased, but it is increased by 
food rich in nucleine — for example, liver or sweetbread. The formation of uric 
acid seems, however, to be particularly favored by the destruction of the nucleines 
already organized in the body, and especially the nucleated white corpuscles, but 
whether there is in gout an actual increase in the amount of uric acid, or whether 
merely a normal amount is formed and its excretion through the kidneys is hin- 
dered, we are entirely unable to say. Many authors have assumed that the blood 
is less alkaline than normal, and consequently uric acid is deposited in the tis- 
sues ; but the most reliable investigations do not indicate any marked change in 
the alkalinity of the blood. In brief, the true riddle of gout, the special role 
which uric acid plays in this disease, is as yet unsolved. 

Diagnosis. — It is usually easy to recognize an acute attack of gout. The sud- 
den onset of the pain and its localization in one of the great toes are very char- 
acteristic symptoms, and render it easy to distinguish between it and other acute- 
affections of the joints. When an acute attack of gout affects other joints, 
we have a sudden development of marked swelling and tenderness in one single 
place, and a comparatively rapid abatement of the inflammation, while in acute 
articular rheumatism the disease attacks several joints, and moves quickly from 
one to another; so that usually the two diseases can be readily distinguished. 
The diagnosis is more difficult in advanced stages of the disease, in which the 
symptoms are more obscure, but in such cases we can usually obtain, by careful 
questioning, an account of the previous occurrence of typical gouty paroxysms 
and the existence of certain serological factors, such as heredity, mode of life, 
or chronic poisoning from alcohol or lead, which are of considerable diagnostic 



GOUT 



777 



importance. In chronic articular gout the main question is its diagnosis from 
ordinary arthritis deformans. The external appearance of the diseased joints 
is not of itself decisive, although the gouty arthritis leads to greater and more 
diffuse enlargement, especially in the fingers, and much oftener occasions com- 
plete anchylosis in individual joints than does arthritis deformans. The most im- 
portant means of diagnosis, however, in every case, are a careful inquiry into the 
previous history with regard to typical attacks of gout, and a consideration of the 
characteristic gouty changes — such as tophi breaking open. We should also bear in 
mind, with regard to differential diagnosis, the chronic arthritis of gonorrhoea. 

If there is chronic nephritis of gouty origin, its source can be recognized only 
from its association with other indubitable symptoms of gout, particularly typi- 
cal gouty paroxysms, unless possibly the knowledge of certain serological factors, 
such as a history of gout in the family or of chronic lead-poisoning, should put us 
upon the right track. Ebstein has reported cases of " primary renal gout " where 
there was no arthritis during the whole course of the disease. Such cases can 
seldom be correctly diagnosticated during life. 

Brief mention should here be made of an experiment performed by Garrod, 
which may be employed to demonstrate the existence of uric acid in the blood, for 
diagnostic purposes. A drachm or two of blood-serum, or of the serum obtained 
from a fly-blister, is put into a shallow watch-glass, and six or eight drops of a 
thirty-per-cent. solution of acetic acid are added to it. A linen thread is then 
laid in the fluid, and the whole allowed to remain at a moderate temperature for 
about a day. If the proportion of uric acid in the fluid is sufficiently large, crystals 
of that acid will now be found on the thread and may be recognized by their shape 
and chemical reaction. This " thread test " of Garrod's is not extensively used, 
because it does not succeed unless there is a comparatively large amount of uric 
acid in the blood, and, furthermore, uric acid may exist in the blood in health, or 
in other diseases than gout. 

Prognosis. — However favorable the prognosis may be with regard to the sin- 
gle gouty attack, yet a permanent release from the disease is rarely to be hoped 
for. Only such patients as, from the first appearance of gout, pursue most care- 
fully all the requisite prophylactic and dietetic measures, can expect that future 
attacks will be rare and comparatively mild, and that severe lesions of the internal 
organs will not occur. So long as the kidneys and other viscera are intact, there 
is no immediate danger to life, and the patient may attain advanced years 
despite his gout. The gradual and chronic alterations in the joints may, how- 
ever, impede locomotion as well as all other movements of the body. Except for 
this, the general condition of the patient in the intervals between the attacks is 
often one of tolerable comfort. Indeed, it is frequently the case that the patient 
will feel at his very best directly after a severe paroxysm, while rudimentary or 
atypical attacks are often regarded as an ill omen. Really, however, there is no 
serious danger until chronic nephritis has developed. The prognosis then be- 
comes as unfavorable as in the other forms of contracted kidney (q. v.), and 
involves the same possibilities. 

Treatment, — All authorities agree that the first essential in treating gout is a 
proper regimen. Unless the patient has energy enough to yield the most implicit 
obedience to the injunctions regarding diet and mode of life in general, from the 
first appearance of his disease, no great benefit can be obtained from treatment. 

Various authorities have, of late, prescribed special diets for the gouty. The 
various and almost contradictory theories as to the nature of gout have led to 
extremely diverse dietetic injunctions. If we cling to simple practical experi- 
ence, the general conclusion for centuries has been that we should enjoin upon 
gouty subjects moderation in everything, most of all in alcoholic beverages, and 
in meat. 



778 



CONSTITUTIONAL DISEASES 



We should advise, therefore, that the total •amount of meat eaten should be 
limited, and that so-called " white " meat (veal, mutton, fowl, fish) should, on the 
whole, be preferred to " red" meat (beef and game). The cellular organs (liver, 
kidneys, sweetbread, brain) are now usually forbidden, out of regard to the above- 
mentioned views as to the formation of uric acid. Milk and eggs may be allowed, 
fat and carbohydrates are to be given freely, or to be limited, according to the 
.general nutrition of the patient. Gouty subjects who are obese should have less 
of such articles of diet, while emaciated patients should be encouraged to par- 
take of them. Green vegetables that are easily digested, such as spinach, salad, 
kohl rabi, cauliflower, Brussels sprouts, and asparagus, have long been regarded as 
especially suitable. The most appropriate beverages are water, milk, tea, and 
coffee, also the ordinary mineral waters, Seltzer, Giesshiibler, and lemonade. 
Fruits, especially when cooked, are usually permissible and to be recommended. 
Such alcoholic beverages as beer and wine are to be allowed in very small quan- 
tities, if at all. In general, we should not be schematic and theoretical in our 
dietetic prescriptions, but should consider the individual. The quality of the 
articles of food eaten is, on the whole, usually less important than the total 
quantity. 

[Many gouty persons, especially those suffering from the irregular form of the 
disease and acid dyspepsia, are more comfortable and seem to do better on a diet 
which is largely nitrogenous, the starches and sugars being greatly limited in 
amount. The diet, in fact, should be similar to that laid down for diabetes melli- 
tus, though not so strictly carried out. In chronic and irregular cases it is often 
desirable to prescribe a stimulant, for a time at least; brandy, whisky, or gin, 
well diluted with water, is perhaps the best form.] 

By thus limiting the amount of food taken, we shall avoid any excessive for- 
mation of uric acid, and perhaps other harmful substances ; but a direct means 
of promoting metabolism is muscular exercise. If a corpulent patient is still 
vigorous and is not threatened by any serious internal disease, he should be urged 
to take a large amount of exercise in mountain-climbing, gymnastics, gardening, 
or similar pursuits. This same indication of accelerating tissue-metamorphosis 
is fulfilled also by bathing. In early stages cool baths and sponging are useful, 
as are also baths containing common salt, or perhaps even sea-bathing cautiously 
employed. In more advanced cases, particularly if the joints present permanent 
lesions, the warmer baths are more desirable, such as are found in Wiesbaden, 
Baden-Baden, Teplitz, Ems, and Aix. 

The internal administration of alkalies is an efficient adjuvant to the dietetic 
and hygienic prescriptions above enumerated. Although there may be doubt 
about the correctness of the ordinary theoretical basis for this prescription — viz., 
that alkalies prevent the deposit of uric acid in the tissues — yet simple practical 
experience justifies the employment of suitable mineral waters. These waters 
stimulate the conversion of the albuminoids, increase the activity of the kidneys, 
benefit gastric catarrh, and overcome constipation, and in all these ways combine 
to produce a favorable effect upon the patient's health. Still another factor is the 
judicious diet and mode of life at such health-resorts. The waters of Carlsbad 
and Vichy have gained the greatest repute in gout, although the waters of Ems 
and Neuenahr have an analogous composition, and doubtless they would produce 
similar effects. The same is true of Kronenquelle and Fachinger-water. Most of 
these waters can be taken very well in the patient's own home. The salts of 
lithium especially promote the solution of uric acid, and the waters which contain 
lithium have been strongly recommended. The natural springs of this sort, such 
as the Crown Spring in Obersalzbrunn, and those of Assmannshausen and Salz- 
chlirf, contain comparatively insignificant amounts of lithium; and it might be 
a better way to use the artificial lithium waters, such as are made by Struve or 



OBESITY 



779 



Ewich. Another way is to prescribe carbonate of lithium, in powders containing 
two or three grains each (gramme 0.10-0.20), one powder two or three times a day, 
in a glass of Seltzer or Biliner water. 

As to the treatment of the acute attack, it has ceased to be customary to em- 
ploy any potent remedies. The patient must, of course, keep his bed. The 
affected joint should be wrapped up in cotton wool, the whole leg elevated, and a 
proper diet strictly enjoined. Free movement of the bowels should be maintained 
by means of enemata. If there is considerable gastric disturbance, bicarbonate 
of sodium, magnesia, or some bitter may be prescribed. The most certain remedy 
for severe pain is a subcutaneous injection of morphine. Less efficient are nar- 
cotics locally applied, and warm compresses. Whether any internal remedies are 
calculated to abbreviate the attack is doubtful. Formerly colchicum (twenty or 
thirty drops of vinum colchici seminis three or four times a day) was the favorite 
medicine, but it seems to be going out of use. Salicylic acid and salicylate of 
sodium may be administered in the same way as in acute articular rheumatism, 
and sometimes, although not always, they are followed by improvement. Anti- 
pyrine, salipyrine, salol, and similar remedies sometimes succeed in allaying the 
pain in the joints. Some physicians recommend subcutaneous injections of anti- 
pyrine in the neighborhood of the joint, but we have no personal experience on 
this point. On the basis of dubious theoretical assumptions, a number of drugs 
have been recommended recently which possess the power of dissolving large 
amounts of uric acid. Prominent among these are piperazine, of which about 
eight grains (gramme 0.5) are given daily in soda-water; and lysidine, fifteen to 
seventy-five minims (cubic centimetres 1-5) of a fifty-per-cent. solution daily. 
Many physicians report favorable results with these remedies ; others, on the con- 
trary, have found no virtue in them. 

[One reason why colchicum has fallen into relative disuse is that the relief 
obtained from it is often so prompt and complete that patients are tempted into 
■continued indulgence in a faulty manner of life. It is also supposed by some 
that the drug interferes with the effort of nature to eliminate the poison, which 
becomes generally diffused, and sets up changes in the vessels and internal 
organs. Precisely how colchicum acts we do not know, but that it does act, and 
sometimes with marvelous success, there can be no question.] 

The chronic affections of the joints in gout are treated as are other varieties 
•of chronic arthritis. The most efficient remedies are cautious massage and baths, 
including hot sulphur baths and mud-and-sulphur baths. The internal adminis- 
tration of the alkalies, lithium, and similar drugs, to combat the general gouty 
•diathesis, should be associated with these external remedies. Some physicians 
Teport that iodide of potassium favors the absorption of the gouty deposits. 

The treatment of the nephritis and other complications need not be discussed 
at length. The gout itself should always be the main object of our therapeutic 
efforts, and beyond this we may be guided by general principles. 



CHAPTEE XII 

OBESITY 

{Corpulence. Polysarcia adiposa) 

Definition and iEtiology. — The amount of adipose tissue in the body is sub- 
ject to considerable variation, and it is not possible to state absolutely what 
should be considered as normal and what as abnormal. For practical purposes we 



780 



CONSTITUTIONAL DISEASES 



may draw the line where the increased size grows burdensome to the individual. 
After a certain point, any further addition to the amount of fatty tissue is almost 
sure to work serious injury, and is therefore to be regarded as an actual disease, 
and not merely an inconvenience. It should be said, however, that in such cases 
the symptoms of obesity are very frequently confounded with those springing 
from other disorders — these latter possessing, indeed, the same aetiology as obes- 
ity, but distinct from it. 

The most frequent and important cause of obesity is the habitual ingestion of 
too large an amount of food. By " too large " is meant an amount sufficient to 
occasion a continual increase of the adipose tissue of the body, when this is 
already fairly well developed. It is a matter of indifference whether the excess is 
composed mainly of albuminoids, carbohydrates, or fats; for in either case, if 
the quantity be sufficient, an increase of adipose tissue may take place. We 
shall soon see, however, that the excess is usually in fat and carbohydrates. Inas- 
much as this overfeeding is almost certain to be habitual, the excess at any one 
time need not be at all large. We often hear a corpulent person express his sur- 
prise that he grows heavier every day, although he " does not eat any more than 
others who are lean." The explanation is easy if we consider that a daily in- 
crease of five grammes of fat (one and one fourth drachm) suffices to increase 
the weight in ten years — for example, between the thirty-fifth and forty-fifth 
years — forty pounds avoirdupois. In reality the daily increase is sometimes 
greater than this. 

The basis for a detailed consideration of the causes which lead to the deposit 
of fat will be gained by a consideration of the physiological laws relating to nutri- 
tion discovered by Voit, Pettenkofer, and their pupils. It has been shown that 
both the albuminoids and the carbohydrates of the food may be a source of fat, 
formed within the economy, and also that the fat contained in the food may be to 
a large extent directly deposited in the fat-cells of the body. One product of the 
decomposition of albuminoid substances is invariably fat. This usually under- 
goes further oxidation, but it is sometimes retained unaltered in the system. It 
would even seem that the albuminoids give rise to much more of the fatty tissues 
of the body than are produced from the carbohydrates ingested, although there is 
no doubt that these latter may also yield fat. Carbohydrates do promote obesity,, 
but less because they are a direct source of fat than because they are easily de- 
composed, and so shield both the ingested fat and that which is formed out of 
the albuminoids from oxidation. In this indirect way they do greatly favor a 
tendency to corpulence. 

We thus perceive that various diets may, each one of them, permit of an 
increase of adipose tissue. In actual life, of course, the most frequent conditions 
are such as result from the customs and habits of the population in general. The 
diet is almost invariably a " mixed " one — that is, it contains albumen, fat, and 
carbohydrates — and in most instances the obesity is due to an excessive amount 
of all three elements, or at least of the fat and carbohydrates. A person may, 
however, become corpulent who eats very little fat, provided he consumes a large 
quantity of albuminoids and carbohydrates; or if he eats verv little starchy food, 
provided he consumes a large amount of meat and fat. Perhaps these facts may 
be made clearer by giving a concrete example. Yoit tells us that a vigorous 
man who requires daily 118 grammes of albumen and 259 grammes of fat to 
maintain a physiological equilibrium as regards fat and albumen will, other 
things being equal, begin to store up fat if there is any further increase in the 
amount of fat in his diet. The same result will also take place if, instead of the 
rations previously stated, he ingests more than 118 grammes of albumen and 
600 grammes of starch, or more than 664 grammes of albumen alone, or, finally, 
more than 118 grammes of albumen, 100 grammes of fat, and 368 grammes of 



OBESITY 



781 



starch.* It is obvious that this last diet, which closely resembles the average 
diet of an adult + in good circumstances, whose weight is neither increasing nor 
diminishing, is the one most likely to be exceeded; whereupon there must take 
place a deposition within the system of the superfluous fat. 

Among the various kinds of food is one group which deserves mention, as 
being an important factor in many cases of obesity; we refer to alcoholic bever- 
ages. There can be no doubt that intemperance in this regard plays a prominent 
part in many instances. Sufficient illustration is furnished by brewers, hotel- 
keepers, and the inhabitants of countries like Bavaria, where beer-drinking is 
prevalent. In this particular it is evident that beer works more harm than does 
wine or strong liquor; for beer contains, in addition to the alcohol, an appreciable 
amount of starchy material, making the sum total from the beer drunk during 
the entire day a considerable one. Many persons who would be extremely indig- 
nant if called " tipplers," habitually take five or six glasses of beer a day, equiva- 
lent to 150 grammes of starch, or, in other words, to one half the total amount of 
starch required by the system. Even this quantity is frequently exceeded. Of 
course, the three or four per cent, of alcohol which the beer contains also pro- 
motes the deposition of fat. Alcohol is readily oxidizable, and it thus shields to a 
considerable extent the fat already present in the body ; and it also, in all proba- 
bility, works such injury to the tissues as to diminish their power of effecting 
decomposition. We must also remember that most beer drinkers take little exer- 
cise. The long sitting at the beer table, and the mental and physical sluggishness 
which immoderate indulgence in beer always causes, and finally the increasing 
corpulence itself, explain why most beer drinkers dislike protracted exercise. 

We have thus seen that in by far the larger number of cases obesity is mainly 
due to the ingestion of too much food. ~No weight need be attached to the usual 
statement of corpulent persons, that they eat no more than others. Few of them 
have any idea how much nourishment they do consume. Others, having already 
become corpulent, eat less, to be sure, than they used to, but nevertheless an 
amount sufficient to maintain the acquired weight. 

Other factors may no doubt exert an influence upon the increase of adipose 
tissue by diminishing the consumption of fat in the system. The most important 
factor of this class is physical inactivity. Muscular contractions lead to the de- 
composition of a large amount of fat. This explains why people of sedentary 
habits, and those who sleep long and exercise little, are more apt to become corpu- 
lent than are manual laborers. Again, there are certain diseases which seem to 
promote corpulence. In anaemia there is sometimes a striking tendency to obesity, 
due in part to the diminished supply of oxygen and in part to diminished muscu- 
lar activity. This same inactivity is probably the main cause of corpulence in 
paralysis (hemiplegia). It may be, however, that disturbances of the nervous 
system may directly affect metamorphosis. Thus, idiots and other subjects of 
congenital defects of the brain are liable to obesity. Disturbances of the circu- 
latory system seem to favor the production of corpulence by impairing oxidation. 
This is seen in many young persons with cardiac disease, although it is not easy 
to exclude in this case the influence of still other factors, such as a sedentary life. 

Finally, some cases of obesity seem to result from a constitutional and inborn 



* This statement is founded upon an important discovery of Eubner, that, as far as the storing up 
of fat is concerned, the measure of value for different foods is the amount of heat given off by them 
when they undergo oxidation into carbonic-dioxide gas and water. Measured in this way, 100 grm. 
fat = 211 grm. albumen = 232 grm. starch - 234 grm. cane-sugar = 256 grm. grape-sugar. 

+ Probably the amount of fat contained in the food is often less than the above, and the amounts 
of albumen and starch somewhat larger. Voit estimates the diet of a well-to-do person at 127 grm. 
albumen, 89 grm. fat, and 362 grm. starch ; and that for a vigorous laborer at 118 grm. albumen, 56 
grm. fat, and 500 grm. starch. Of course, these figures are merely approximate. 



782 



CONSTITUTIONAL DISEASES 



predisposition. Young children sometimes suffer from obesity; and the condi- 
tion seems in many cases to be hereditary. Many races and nations exhibit an 
especial tendency to corpulence — for example, the Jews. Age and sex have some 
importance in this regard : extreme obesity is seldom seen previously to the thir- 
tieth year; and women appear to be somewhat more subject to the disease than 
men. The importance of a " tendency " to obesity should not be overrated. Upon 
careful investigation, we shall almost invariably find in the habits of the indi- 
vidual, as regards food and exercise, a satisfactory explanation of his obesity. 
Still, it may be possible that upon accurate examinations into metabolism it 
would be found that the power of fat-combustion is subnormal in many persons,, 
analogous to the impaired combustion of carbohydrates in diabetics. This dimi- 
nution of the oxidizing function might be due to congenital or acquired anoma- 
lies. If our supposition prove correct, it might explain the not infrequent com- 
bination of obesity and diabetes (q. v.), or obesity and gout. Strictly speak- 
ing, the condition can not be regarded as a disease unless the habits as to diet 
and exercise fail to account for it. 

Pathology. — After corpulence has passed a certain point the condition is evi- 
dent at the first glance. The subcutaneous cellular tissue is one of the chief 
places in which the fat is deposited. Consequently, the panniculus adiposus soon 
attains considerable thickness. The countenance grows more round and plump; 
beneath the chin is formed a second prominence known as the " double chin " ; the 
chest appears broadened; the waist enlarges; and, particularly in women, the 
breasts are changed to great shapeless masses, over which the skin is so tightly 
stretched as to present lineas albicantes. The abdominal walls are greatly altered. 
The belly projects more and more until it becomes actually pendulous, and its 
lower surface touches the interior surface of the thighs. Intertrigo is apt to 
occur in the groins, below the breasts, and between the buttocks. The skin every- 
where has a fatty feel, due to the increased secretion of the sebaceous glands. 
This hyperplasia of the fatty tissue in the panniculus adiposus is associated with 
a deposit of fat in many parts of the interior of the body, including the mesen- 
tery, mediastinum, pericardium, and the capsules of the kidneys. Some of these 
will be mentioned again further on. 

Of course, the circumference and weight of the body become greatly increased. 
As an approximate measure it may be stated that for men of middle height a 
weight exceeding ninety kilogrammes (200 pounds), and for women seventy-five 
kilogrammes (165 pounds), may be regarded as abnormal.* This increase in bulk 
is the first cause of subjective symptoms. An obese person has to exert a greater 
effort in making any motion than do other people, and as a necessary consequence 
he gets easily tired, and seeks as far as possible to avoid exertion. The increased 
demand upon the muscles explains the familiar fact that corpulent persons per- 
spire readily. 

The graver symptoms of obesity, and properly the first pathological phe- 
nomena of the condition, relate to the respiration and the circulation. The 
patient begins to complain of shortness of breath, and is subject to marked dysp- 
noea upon running or climbing stairs. There may be, at the same time, cardiac 
disturbance, indicated by a rapid pulse, palpitation, intermission of the pulse, or 
other slight irregularities in cardiac action. All these symptoms grow gradually 
worse ; and to them are added symptoms of cardiac failure and consequent passive 
congestion. There is a tendency to bronchitis and other catarrhal troubles. The 
appetite and digestion are affected, and oedema appears. 

A careful analysis of all these symptoms shows that many causes combine to 
produce them, all having a common tendency to impede respiration, and, still 



* A weight of even 150 kilogrammes (330 pounds) has been repeatedly observed. 



OBESITY 



783- 



more, circulation. One source of disturbance is the increased deposit of fat upon 
the framework of the body. It is probable that the excess of adipose tissue cover- 
ing the thorax exerts a direct influence in obstructing the respiratory motion of 
the thoracic walls, and renders the respiration more superficial. In this way the 
return of venous blood to the heart and the pulmonary circulation are both im- 
peded, because the negative pressure in the chest is less than normal. Likewise 
the diminished amount of bodily exercise affects the circulation unfavorably. 
Brauner has shown how numerous are the arrangements connected with the 
fasciae for promoting the venous currents, by means of the negative pressure 
resulting from the movements of the body. Whether the fat deposited arOund 
the heart directly obstructs the cardiac movements is somewhat doubtful, though 
this view is held by many. The fatty infiltration of the myocardium is of more 
importance : the fat is deposited in the intermuscular connective tissue. Still, 
it is doubtful whether this condition, which is not so very frequent, after all,, 
occurs as a primary change, or whether it is not rather a result of previous 
atrophy of the myocardium (compare the chapter on fatty heart). 

There is no doubt that, in almost all cases where the corpulence actually in- 
duces grave disturbance, the cardiac symptoms are of prime importance. These 
are due, as has just been indicated, in part to the increased amount of adipose 
tissue, and in still greater part to complications, most of which are excited by the 
same causes as is the obesity itself. The abundant adipose tissue may obstruct 
the circulation in the smaller blood-vessels and capillaries inclosed within it. 
Furthermore, the excessive development of fatty tissue probably leads to the 
growth of new blood-vessels, and, as a consequence, to an increase in the total vol- 
ume of the blood. This is one way in which the demands made upon the heart 
are rendered greater than normal, and explains why the corpulent frequently 
exhibit cardiac hypertrophy. Other influences are also at work to produce this 
same result: they are, in the first place, the same factor which occasions the 
obesity itself, namely, the ingestion of increased amounts of food and drink (see 
the chapter on cardiac hypertrophy), and, secondly, certain other lesions which 
are frequently associated with obesity and are referable to the same causes as it 
is. Chief among this latter class is general arterio-sclerosis. If this involve the 
coronary arteries, it may in turn occasion still further damage — for example, de- 
generative myocarditis (compare page 341). Chronic interstitial nephritis is an- 
other not infrequent complication. This is referable in part to the same causes 
as is the obesity. Gout and diabetes are less frequent. 

We thus see that obesity is often merely one of many injurious results occa- 
sioned by an improper mode of life. It is, in a certain sense, the first danger- 
signal, warning the patient and his physician to avoid the graver disturbances 
which threaten. This is a point of great practical importance; for, when once 
we have a combination of obesity with cardiac hypertrophy, fatty infiltration of 
the heart, arterio-sclerosis, or interstitial nephritis, the various causes and effects 
act and react upon one another in a way most perilous to health, and even to life. 
There is no need of describing the grave disturbances which invariably develop 
at the close of the scene. They are the result of chronic cardiac insufficiency, and 
have been fully described under cardiac disease. 

In every case of obesity the physician should examine the heart, lungs, vascu- 
lar system, and kidneys, particularly if there be already subjective disturbances. 
The examination of the heart may present considerable difficulties, because the 
results of palpation and percussion are so much obscured by the thick cushion of 
fat which covers the thorax. We can, however, have recourse to auscultation, 
and can feel the pulse. The pulse may be either rapid, slow, or irregular. 
We need not mention any minute particulars as to the examination. It may 
be stated, however, that a hepatic enlargement is often found, but it is much 



784 



CONSTITUTIONAL DISEASES 



less often the result of fatty infiltration than of simple hypertrophy or passive 
congestion. 

We have thus seen that corpulence may sometimes be associated with grave 
and dangerous lesions ; but, on the other hand, it should be stated that this unfor- 
tunate condition by no means invariably exists. Not infrequently the corpulence 
remains moderate, in which case it is not really dangerous, however incon- 
venient. This is true of a proportion of those cases which are due to the in- 
gestion of a large amount of nourishment, associated with defective oxidation, 
and where there are no other unfavorable influences at work. The obesity of 
hard drinkers is almost always a more or less dangerous condition, while that 
seen in many elderly persons and in women is often comparatively free from 
peril. These latter individuals are, to be sure, discommoded by their great 
weight, they can accomplish less than they used to, they are easily put out of 
breath, and have a certain tendency to catarrhal inflammations and rheumatic 
difficulties; but they escape the severer lesions above enumerated. Even these 
apparently harmless conditions should not be disregarded by the physician, as he 
can never be absolutely certain that grave complications may not be developed 
eventually. 

Treatment of Obesity. — To cause the disappearance of the accumulated fat, it 
is necessary to promote its oxidation in the system and to prevent the ingestion 
of new supplies of fat. To accomplish this purpose we possess only two means — 
first, a limitation of the ingestion of such kinds of food as may lead to the forma- 
tion of fat in the system, and, secondly, stimulation of muscular activity and 
other factors which occasion the destruction of the fat already present. All the 
various methods of treating obesity, without exception, aim either to diminish 
the supply or to increase the destruction of fat. 

The methods vary greatly. It must be borne in mind that the diminution of 
the adipose tissue must not involve injury to the body itself. The treatment 
should not weaken the constitution, but should invigorate the patient, or at least 
be innocuous. 

It is of prime importance, in every method of treatment, that the total quan- 
tity of ingested food should be diminished. It is a mistake to forbid the patient 
some particular kind of food — for instance, the carbohydrates or the fats — with 
the idea that they alone do harm, or to allow him unlimited quantities of other 
kinds of food, in the belief that they are harmless. Any person can eat albu- 
minoids, fat, and starch at every meal, and yet not grow fat ; while, on the other 
hand, too much of any one of these may lead to an increase of adipose tissue. 
The amount of food which a person can take without increasing the amount of 
adipose tissue varies with the individual. It depends upon the amount of mate- 
rial already present in the body, and upon the various demands made upon the 
system, as well as other factors. This renders it difficult to draw up a universal 
dietary for the obese. We can best judge of the value of any course of treatment 
by its results, and these are best measured by the weight and the subjective con- 
dition of the individual patient. 

Of the various elements of food, the albuminoids should be diminished least 
of any, because it would be sure to work injury to the system if they were sup- 
plied in too small an amount. Of course, the albuminoids must not be eaten to 
such an extent that the fat into which they decompose remains intact in the body. 
An increase in the amount of nitrogenous tissue is, however, desirable, because 
this promotes the vigor of the muscles and the heart, and so leads to the oxidation 
of larger quantities of the non-nitrogenous tissues. 

The amount of fat and starch must be much more limited. The fats and 
starches are more potent in increasing adipose tissue and in shielding from oxida- 
tion the fat already stored up in the body than is nitrogenous food. It would 



OBESITY 



785 



not be at all advisable to forbid the use of either one of these two constituents of 
a mixed diet, allowing the other alone to be eaten. A. varied diet is extremely 
desirable, even for one who is corpulent ; and we should exclude neither fat nor 
starch wholly from the dietary, but we should merely limit the amounts to be 
taken. As already indicated, the amount of albuminoid food remaining un- 
changed, a person can eat double the quantity of starchy food that he can of fat, 
without increasing his adipose tissue. It is therefore irrational to allow the cor- 
pulent fat in larger proportions than starchy foods. The diet which Ebstein has 
recently proposed for the treatment of obesity does prove successful, but the ex- 
planation of its success lies in the comparatively small amounts of meat and fat 
ingested. Precisely the same results would be attained if a corresponding 
amount of starch were substituted for all or a portion of the fat ; and in practice 
it is desirable, at least in most cases, to allow the patient both starches and fats. 
Of course, the likings and experience of the individual should be considered in 
-each separate case. The Banting treatment, introduced in 1864, enjoyed for a 
time a great reputation. Its inventor applied it first of all to his own case, and 
with success. It rests upon a rational basis, inasmuch as the albuminoids are 
allowed in abundance, and the ingestion of fat and starch is limited. It lays 
too much stress, however, upon the exclusion of fat as compared with starch. Of 
great practical importance in many cases is the strict prohibition of beer drink- 
ing. Many cases of obesity are due merely to the excessive amount of carbo- 
hydrates contained in the unreasonable quantity of beer drunk daily. If corpu- 
lent beer drinkers of this sort change their mode of life in this single particular, 
and drink no beer whatever for from three to six months, they are almost sure to 
lose a great deal of weight. 

The physician who bears in mind the principles just expounded can lay down 
lis own rules for the diet of his patient. As already stated, it is impossible to 
give figures which will apply to every case. If we take as a basis the average 
diet for an adult — that is, about 125 grammes of albumen, 80 grammes of fat, and 
350 grammes of starch — we might say that most cases of obesity would be sure to 
undergo improvement upon a diet containing 125 grammes albumen (or possibly 
even more than this), 40 grammes fat, and 150 grammes starch. The amounts of 
fat and starch could be even more diminished, but it is usually best not to be too 
precipitate. A gradual diminution of two or three pounds a week, extending 
over a long period without interruption, is to be preferred to the rapid treatment 
common at many health-resorts. Of course, the loss of fat is greater at the com- 
mencement of treatment than later on, when the amount of adipose tissue has 
already approached more nearly to normal, and the diet must undergo a gradual 
and corresponding change. It is of particular importance to increase the amount 
of non-nitrogenous foods in the later stages of treatment, lest the albuminoid 
tissues of the body become wasted. 

The following dietary may be taken as an illustration of what would be suit- 
able for a patient in the beginning of treatment : For breakfast, a cup of coffee 
with milk, and about 75 grammes of bread. At noon, a plate of soup, 150 to 175 
grammes of lean meat or fish, lettuce, green vegetables, and about 25 grammes of 
bread. For dessert, about 75 grammes of boiled rice, or some simple pudding, or 
100 grammes of fruit. To quench the thirst, water, or half a pint of light wine. 
In the afternoon, a cup of coffee, and with it not more than 20 to 30 grammes of 
bread. For supper, two eggs, or 100 to 120 grammes of meat, with 30 grammes of 
bread, a little fruit, lettuce, half a pint of wine, or one or two cups of tea, not much 
sweetened. Butter should be entirely proscribed at first ; later on it may be used 
in small amounts. 

Some approach to this bill of fare must be enforced not merely for a few weeks, 
but for months. It is absolutely necessary that the patient should be weighed 
50 



786 



CONSTITUTIONAL DISEASES 



every two or three weeks. If the weight diminishes slowly and gradually, with- 
out any subjective disturbance, we have the best proof that the diet is a suitable 
one. If the weight does not diminish, then the amount of ingesta must undergo 
further reduction. If more food can be taken without the weight increasing 
again, a larger amount may be unhesitatingly permitted, and indeed may even 
be advisable if the patient be languid. The increase should at first, however, 
be mainly in the amount of albuminous food, the amount of starches and fats 
not being much increased. The " cure " can not be regarded as complete until 
the weight has been brought down to that of the average individual of the 
given age and sex. This goal having been reached, greater freedom in diet is 
permissible. 

The object of the treatment just suggested is exclusively the limitation of the 
production of fat. We may also promote the destruction of the fat already stored 
up in the system. A chief means to this end is muscular exercise, which undoubt- 
edly increases the oxidation of the adipose tissues. Carried out in a proper man- 
ner, it is therefore a most valuable adjuvant to treatment. Oertel has recently 
pointed out that muscular exertion does good in still another way — namely, by 
promoting cardiac activity and inducing deep respiratory efforts. Thus the heart 
is strengthened and circulation promoted. Mountain-climbing is one of the best 
modes in which to take the desired exercise. We need hardly say that the 
increased muscular activity makes it possible for the patient to take an increased 
amount of food without injury. In dealing with cases of obesity in which the 
condition is due less to overfeeding than to lack of muscular exercise, it might 
be decidedly advisable to lay the most stress upon the increase in muscular activ- 
ity; for certainly it is more advantageous for the organism to get rid of its excess 
of fat by means of lively metabolism, while nutrition is well maintained, than 
to be more or less starved by an excessive limitation of diet. We should not rest 
satisfied with a single mountain tour, but should insist upon a persistent and 
considerable employment of the muscles in gymnastics, walking, and the like. 

Baths also promote oxidation, but they are far less potent than is muscular 
exercise. Cold baths, brine baths, or baths containing carbonic-acid gas, may be 
employed. One way in which they do good is by stimulating the nervous system. 
Oertel regards it of great importance to diminish the amount of water in the sys- 
tem, a point which has until very lately received little attention. The diminution 
in the amount of fluids may ameliorate any circulatory disturbance {vide supra) 
and relieve venous congestion, and it undoubtedly has some value in the treat- 
ment of obesity. Oertel has shown that a simple diminution in the amount of 
fluids ingested, when there is no other change in the diet or mode of life, will 
effect a diminution of the adipose tissues. This result is probably due mainly to 
the diminished strain upon the heart and the consequent increase of oxidation; 
but the chief cause of the rapid loss of weight, which we actually see in the cor- 
pulent as a result of the deprivation of fluid, is to be found not in the loss of fat, 
but in the marked loss of water contained in the body. " Desiccation " may fur- 
ther be promoted by stimulating the perspiration by bodily exercise or by steam 
baths. This withdrawal of liquid from the system, however, is advisable only in 
cases where there is already incipient cardiac failure. ' 

It is evident that numerous excellent methods are at our disposal for the treat- 
ment of obesity ; but their application to any particular case should be the result 
of a careful consideration of the special circumstances presented. A very essen- 
tial point is that the injunctions of the physician should not merely be made, but 
be carried out ; and it is precisely here that the treatment of many cases suffers 
shipwreck. We may be baffled by the patient's lack of energy and persistence, 
or by the importunate demands which his profession or social position make upon 
him. Indeed, it is sometimes absolutely impossible to prosecute the treatment at 



SCROFULA 



home, in which case bathing- and health-resorts are to be urgently recommended. 
There alone can the patient muster up the resolution necessary for carrying out 
the desired changes in his mode of life. The incontestable success of treatment at 
Carlsbad, Marienbad, Kissingen, Tarasp, and similar resorts is doubtless only to a 
very small extent the result of their specific medicinal influence, but it is mainly 
due to a strict observance of the above-described diet and regimen. The internal 
use of mineral waters is not entirely without a beneficial effect. Their laxative 
qualities diminish the absorption of food from the intestinal canal. It should be 
said, however, that the patient is at the same time exposed to the danger of a 
waste of his nitrogenous tissues. This is why patients frequently complain of the 
debilitating effect of these mineral springs ; to avoid which, it would be well to 
increase the amount of albuminoids in the diet. We must also consider the need 
of guarding against too great a supply of fluid, with regard to what was said 
above as to the occasional service of " desiccation " of the body. 



CHAPTER XIII 
SCROFULA 

Definition and Symptoms of what is called Scrofula. — We desire to present, 
at the close of this section, a brief description of scrofula, but merely from a prac- 
tical standpoint. From a scientific point of view scrofula is not to be regarded as 
any special variety of disease. The term is applied to a group of symptoms seen 
most frequently in childhood, the essential features of which consist in the ap- 
pearance of chronic enlargements of the lymph-glands, and in certain diseases of 
the skin and mucous membranes. The simultaneous appearance of these various 
phenomena does really produce a somewhat characteristic picture, which can fre- 
quently be recognized at the first glance. 

Most scrofulous children appear pale, with a flabby skin and soft muscles. 
The panniculus adiposus may nevertheless be tolerably well developed. Not 
infrequently the face is puffy, with prominent lips. This is called the " torpid 
habitus." In other cases the child has small features and a remarkably delicate 
white skin, which but partly conceals the superficial veins, and is readily suf- 
fused with blushes. To these the name " erethitic habitus " is applied. Enlarged 
lymph-glands are to be felt in the throat, at the angles of the lower jaw, and in 
the back of the neck, and occasionally in other parts of the body. These glands 
may remain indolent for a long while, or they may suppurate and break exter- 
nally. Chronic cutaneous eruptions are often seen in various places. The most 
common of these is a scaly or impetiginous eczema, affecting the face, scalp, or 
extremities. More severe affections are lupus ("lupus scrophulosorum''''), pru- 
rigo, and lichen scrophulosorum. 

Of the mucous membranes, the conjunctiva and the lining* membrane of the 
nostrils are most frequently affected. Conjunctivitis in various forms is a char- 
acteristic symptom of scrofula ; as are also blepharitis ciliaris, keratitis, and 
chronic rhinitis, which last often terminates in a pronounced ozama (q. v.). 
Chronic diseases of the ear are also frequent, such as otitis media, with perfora- 
tion of the tympanum, and occasionally caries of the mastoid cells and its unfor- 
tunate results. 

Of the deeper-lying tissues, the bones and joints are most apt to suffer. The 
affections located here are almost exclusively " fungous " — namely, fungous 
ostitis and periostitis, white swelling, and caries. Formerly there was frequent 



788 



CONSTITUTIONAL DISEASES 



use of such terms as " scrofulous inflammation of the knee-joint," or " scrofulous 
caries of the ribs." 

If we inquire into the nature of this strange group of symptoms thus briefly 
enumerated, we shall find that by far the greater number of cases of well-marked 
scrofula are examples of tuberculosis. Tubercle bacilli have been demonstrated 
in connection with most of the fungous or " scrofulous " diseases of the bones and 
joints. Ozaena is often a tubercular disease of the nose, lupus is a tuberculosis of 
the skin, and many forms of otorrhcea are really tuberculosis of the ear. The 
aetiology of " scrofula " is therefore in the main identical with that of tuberculosis 
(q. v.), and this explains why the old physicians habitually insisted upon the inti- 
mate relationship between the two diseases. It was formerly thought that scrof- 
ula often terminated in tuberculosis — that is, a scrofulous child is apt to suffer 
eventually from tuberculosis of the lungs, intestine, or brain. To-day we know 
that most scrofulous children do not become, but that they are already, tuberculous. 

It must, however, be borne in mind that in practice many diseases are termed 
scrofulous which have nothing to do with tuberculosis. Many cases of perfectly 
innocent eczema of the face and scalp lead to swelling of the glands in the throat, 
and are therefore termed scrofulous eczema. These cases are probably most of 
them secondary, and the result of external irritation and the like. Again, many en- 
larged glands in the neck are the result of pharyngeal trouble, as after scarlet fever, 
and are equally devoid of a tubercular taint. Pseudo-leuksemic lymphomata may 
also occur in children ; and it should be borne in mind that hereditary or acquired 
syphilis may produce in children lesions closely resembling those of scrofula. 

It is therefore the duty of the physician in every case of " scrofula " to analyze 
the aetiology and symptoms carefully, in order to determine with what he has to 
deal. " Scrofula " should be regarded merely as a short way of naming a certain 
group of symptoms. It is convenient to retain the term as being less likely to 
startle the friends of the child than would the true name of the disease. 

Treatment. — In the treatment of scrofula we have first to attack the various 
local diseases, and, second, to invigorate the general health. We can not here 
enter into all the details of local treatment, but we must refer the reader to the 
special descriptions already given of the various local affections. We may, how- 
ever, briefly mention a few facts with regard to the treatment of scrofulous swell- 
ing of the lymph-glands. Painting the overlying skin with tincture of iodine is 
a very common practice, but it seldom does much good. We have obtained more 
satisfactory results from iodoform ointment, or from the repeated inunction of 
sapo viridis. For particulars as to the opening of abscesses, or the extirpation of 
glands, we must refer to works on surgery. 

Second, in the general treatment of scrofula every possible means is to be 
employed to invigorate the system. Abundant nourishment and fresh air are 
essential. The child may be taken either to the country, the mountains, or the 
seashore. Cod-liver oil is regarded by some as a specific in scrofula ; but its un- 
doubted value really lies in the fact that it is an easily digested fat. Some children 
can take a considerably larger dose than others without its disturbing the stomach. 
Usually we prescribe two or three tablespoonfuls per diem. Salt baths enjoy a great 
reputation, as a remedy in scrofula. If circumstances permit, the best way is to 
visit some place where there are brine baths, such as Kosen, Suiza, Salzungen, 
Arnstadt, Kreuznach, Minister am Stein, Rehme, Reichenhall, Ischl, or Colberg. 

Treatment at these resorts is preferable to the use of artificial baths at home, 
because it is under more favorable hygienic surroundings. 

The chief internal remedies are iron, iodine, and arsenic. A favorite prescrip- 
tion is syrup of the iodide of iron. Arsenic may have a slight specific influence 
upon the tuberculous adenitis and bone diseases, as also upon lupus, but beyond 
this we can not expect any great benefit from internal remedies. 



DISEASES OF THE NERVOUS SYSTEM 



I.— THE DISEASES OF THE PERIPHERAL NERVES 

SECTION I 

Diseases of the Sensory Nerves 
CHAPTEE I 

GENERAL REMARKS UPON THE DISTURBANCES OF SENSIBILITY 

The disturbances of sensibility, like all other functions of the nerves, are mani- 
fested in two directions. Under pathological conditions we observe either an 
abnormal diminution or a complete absence of sensibility — anaesthesia — or a mor- 
bid increase — hyperaesthesia. While, in anaesthesia, the ordinary or even the 
strongest irritations which excite the sensory nerves produce only a weak and in- 
significant sensation, or even no corresponding sensation at all, in hyperassthesia 
very severe and painful sensations are caused by weak irritations. The " symp- 
toms of sensory irritation " are to be distinguished from hyperassthesia, although 
they are often present along with it. By this term we mean sensations which cause 
internal irritation, not from without, but from certain abnormal morbid condi- 
tions in the nerve itself. In the region of cutaneous sensibility, with which we 
shall chiefly concern ourselves in what follows, these symptoms of sensory irrita- 
tion show themselves partly as actual pain and partly as the so-called pares- 
thesias — that is, abnormal sensations in the skin, which are termed " formication " 
(the crawling of ants), "prickling," "numbness," "a furry feeling," "hot and 
cold feelings," etc. 

The Different Varieties of Cutaneous Sensibility and the Methods of testing 
them. — As is known from physiology, the irritation of the sensory cutaneous 
nerves produces in us a number of sensations, differing in quality according to 
the manner in which the irritation acts. If, therefore, we would obtain an accu- 
rate estimate of the condition of the patient's cutaneous sensibility, we must 
make a special test of all the different forms of sensation; for we often see that 
the disturbances of sensibility do not involve all the forms mentioned alike, but 
that one kind of irritation is followed by perfectly normal sensation, while there is 
more or less complete anaesthesia for another kind. We term such partial anaes- 
thesias of the skin, which are manifest toward only one or more forms of irrita- 
tion, " dissociated " or " partial anaesthesias." The study of these partial anaes- 
thesias is the more interesting, since, according to recent physiological theories 
(Blix, Goldscheider, etc.), the different qualities of cutaneous sensibility are 
transmitted to the consciousness by special nerve-fibers, so that there are probably 
in the skin different terminal nervous organs for the perception of sensations of 
pressure, cold, heat, etc. Such a condition recalls the well-known specific energy 
of the different fibers of the optic nerve to colors, assumed by many physiologists. 

789 



790 



DISEASES OF THE XEEVOUS SYSTEM 



The separate varieties of cutaneous sensibility, and the chief practical methods of 
testing them, are as follows : 

1. Sensibility to Contact. — The examination of the sensibility of the skin 
to simple contact is usually performed by repeatedly touching or stroking the 
part of the skin to be tested with the finger, a fine brush, or some other blunt 
object (not of metal, in order to exclude sensations of cold) while the patient's 
eyes are shut, and asking the patient to say whether he has felt the touch or not. 
When it is necessary to call the patient's attention to the investigation, it is 
always best to do so afresh by asking "Xow?" and then either really to touch 
the skin or else to ask the question when only pretending to touch it. In this way 
we are safest from the error, which otherwise may readily arise, from a lack of 
attention or of practice on the part of the patient. We may often make the patient 
close his eyes and then count the number of times we touch the skin, or we touch 
the skin alike in different parts of the body (alternating on the two legs, etc.), and 
then ask him to tell merely the place where he is touched (vide infra). The degree 
of correctness of his answer of course shows the condition of the sense of contact. 
The comparison of the sensibility in symmetrical parts of the body is of impor- 
tance, especially in unilateral disturbances. 

In a good many cases the patients feel the slightest touch, but nevertheless 
they say that the touch on the affected part is " more indistinct," " duller," in 
short, " different " from that on the normal part of the skin. 

2. Sense of Locality (Localization of Sensation). — Under normal conditions, 
as we know, not only do we feel the touch of an object, but we can tell with a 
good deal of accuracy the place on our skin which was touched. This power we 
term the ability to localize our sensation. In nervous patients we often see that, 
while cutaneous sensibility is still present (we refer not only to tactile sensibility 
but also to the other forms), it is localized more poorly and with less accuracy 
than is the case under normal conditions. 

In the simple test of the sense of contact we may also examine, at least rough- 
ly, the power of localization if we ask the patient also to state where the touch 
is felt, or if we ask him to designate with his hand as accurately as possible the 
part of the skin touched. A more accurate method was proposed by E. H. Weber. 
It consists in determining the smallest distance which must separate two simulta- 
neous cutaneous irritants from each other, in order that they may be perceived 
as two locally distinct sensations. Weber has found that this distance differs 
very much in different parts of the body, and from this he has divided the whole 
surface of the skin into so-called tactile circles. As data for the examination of 
patients, some of the figures obtained by Weber in healthy individuals may here 
be given : The smallest distance at which the two points of a pair of compasses * 
applied at the same time to the skin may plainly be distinguished from each other 
is 11 to 15 millimetres on the cheeks, 6 millimetres at the tip of the nose, 22 milli- 
metres on the forehead, 1.2 millimetre at the tip of the tongue, 4 to 5 millimetres 
at the back of the tongue and on the lips, 34 millimetres on the neck, 77 milli- 
metres on the upper arm, 40 millimetres on the forearm, 31 millimetres on the 
backs of the hands, 11 to 16 millimetres on the backs of the 'fingers. 2 to 3 milli- 
metres at the tips of the fingers, 55 to 77 millimetres on the back, 45 millimetres 
on the chest, 77 millimetres on the thigh, 40 millimetres on the leg, 40 milli- 
metres on the instep; but these figures show certain variations in different indi- 
viduals, so that they are to be regarded as only average values. 

Testing the sense of locality by Weber's method has no great practical impor- 
tance; it also takes very much time and demands intelligence, patience, and 
good will on the part of the patient. The influence of practice is manifested 



* There are special "tactile compasses " with blunt ivory points and graduated quadrants. 



REMARKS UPON THE DISTURBANCES OF SENSIBILITY 791 



in a very remarkable way, since trie perceptible difference becomes considerably 
less if the examinations are often repeated. On the other hand, a single exami- 
nation, as in testing any form of sensibility, must not be too long protracted, for 
otherwise the patient may easily become fatigued, and the data obtained will be 
entirely contradictory. If we test the sense of locality by bringing down the two 
points not at the same time but one after the other, and vary it by touching the 
same place twice, or a different place each time, we obtain from the outset, as we 
have repeatedly proved, smaller numbers than if we touch the skin with the two 
points of the compasses at the same time. We also obtain somewhat different val- 
ues for the fineness of the sense of locality if we test the so-called sensations of 
motion (Leube) — that is, the distinction between a simple circumscribed touch of 
the skin, and a very short line drawn with a stick on the skin. In this way we 
can also determine whether the patient can distinguish accurately the direction 
of transverse and longitudinal lines. 

We may also mention here two peculiar anomalies of sensibility, polycesthesia 
(G. Eischer) and allochiria (Obersteiner). Polysesthesia is a symptom shown by 
certain patients (especially patients with tabes), who, when the skin is touched 
with only one point of the compasses, have a sensation as if they felt two or even 
more points. The cause of this remarkable anomaly of sensation is not yet ade- 
quately explained. In allochiria a stimulation of the skin (touch, pain) is felt 
not on the part touched, but on the corresponding point on the other half of the 
body. This remarkable symptom has been observed a few times in cerebral hemi- 
plegia, tabes, etc. 

3. Sense of Pressure. — The healthy man distinguishes with ease whether an 
object merely touches the skin or exerts pressure upon it. In the perception of 
pressure we must consider not merely the sensibility of the skin, but probably 
even more the sensibility of the deep parts below the skin (fascia?, muscles, peri- 
osteum). If a fold of the skin be raised, differences of pressure are felt much less 
plainly than when pressure is at the same time exerted on the deeper parts. Since 
E. H. Weber's investigations we know that we estimate the difference in the in- 
tensity of our sensations of pressure, not according to the absolute, but according 
to the relative increase in the pressure. If, for example, a part of the skin has 
a weight of nineteen grammes on it, and we perceive the first manifest increase 
in our sensation of pressure when a weight of one gramme is added to it; when 
the skin has a weight of one hundred and ninety grammes on it, we first perceive 
the increase of pressure not when one gramme is added, but when we add ten 
grammes. If this law, on more accurate testing, has not proved so simple as it 
would seem according to the results of Weber's first investigations, still it is gen- 
erally a fact that under normal conditions an increase of pressure of about one 
twentieth to one thirtieth of the original pressure may be plainly perceived in the 
different parts of the body. 

Different methods and instruments, such as Eulenburg's " baraBsthesiometer," 
have been devised for testing accurately the sense of pressure in patients, but they 
have entered but little into practice on account of their elaborate character. We 
usually content ourselves with testing the sense of pressure by applying different 
weights, or coins. We must mention here that the part of the body to be tested 
must be fully supported, that we must also exclude sensations of temperature at 
the same time by putting some non-conductor beneath the weights, and that we 
must apply the separate weights to the same place on the skin at equal intervals of 
time, which must not be too long after one another. For the ordinary needs of 
practice it is wholly sufficient to test the pressure sense simply with the finger or 
any blunt object. By pressing with the finger we can vary the pressure, make it 
weaker or stronger, and thus learn whether the patient is able correctly to state 
all these differences. 



792 



DISEASES OF THE NEKVOUS SYSTEM 



We should never fail to test the pressure sense in patients with nervous dis- 
ease, since anaesthesia of the pressure sense, or at least a diminution, is by no 
means rare. We find quite often, especially in spinal diseases (tabes, myelitis, 
compression), that the patient feels a light touch on the skin, but that he can not 
distinguish a marked pressure at all, or only obscurely. On the other hand, the 
sense of pressure is sometimes well preserved when the other forms of cutaneous 
sensibility are much impaired (as in syringomyelia). 

4. Sense of Temperature. — As we have already said (p. 789), we have lately 
been led by physiological investigations (Goldscheider, etc.) to believe more and 
more strongly that sensations of heat and cold are to be regarded as due to two 
wholly distinct functions of the cutaneous nerves. These functions are probably 
performed by special nerve terminations and nerve-fibers. If we test the sensi- 
bility of the skin for heat and cold with a pointed metal rod, heated or cooled, 
we can easily be convinced that the hot rod excites a sensation of warmth only on 
definite parts of the skin, and that the cold rod excites a sensation of cold only on 
other definite points ("warm points," "cold points"), but on the intervening 
points these rods excite no sensation of temperature. From repeated personal 
observation we can state that pathological symptoms agree completely with this 
theory of the existence of special nerve conduction for sensations of heat and cold, 
for we see that changes in the temperature sense in the skin by no means affect 
the heat sense and the cold sense equally. It is therefore always necessary to test 
both forms of the temperature sense separately. We often find that while one 
form of temperature sense is in normal activity, the other is much altered — a 
pronounced partial anaesthesia to heat or cold. The affected sense may be wholly 
lost or merely blunted, so that hot water is felt merely as tepid, or ice as cool. 
If the temperature sense be lost, the application of a hot or cold object will cause 
only a sensation of touch, and not of temperature. Extreme temperatures, espe- 
cially extreme heat, excite, as is well known, a sensation of pain. This may, of 
course, remain normal; but if there is also analgesia (vide infra), it disappears. 

If anaesthesia to cold be present, patients often speak of having a distinct 
sensation of warmth when the skin is touched with a bit of ice. This symptom, 
which we discovered and called " perverted temperature sense," may perhaps be 
explained by supposing that the heat nerves are excited by the severe irritation 
from cold. The contrary symptom, that heat excites a distinct sensation of cold, 
is very much less common. 

Besides the sensations of temperature we usually test also the patient's ca- 
pacity to distinguish differences of temperature. Within the moderate degrees of 
temperature, 80° to 100° (25°-35° C), differences of a degree Fahrenheit (0.5° 
C.) are easily distinguishable under normal conditions, and even half a degree 
(0.2° C.) can be distinguished on the face and fingers, but only about two degrees 
(1° C.) on the back. 

Variations in the temperature sense are very common. We often find them 
(especially in spinal disease) in those cases where the simple sensibility to touch 
is fully retained. The test of the sensibility to heat and cold should therefore 
never be omitted in testing the sensibility. It can be done with sufficient accu- 
racy for all practical diagnostic purposes simply by touching the skin with large 
test-tubes filled with ice or hot water. The various thermaesthesiometers that 
have been devised are too complicated for practical purposes. For a hasty test 
it is sometimes quite serviceable to try whether the patient can distinguish warm 
breathing upon a given portion of the skin from cool blowing upon it. 

5. Sensation of Pain. — Tbe sensibility to pain, also, can not be excited in all 
parts of the skin by circumscribed irritation, such as a pin-prick. We find " pain 
points " and parts insensible to pain. From this fact and for other reasons, 
which can not be detailed here, von Frey has concluded that there are special 



REMARKS UPON THE DISTUBBAXCES OE SEXSIBILITY 793 



pain nerves, whose terminal apparatus is to be found in the free intra-epithelial 
nerve endings. It is a fact that the sensibility of the .skin for touch and that 
for pain are not always parallel under pathological conditions. AVe sometimes see 
that a patient does not feel a simple touch on the skin, when sticking- a needle 
into it is immediately painful ; while, on the other hand, we still more frequently 
find that a patient feels quite a light touch on the skin, but that the most marked 
irritation, such as pinching or pricking it, does not excite the slightest pain, but is 
felt only as a simple touch, or at most as a slight pressure. This latter con- 
dition of sensibility, the loss of cutaneous sensibility to pain with retained tactile 
sensibility, is termed analgesia. Both in peripheral and in central nervous dis- 
eases analgesia is a symptom that may be quite frequently observed. 

The test of sensibility to pain may be best performed by pricking with the 
point of a pin, and also by pinching a fold of the skin with considerable force. 
The simple test, whether a patient is able to distinguish between the head and the 
point of a pin, is much employed. We thus obtain information at the same time 
of the sensibility to pressure or touch; for a prick with the point of a pin nor- 
mally excites a slight pain, while the application of the pin-head causes a sensa- 
tion of simple touch or slight pressure. In testing the sensibility to pain we must 
be careful to prick deep enough (penetrating the epidermis), but at first we must 
employ only brief pin-pricks. Only when these are not felt as painful should we 
use long-continued pin-pricks. Very often by summation of the irritation ( vide 
infra) a lively sensation of pain is produced. If there be marked analgesia we 
can of course stick a pin deep into the skin or push it through a fold of skin with- 
out causing pain. 

It is well known that various kinds of irritation may produce pain: severe 
pressure, extreme temperature, strong electrical currents, etc., as well as wounds 
of the skin (for pin-pricks are to be regarded as such). It is always some irrita- 
tion which acts on the deeper layers of the skin. 

6. Electro-cutaneous Sensibility. — The test of cutaneous sensibility by 
means of the electric current has been proposed by various observers. The 
advantage of it is that in this way the intensity of the irritation can be very 
easily and accurately graded and expressed in numbers, by the position of the 
coil in using the faradic current, or by the galvanometer in using the con- 
stant current. The faradic current is usually sufficient in testing the sensibility, 
and- we designate it by the position of the coil when the first sensation is felt 
and the position when the first pain is felt. In general, the differences of the 
farado-cutaneous sensibility are not very marked. Pathological deviations are 
given by comparison with normal portions of the skin (testing, if possible, sym- 
metrical parts) or with healthy people. The galvanic current is also used to test 
sensibility, noting the occurrence of a burning sensation at the cathode. Eor 
practical purposes, the test of electro-cutaneous sensibility is unnecessary, since 
its results are the same as in testing the sensibility to touch and to pain. 

7. Delay of Sensation (so-called Delayed Conduction), Summation of Irri- 
tation and After-sensations. — Quite frequently in diseases of the spinal cord, 
especially in compression paralysis and tabes (q. v.). and not infrequently in 
peripheral nerve disease (neuritis), we see a marked delay in sensation after the 
action of an irritant. This symptom affects chiefly the sensibility to pain. If 
in such a case we stick a pin into the sole of a patient's foot, several seconds 
elapse, even ten or twenty, it is said, before the pain is felt. As was first observed 
by Xaunyn and E. Eemak in tabes, and as has often been confirmed since, after 
sticking a pin into the foot there is in such cases first a simple sensation of slight 
pressure, and some seconds later the peculiar sensation of pain, so that the 
patient at once responds to the prick with " Now/ 5 and a little later with " Ow ! ?r 
as an expression of pain. 



794 



DISEASES OF THE KEKVOUS SYSTEM 



On analyzing this symptom somewhat more closely we will have to distinguish 
between single brief and continuous irritations (pin-pricks). If we make, for 
example, a single short prick in the skin, it may happen that the pain thus caused 
appears comparatively late. This symptom depends perhaps upon a " delay of 
conduction," although it is still undetermined, of course, whether this delay takes 
place actually in the peripheral-nerve fiber or in the interpolated ganglion cells. 
The conditions in permanent painful excitation (continued pin-prick) are dif- 
ferent. In these cases we notice very often that immediately after the insertion 
of the pin the patient feels nothing or only a simple touch. If the prick be con- 
tinued, however, there is felt a lively sensation of pain, often only after a few 
seconds. This phenomenon is apparently due, not to a delay of conduction, but 
to a summation of the irritant action, which thus gradually attains sufficient 
intensity finally to break through the existing resistance and to reach the con- 
sciousness in full strength. At the same time with the sensation of pain there is 
usually a reflex twitching, and the same conditions are therefore to be considered 
in testing the cutaneous reflexes (vide infra). 

In this connection, it is well to mention briefly the after-sensations, which 
we have noted in the most striking fashion, especially in cases of tabes. After a 
single short prick these after-sensations appear as a burning feeling in the skin, 
which lasts a strikingly long time, or else the first sensation soon ceases after the 
prick, and then, in the same spot on the skin, new sudden sensations of pain are 
felt several times, just as if the patient had been pricked anew. 

8. The Sensibility of the Muscles and Joints. — A number of sensations are 
classed together under the names of " muscular sense " or " muscular sensibil- 
ity." They are not all wholly of the same value, and, under pathological condi- 
tions, they must be tested separately. 

Ordinarily we call our power to be informed of the position of any of our 
limbs without the help of our eyes, and of the extent of any motion made by them, 
the " muscular sense." If we put a healthy person's arm into a given position 
when his eyes are closed, and tell him to put the other arm into the same position, 
he can do it with considerable accuracy. If we make passive movements in any of 
the joints of the extremities, a healthy person whose eyes are closed can easily 
and correctly state the form and direction of these movements. In nervous pa- 
tients, however, this power may be diminished or lost, and we often speak of " dis- 
turbances of the muscular sense " ; but we must note that the judgment as to the 
position of the limbs and the passive movements executed with them is not chiefly, 
much less exclusively, due to the sensibility of the muscles. In all probability it 
depends much more upon the sensibility of the articular surfaces, the ligaments 
and tendons, and in part even of the skin, all of which tissues are relaxed or made 
tense in the different movements. It would therefore be more correct to speak 
of sense of position (the sensation of position of the limbs) and sense of motion 
(sensation of passive movements) instead of the " muscular sense." The sensi- 
bility to movement is tested simply by making the patient close his eyes, by tak- 
ing an arm or a leg firmly in both hands, and then by making passive movements 
up and down, right and left, at first extensive and then gradually less. The pa- 
tient should state the direction of the movement made. We may also describe 
with the extremities different letters or figures in the air, which the patient should 
recognize with his eyes closed. If the test is to be absolutely accurate, passive 
movements must be tested in all the joints individually (shoulder, elbow, hip, 
knee, etc.), but as a rule we can judge correctly if we test the passive movements 
for the whole extremity at the shoulder or hip. By control experiments on healthy 
persons we can readily convince ourselves how uncommonly sharp and accurate 
the sensation of passive motion is under normal conditions. 

The sensation of the position of the limbs is tested by putting one extremity 



KEMAKKS UPON THE DISTURBANCES OF SENSIBILITY 795 



passively into a given position and then asking the patient to put the other cor- 
responding extremity into the same position, as nearly as possible. It is still bet- 
ter to have the patient make some definite movement, especially pointing to or 
seizing some object, at first with the eyes open; then to let him close his eyes and 
repeat the movement as well as he can. 

The sensation of the strength of voluntary muscular contraction, the so- 
called " sense of power," is quite different from the sensations just described. 
Besides the peripheral sensations in the muscles and tendons we perhaps have to 
do with special sensations of innervation. In raising weights we can distinguish 
with considerable accuracy the lighter from the heavier, when the pressure on the 
skin is excluded as far as possible. In such cases, also, we do not deal with the 
absolute, but with the relative differences in weight; we can usually tell quite 
plainly when one fortieth of the original weight has been added or taken away. 
The sense of power, then, is somewhat finer than the sense of pressure. In order 
to exclude the latter in the test we have the patient lift the weight, suspended in 
a towel, with his hand or foot, but in the lower extremities it is scarcely possible 
to exclude entirely the co-existing sensations of pressure. 

We must mention, in conclusion, that muscular contraction is in itself ac- 
companied by a sensation, as may be proved, for example, in irritating the mus- 
cles by faradism — electro-muscular sensibility. In certain forms of spasm the 
muscular contraction becomes so strong that it causes a decided pain, which 
is probably due to irritation of the sensory muscular nerves discovered by C. 
Sachs. 

Tests of the sense of power and of the electro-muscular sensibility have thus 
far been but little employed in nervous diseases. They also have no great prac- 
tical significance, but the test of the sensations of position and motion are often 
of great importance. Marked disturbances in these functions are often found in 
advanced cases of tabes and sometimes in other spinal diseases and in cerebral 
(especially cortical) paralyses. Complete loss of " muscular sense " is also found 
quite frequently in severe hysterical affections, usually associated with other 
hysterical anaesthesias and hysterical paralysis. 

9. The Special Sensibility to Touch (Stereognostic Sense, Active Touch). — 
The highest and most valuable function of the skin as a sensory organ is the judg- 
ment we can often make of the size, form, hardness, and consistency of objects 
solely by feeling of them — in short, the recognition of them. This function, the 
special sense of touch, is apparently a complicated estimate of all the separate 
sensations derived from the different cutaneous nerves, to which are always added 
at the same time a large number of sensations of movement. For " touch " and 
" feeling " always imply a movement of the parts which touch. "We see, therefore, 
that a patient whose hand is completely paralyzed can recognize objects either 
with difficulty or not at all by the touch, although the cutaneous sensibility is 
retained. If there be actual anaesthesia of the skin it is, of course, also impossible 
to recognize objects by the sense of touch, although mobility is retained. There 
are, however, also cases where the hand can be moved well enough and where the 
sensibility of the skin and muscles for the different qualities of sensation is re- 
tained, but nevertheless the recognition of objects by the sense of touch is mark- 
edly impaired. In such cases there is probably always some cerebral (cortical) 
disturbance, which may be regarded as analogous to cortical blindness and corti- 
cal deafness — that is, the normal mental estimate, the " understanding " of the 
various cutaneous sensations received. The author has seen such conditions, 
especially in cerebral infantile paralysis ; the intelligent child feels every touch 
on the skin perfectly well, but, when his eyes are closed, he can not recognize by 
feeling of them with the affected hand the most familiar objects (key. knife, ring, 
money, etc.). At any rate it is very important, especially in cerebral diseases, 



796 



DISEASES OF THE NERVOUS SYSTEM 



not to neglect this mode of investigating the special " sense of touch." If we 
choose for our tests simple stereometric figures (sphere, cube, cone, octahedron),, 
we may also speak of a " stereognostic sense." 



CHAPTER II 

THE SENSORY CONDUCTION TRACTS AND ANESTHESIA OF 

THE SKIN 



1. Course of the Sensory Conduction Tracts— In every tract of the conduct- 
ing path, which runs from the terminal apparatus of the sensory cutaneous 
nerves to the centers for the perception of sensation in the cerebral cortex, we 

may have, under pathological conditions, 
a break in the conduction, and, as a result 
of it, a complete or partial ansesthesia of 
the corresponding part of the skin. We 
speak of a peripheral, spinal, or cerebral 
anaesthesia, according to the place where 
this break in the conduction occurs. The 
anatomical course of the sensory fibers 
(Fig. 84) is, however, not yet known as 
accurately as we could desire; the course 
of the sensory tract is also apparently far 
more complicated than that of the chief 
motor tract (vide infra, Section II). This 
is dependent partly upon the different 
qualities of sensation, and partly on the 
fact that the sensory tracts enter into 
many combinations with motor cells for 
the excitation of reflex movements or for 
the purpose of co-ordination of motion. 

We must regard the sensory nerve- 
fiber, like every fiber in the nervous sys- 
tem, as the direct process of a nerve-cell 
(ganglion-cell) . This sensory fiber receives 
the external impressions made upon its 
peripheral terminal organs in the skin. 
We now know definitely that all peripheral 
sensory nerve-fibers come from the cells 
of the spinal ganglia (intervertebral gan- 
glia). All, or at least most of these cells, 
have a short process which soon divides 
into two offshoots 1 from the cell : one 
long one, going to the surface of the body 
(the peripheral sensory nerve), and a 
shorter one, which enters the posterior 
root of the spinal cord and is intended 
for the further conduction of sensory im- 
pressions. Almost all the fibers of the 
Vorder 'Seitenstr. = Antero-iaterai columns, posterior roots accordingly come from the 

Kleinlurn. Seiten. B. = Lateral cerebellar x . . ~ 17 . - 

tract. spinal ganglia; during toetal development 




Fig. 84. (From Edinger.) — Diagram of the 
course of the posterior sensory root-fibers 
in the spinal cord and medulla oblongata. 



ANAESTHESIA OF THE SKIN 



79? 



they grow from their cells of origin into the spinal cord. The spinal gan- 
glion cell with its processes forms the first (peripheral) sensory neurone. The 
posterior root-fibers, entering the spinal cord with their branches (collaterals, 
vide infra), take very different courses, apparently according to their different 
functions (see Figs. 84 and 85). A part of them (Fig. 85, 4) go to the anterior 




Fig. 85.— (From Edinger.) Diagram of a transverse section of the spinal cord with especial regard to the 
course of the posterior root-fibers : 1. Fibers in the posterior column. 2. Fibers to the cells of Clarke's 
column, whose processes enter the lateral cerebellar tract. 3 Direct fibers in the i; lateral limiting 
layer 11 of the lateral column (not mentioned in the text). 4. Fibers to the motor cells of the anterior 
horn (reflex fibers). 5. Fibers in the posterior horn splitting up about its cells. Balm, tract ; Grenz- 
schicht. limiting layer ; Grund-Biindel, ground bundle ; Kleinhirn, cerebellum ; Pyramiden, pyramid ; 
Seitenstrang, lateral column ; Vorder Strang, anterior column ; Strangzellen, cells to columns. 

horns and break up about their motor ganglion cells ; these are apparently tracts 
for the reflex movements. Another part go to the cells of Clarke's columns, from 
which arise fibers for the lateral cerebellar tract (see Fig. 84 and Fig. 85 in the 
right half of the figure) ; these fibers seem to serve for the maintenance of the 
bodily equilibrium and perhaps for the co-ordination of movements. The special 
sensory fibers, however, divide into two main groups (Figs. 84-86) ; a part of 
them, chiefly the median root-fibers, enter directly into the posterior column of 
the same side. Soon after their entrance the fibers divide again into a short 
descending and a long ascending branch. The short descending branches serve, 
as I suspect, for reflex processes, while the ascending fibers in the posterior col- 
umns form the special continuation of the centripetal tract. That portion of the 
posterior columns, into which these root-fibers enter, is called the " posterior root- 
zone," or " root entrance zone " ; in the lumbar cord it lies in the middle part of the 
posterior columns, in the dorsal and cervical cord in the lateral parts (columns of 
Burdach). Since new root-fibers are constantly entering the cord as we go up- 
ward, the fibers coming from the lower portions, and especially from the lumbar 
cord, are gradually pressed toward the median line by the new fibers that enter. 



798 



DISEASES OF THE NEKVOUS SYSTEM 




Fig. 86.— Diagram of the course of the sensory conduction tracts : A. En- 
trance of the posterior sensory root-fibers in the lumbar cord; gi, in- 
tervertebral ganglion ; rp, posterior root. A part of the fibers that 
enter end in the posterior horns, from whose cells new fibers arise 
and enter the lateral columns, partly crossed, partly uncrossed. An- 
other part of the fibers from the posterior roots pass upward in the 
posterior columns and form in B the so-called columns of Goll ((?). 
B. Cervical cord. Lettering as in A. B. Columns of Burdach. C. 
Medulla oblongata. Region of the decussation of the lemniscus. 
The fibers from the posterior columns end in the nuclei of GolPs 
and Burdach's columns (G and B). New fibers arise from the cells 
of these nuclei, which form the decussation of the lemniscus. Py. 
Motor pyramids. D. L, sensory lemniscus : o/, olivary body ; cr, cor- 
pus restiforme. E. Section through the pons. L, lemniscus ; &, su- 
perior cerebellar peduncle ; iv, fourth ventricle. F. Frontal section 
through the region of the corpora quadrigemina : i, lemniscus ; nr, 
red nucleus ; Py, pyramidal tract in the crusta of the crus cerebri ; 
nL, lenticular nucleus ; T/i, optic thalamus (interruption of the sen- 
sory tract ? Beginning of a third sensory neurone ?) ; cqa, anterior 
corpora quadrigemina ; n, corpus geniculatum externum and optic 
nerve ; cc, corpus callosum. 



Thus it happens that the 
fibers from the lumbar 
and the lower dorsal 
cords are in quite a me- 
dian position in the cer- 
vical cord, in the region 
of the so-called columns 
of GolL All these fibers 
end in the nuclei of 
Goll's and Burdach's col- 
umns in the beginning 
of the medulla oblonga- 
ta. From the cells of' 
these nuclei come the 
secondary sensory neu- 
rones, whose fibers de- 
cussate in the medulla 
oblongata (fibra3 arcua- 
tse internae, or sensory 
decussation in the lem- 
niscus, Fig. 86), and in 
their further course 
form the so-called lem- 
niscus, which passes 
through the medulla, 
pons, and tegmentum of 
the crus to the cere- 
brum. 

A second (lateral) 
portion of the fibers of 
the posterior roots enter 
at once the gray matter 
of the posterior horn. 
These fibers also divide 
into an ascending and a 
descending branch. A 
number of especially fine 
fibers remain in the 
periphery of the poste- 
rior horn (zona termi- 
nalis, Fig. 85, also called 
Lissauer's zone). The 
fine collaterals of these 
fibers probably enter the 
posterior horn through 
the zona spongiosa, and 
enter into similar rela- 
tions with the ganglion- 
cells as the other coarser 
fibers of this portion of 
the posterior root-fibers, 
which enter the pos- 
terior horns directly 
through the substantia 



ANESTHESIA OF THE SKIN 



799 



gelatinosa, and after a short course split up in so-called terminal arborization 
about the ganglion-cells there. With these cells begin .the second sensory neu- 
rones for this part of the sensory tract; the processes (fibers) of these cells at 
once enter the lateral column of the opposite side through the anterior commis- 
sure, decussate therefore in the anterior commissure of the cord, ascend in the 
anterior and middle portions of the antero-lateral columns (anterior and internal 
to the motor pyramidal lateral tract), reach the medulla oblongata also in the lem- 
niscus, and unite here with the above-described fibers from the cells of Goll's and 
Burdach's nuclei. The diagram on the opposite page (Fig. 86, the red portion, L, 
signifying the lemniscus) gives an idea of the position of the lemniscus — that is, 
of the chief sensory tract — farther upward in the pons and tegmentum. Higher 
still, in the internal capsule, the sensory tract lies in the posterior limb behind the 
motor pyramidal tract (vide infra, Fig. 95). There is still considerable obscurity 
as to its further course. A part of the lemniscus fibers probably end in the optic 
thalamus, from whose cells, to all appearances, a third sensory neurone arises, 
sending its fibers to the cerebral cortex. Another part of the lemniscus fibers, 
however, pass directly to the cerebral cortex without interruption. "The sensory 
fibers from the posterior columns probably end in the cerebral cortex in the cen- 
tral convolutions, especially in the posterior central convolution and in the neigh- 
boring portion of the parietal lobe, and perhaps also of the frontal lobe. It is ex- 
tremely interesting physiologically that the central terminal region of the sensory 
fibers in part quite coincides in its localization with the motor centers (vide 
infra). 

It would be extremely valuable if we knew the centripetal conduction tracts 
to the cerebrum for the different kinds of cutaneous and muscular sensibility 
(see the preceding chapter). Unfortunately, our knowledge in this regard is still 
extremely defective and uncertain. The hypothesis, which seems relatively the 
most certain, is that the sensory fibers entering directly into the gray posterior 
horns serve chiefly for the conduction of sensations of pain and temperature. 
This is supported especially by the observations on syringomyelia (vide infra). 
It has also long been claimed by the physiologists (Schiff) that section of the 
posterior gray matter causes analgesia. The posterior root-fibers, which ascend 
in the posterior columns, seem to serve especially for the conduction of muscular 
sensations and the co-ordination of motion (vide infra). Many ways seem to be 
open for the conduction of simple sensations of contact : it is striking how rarely 
total anaesthesia of the skin occurs in organic diseases of the spinal cord, and it 
almost never occurs in organic diseases of the brain. 

2. The General Causes of Cutaneous Anaesthesia. — Kegarding the separate 
causes of anaesthesia, we see, in the first place, peripheral anaesthesia under con- 
ditions where the terminal organs of the sensory cutaneous nerves have lost their 
direct irritability. After chilling the skin, after the local action of ether and 
similar substances, after the corrosive action of acids and alkalies, carbolic acid, 
etc., as well as after the use of certain narcotics, such as cocaine, we see an 
anaesthesia of the skin, which is due to injury of the terminal sensory organs. 
We may probably put the frequent anaesthesia of washerwomen in this class, for 
their hands and forearms are exposed all day to the action of cold, lye, etc. The 
anaesthesias which develop in circulatory disturbances of the skin also have the 
same peripheral origin, especially the " spastic anaemia " which sometimes comes 
in the hands and is due to a spasm of the small arteries. 

We distinguish the peripheral anaesthesia of conduction, which may be pro- 
duced by all forms of lesion of the nerve-trunks, from the peripheral anaesthesias 
in the strict sense of the term. Traumatic influences, compression from new 
growths, and inflammation and degeneration of the peripheral nerves,, as in neu- 
ritis, are the most frequent causes of this form of anaesthesia, which is often lim- 



800 



DISEASES OF THE NEKVOUS SYSTEM 



ited to the region of distribution of one or more individual nerves. The circum- 
scribed anaesthesias which often come on after acute diseases (typhoid fever, 
diphtheria), and in some chronic diseases (diabetes), are usually peripheral 
(neuritic) anaesthesias. 

Spinal anaesthesia is very often seen in the different diseases of the spinal 
cord, most frequently in tabes, because this, as we shall see later, is a direct dis- 
ease of the peripheral sensory neurone ; but spinal anaesthesia is not infrequent 
in diffuse acute and chronic inflammation of the cord and in compression and 
new growths, and especially in syringomyelia. As a rule, it is bilateral para-an- 
aesthesia, but in unilateral lesion of the cord it may also be unilateral, the anaes- 
thesia being found on the half of the body opposite to the affected half of 
the cord, owing to the decussation of the sensory fibers in the gray matter (vide 
supra). 

Cerebral anaesthesia is seen especially in haemorrhages, foci of softening, and 
tumors, which affect any part of the lemniscus tract or the posterior portion of 
the internal capsule. Such anaesthesias affect the half of the body opposite to the 
lesion, and are called hemianaesthesia. As a rule, experience shows that cerebral 
anaesthesia of organic origin is seldom very intense. Hysterical anaesthesias, 
however, may attain an extreme degree; they are due to a disturbance of the 
perception of sensory impressions by the consciousness. 

3. The Symptoms of Cutaneous Anaesthesia. — In many cases the patient 
himself notices the existence of anaesthesia. He finds that in certain parts of 
the body he no longer feels the pressure of his clothing or the bed-clothes in the 
usual way. Anaesthesia of the hands is soonest noticed, because this affects the 
patient's occupation in diverse ways, so that, for example, he is apt to let fine 
objects, such as needles, drop from his hands. In other cases, of course, the 
anaesthesia is first found on a physical examination. It is worthy of note that 
hysterical anaesthesia especially, even if it be very marked and extensive, may 
often be wholly overlooked by the patients themselves. 

Anaesthesia is very often combined with abnormal subjective sensations, par- 
aesthesiae, in the affected portions of the skin. The patient has a feeling there of 
" numbness," or a " furry feeling," or complains of prickling or formication. The 
anaesthetic parts may even be the seat of very decided pain (anwsthesia dolorosa), 
if there is abnormal irritation of the sensory nerves from the break in the con- 
duction toward the center. The most diverse forms of anomalies of motility and 
of the reflexes, and vaso-motor disturbances, may of course be present in addition 
to the anaesthesia. Special mention must be made of the so-called trophic dis- 
turbances (inflammation, ulceration, bed-sores, etc.) which are often seen in an- 
aesthetic regions. Whether in these cases we actually have to do in part with 
direct injury of the tissues from the failure of normal " tropho-neurotic " influ- 
ences is at present wholly undetermined. The majority of the ordinary so-called 
" trophic " disturbances are without doubt due to external injuries (slight wounds 
with consequent purulent infection). When there is anaesthesia, or especially 
analgesia, of the patient's skin, these injuries do not receive sufficient attention, 
and therefore they are neither avoided nor thoroughly treated (compare especially 
the chapter on syringomyelia). Greater external injuries^-burns, bed-sores, etc. 
— are often not noticed at all when on anaesthetic parts, and therefore they may 
attain an extraordinary size and become very bad. 

Voluntary motion, if we may draw conclusions from existing clinical observa- 
tions, is not disturbed by anaesthesia in itself, of however great a degree, as long 
as the motions can be controlled by the eyes, but finer movements are often con- 
siderably impaired by cutaneous anaesthesia ; thus patients with diminished sen- 
sibility in the fingers can usually no longer sew, because they lose the needle every 
minute. With the eyes shut, however, the motions of the anaesthetic parts be- 



ANAESTHESIA OF THE SKIN 



801 



come very uncertain, both in anaesthesia of the skin and of the deeper parts, the 
muscles and joints; since then the patient loses, to a great degree, his power of 
judging of the extent and of the precise direction of his movements. Very ex- 
tensive anaesthesia of the skin, associated at the same time with anaesthesia of 
the organs of special sense, is sometimes not without influence upon conscious- 
ness. We have had under observation a very remarkable case of total anaes- 
thesia of the whole body associated with unilateral blindness and deafness. If 

we entirely excluded this 
patient from all external 
impressions of sense by 
closing his still service- 
able eye and ear, we could 
at once in this way put 
him into a deep sleep! 
It must, of course, be said 
in this connection that 
such extensive anaesthe- 
sias have thus far been ob- 
served almost exclusively 
in hysteria (vide infra), 





Fig. 87. Fig. 88. Fig. 89. 

Figs. 87 and 88.* — Distribution of the sensory cutaneous nerves in the trunk and upper extremities : 
Fig. 87. Posterior aspect. Fig. 88. Anterior aspect. The shaded portion in Fig. 87 designates the 
territory supplied by the radial nerve. (From Henle.) sc. Supraclavicular nerves (from the cervical 
plexus), ax. Cutaneous branch of the axillary nerve, cps and cpi. Superior and inferior posterior 
cutaneous nerves from the radial (ra). cmd, cm, and cl. Median cutaneous, median, and lateral nerves. 
me. Median nerve, u. Ulnar nerve, du. Second dorsal nerve, dxn. Twelfth dorsal nerve, ih. Ileo- 
hypogastric nerve, ii. Uio-inguinal nerve, il. Lateral perforating branches, and ia, anterior per- 
forating branches of the intercostal nerves. 

Fig. 89.— Detailed distribution of the nerves to the dorsal surface of the fingers. (From Krause.) r. Radial 
nerve, m. Median nerve, u. Ulnar nerve. 



and that therefore special psychical factors have perhaps been of influence in 
the phenomenon just mentioned. 

We can not here go into details of the different forms and varieties in the 
course of anaesthesia, since they will be spoken of under the different diseases 
which lie at the basis of the anaesthesia. The regions of distribution of the 
peripheral sensory nerves of the skin are given diagrammatically in the accom- 
panying cuts (Figs. 87 to 91). Experience shows, however, that complete section 
of a peripheral sensory (or mixed) nerve almost never causes total anaesthesia 
in the corresponding cutaneous region, probably because there are many anasto- 
moses of the terminal branches of the sensory nerves. 



[* Henle's nomenclature of the peripheral nerves has been adopted, 
51 



.— Trans.] 



802 



DISEASES OF THE NERVOUS SYSTEM 



cp 



cl 



li 



Anaesthesia in the region of the trigeminus demands a brief special de- 
scription. 

4. Anaesthesia of the trigeminus is observed in tumors, syphilitic new 
growths, chronic inflammations, and analogous processes at the base of the skull, 
which compress the trunk, the Gasserian ganglion, or one of the three branches of 
the trigeminus, or directly involve the nerves. Traumatic lesions of the tri- 
geminus also are not very uncommon. The distribution of the anaesthesia, ac- 
cording as the affection involves the whole trigeminus, or only one branch of it, 
may be seen in Eigs. 92 and 93, but individual variations occur. In total anaes- 
thesia of the trigeminus, the conjunctiva 
and cornea, the mucous membrane of the 
nose, the cavity of the mouth, the tongue 
J/ V^nI up "to the foramen caecum, and the soft 

palate are anaesthetic on the affected side. 
Hence we often find ulcers on the tongue 
and the mucous membrane, which come 
from being bitten. The " neuro-paralytic 
ophthalmia," not infrequently seen in an- 
aesthesia of the trigeminus is of special in- 
terest, and it has been much studied by 
cr \ I physicians and physiologists. This is an 
tht I \ j ulcerative keratitis, almost always begin- 

ning in the lower segment of the cornea, 
and sometimes passing over into a purulent 
inflammation of the whole eyeball. This 
affection is regarded in many quarters as 
an immediate result of the disturbance of 
special " trophic " functions, but, after 
careful experiments, it seems certain that 
external traumatic influences always occa- 
sion the first trouble, and render the in- 
trusion of inflammatory agents possible. 
As a result of the anaesthesia of the eye 
the patient does not notice the inflamma- 
tory symptoms, which therefore often at- 
CtiJAmfl tain an extremely high degree. It is still 

uncertain, but not wholly improbable, that 
KHPv^ J we must also assume a specially dimin- 

ished power of resistance on the part of 
the tissues and a limitation of all com- 
pensating functions as a result of the 
nervous lesion. 

The skin of the face is often somewhat 
bloated and reddened in anaesthesia of 
the trigeminus, and it is sometimes 
warmer, but often colder, than normal. 
The reflexes are lost in peripheral anaes- 
thesia, and the lachrymal secretion ceases, 
or at least is persistently diminished. The taste is almost always decidedly dimin- 
ished on the anterior two thirds of the tongue on the affected side, the territory 
supplied by the lingual nerve. According to the investigations of Krause on 
patients in whom the Gasserian ganglion has been extirpated (vide infra), the 
trigeminus contains fibers which conduct sensations of taste for sweet, sour, and 
salt from the tip of the tongue and the anterior two thirds of its lateral border; 



qim 



cti\ 



Fig. 



Fig. 90. 

Figs. 90 and 91.— Distribution of the sensory cu- 
taneous nerves to the lower extremities. Fig. 
90. Posterior aspect. Fig. 91. Anterior as- 
pect. (From Hexle. ) it. Ilio inguinal nerve. 
li. Lumbo-inguinal nerve, se. External sper- 
matic, cp. Posterior cutaneous, cl. Lateral 
cutaneous, cr. Crural, obt. Obturator, sa. 
Saphenous, cpe. Peroneal communicating 
nerve, cti. Tibial communicating nerve. 
per'. Superficial branch of the peroneal 
nerve, per". Deep peroneal nerve, cpm. 
Posterior median cutaneous nerve, cpp. Cu- 
taneous plantar nerve. 



ANAESTHESIA OF THE SKIN 



803 



hut Individual variations seem to occur. The secretion of saliva as a rule suffers 
no perceptible change, but we sometimes see a diminished secretion of mucus in 
the nasal cavity on the affected side. 

Besides the peripheral anaesthesias just described, other anaesthesias occur, 
especially in syringomyelia, and more rarely in other diseases of the medulla 
oblongata, which are due to a lesion in the region of the trigeminal nucleus (nu- 
clear anaesthesia). In those cases a remarkable condition is manifest — namely, 
that, in diseases which extend from below upward, the anaesthesia first appears 
in the upper part of the forehead next to the hairy scalp (and usually on the lat- 
eral portion before the median), and that the sensory disturbance extends in a 
curve downward and 
inward to the eye- 
brows, then to the 
outer portion of the 
ejaelids, then to the 
median portion of the 
lids, and finally to the 
skin of the alae nasi 
and the bridge of the 
nose. The frontal 
portion of the first 
branch of the trigem- 
inus, therefore, seems 
to derive its fibers 
from the most dis- 
tal (lowest) nuclear 
groups, next above 
come the nuclei for 
the third branch 
(temporal region), 
and then for the sec- 
ond branch and the 
nasal portion of the 
first branch (see the 
anatomical description in the section on diseases of the medulla oblongata). 
The disturbances of sensibility in the mucous membrane of the mouth are usually 
seen first in the posterior portion of the mucous membrane of the cheeks, then in 
the hard palate, and finally in the region of the soft palate and the tonsils. The 
mucous membrane of the oral cavity, therefore, derives its sensory fibers from the 
distal portion of the trigeminus nuclei (Schlesinger). 

5. Treatment of Cutaneous Anaesthesia. — Since anaesthesia in most cases is 
only a symptom, treatment, of course, must always first be directed against the 
underlying disease. Therefore we will mention here only those measures which 
are to be used symptomatically against anaesthesia. 

The chief remedy is the electric current. We treat the anaesthetic part of the 
skin with the faradic current, using ordinary electrodes, or, better still, the wire 
brush, or with the galvanic current, stroking the skin slowly back and forth with 
the cathode for three or four minutes. Sometimes we can see a result imme- 
diately after the' sitting. Hysterical anaesthesia may often be removed in this 
way in a very short time. 

Besides electricity we prescribe embrocations, such as spirit of camphor, 
formic acid, spirit of thyme, etc., and also baths, and cold or hot local douches, 
combined with rubbing the skin. The action of internal remedies, such as strych- 
nine, is extremely doubtful. 




Fig. 92. Fig. 93. 

Fig 3. 92 and 93.— Distribution of the sensory cutaneous nerves in the head : 
oma and omi. Occipitalis major and minor, am. Auricularis magnus. 
cs. Superficial cervical. V x . V 2 . V 3 . First, second, and third branches 
of the fifth (F). so. Supraorbital, st. Supratrochlear, it. Infratroch- 
lear. e. Ethmoidal. I. Lachrymal, sm. Subcutaneus mate, or zygo- 
matic, at. Auriculotemporal, b. Buccinator, m. Mental. B. Poste- 
rior branches of the third cervical. 



804 



DISEASES OF THE NERVOUS SYSTEM 



It is very important to protect the anaesthetic part against external injuries. 
In anaesthesia of the trigeminus, particularly, we guard the eye as far as possible 
from the development of a neuro-paralytic keratitis, by a carefully applied oc- 
clusive bandage, and treat even the slightest inflammation with the greatest care. 
We can thus almost certainly avoid bad results. 



CHAPTER III 
NEURALGIA IN GENERAL 

Concept and .ZEtiology. — Although every pain is, of course, excited by abnor- 
mal irritation of the nerves, still we are justified in giving a certain special vari- 
ety of pain the name of neuralgia. By that name we understand pain due to a 
disease of a definite sensory nerve (or perhaps sometimes of its central con- 
tinuation). The name neuralgia has therefore both a symptomatical and an ana- 
tomical significance. Symptomatically most neuralgias are characterized by the 
following peculiarities : 1, the pain is felt exactly in the course or in the distribu- 
tion of one or more special nerve-trunks or nerve-branches ; 2, it is usually 
of very considerable intensity; and, 3, as a rule, it is not present continuously, 
but it shows manifest variations. Many neuralgias come on in pronounced parox- 
ysms of pain, which are interrupted by wholly painless intervals. Anatomically, 
neuralgia is not one single disease. Every severe affection of a sensory nerve 
leads to neuralgic pain. The trouble is often merely one symptom of another 
more extensive morbid process (symptomatic neuralgia). In other cases the 
affection of the sensory nerve is an independent disease by itself (idiopathic, 
primary neuralgia). In many idiopathic neuralgias we may with great probabil- 
ity assume an inflammatory affection of the nerve or the nerve-sheath, as in sci- 
atica, but in other cases, and indeed in most typical neuralgias, as in severe 
trigeminal neuralgia, this theory is improbable. In these cases the special nature 
of the " neuralgic disease " is still entirely obscure. At times, in separate at- 
tacks and without any known cause, extremely active irritative processes occur 
in the special nerve territory, causing the most intense pain. Trousseau has 
compared these paroxysms of sensory irritation to the motor discharges of the 
epileptic attack, and hence has spoken of " epileptiform neuralgia." 

In regard to the general occurrence of neuralgia, age has thus far an influ- 
ence that most cases occur in middle life, but neuralgia also occurs in older peo- 
ple and much less frequently in children. Sex exerts an influence so far that 
certain forms, such as sciatica and brachial neuralgia, are more common in 
men. On the other hand, certain phases of the female sexual life, such as 
puberty, pregnancy, childbed, and the climacteric, favor the disposition to neu- 
ralgia. The general neuropathic predisposition, which is hereditary in the ma- 
jority of cases, is of great significance. Neuralgia often appears in people who 
suffer from other neuroses, or in whose families other nervous diseases, such as 
the psychoses, epilepsy, hysteria, or neurasthenia, have repeatedly occurred. The 
physical constitution also seems to be of influence. We often see neuralgia in 
anaemic people, or in those whose constitution has been impaired by physical and 
mental strain, by imprudent living, or by mental excitement. 

We may mention, as exciting or at least as favoring causes of neuralgia : 1. 
Cold, the action of draughts, wind, or wet — the so-called " rheumatic neuralgias." 
It is not perfectly clear how the cold acts in- such cases. We usually assume that 
by its action slight anatomical (inflammatory?) changes arise directly or in a 



NEUEALGIA IN GENEEAL 



805 



reflex manner in the nerves themselves. 2. Mechanical and traumatic action. 
Among' these are, first, wounds and contusions which directly involve the nerves. 
Thus, for example, extremely severe neuralgia sometimes arises from the pres- 
sure of foreign bodies, such as splinters of wood or of bones in wounds, on the 
branch of a nerve. We may also mention here the very severe neuralgia some- 
times met with after amputations. These cases are probably due less to the so- 
called amputation neuromata than to the pulling and stretching of the nerve- 
trunks in the amputation cicatrix, giving rise to the pain. To this class, too, 
belong many diseases in the neighborhood of nerves. Diseases of the bones or 
periosteum, by pressure and mechanical irritation, and often perhaps by the ac- 
companying inflammation, may lead to neuralgia in those nerves which run 
through bony canals or grooves. Lastly, tumors, aneurisms, hernise, or the gravid 
uterus, may lead to neuralgia by pressure on the neighboring nerves; but we 
must call to mind that every pressure on a nerve does not lead to neuralgia in 
the same way, so that we must assume a special consequent change in the nerve 
in " neuralgia from compression." 3. The relation which certain infections and 
poisons have to the development of neuralgia is very important. In the first 
place, it is not impossible that many of the apparently "idiopathic" neuralgias 
are to be referred to infectious causes — an assumption which may be made, for 
instance, in intercostal neuralgia associated with an eruption of zoster (q. v.), or- 
in many acute trigeminal neuralgias. Many neuralgias, however, also have a 
definite relation to other infectious diseases. We may mention in particular 
the malarial neuralgias, which are directly dependent upon the malarial infec- 
tion, often come on at regular intervals, and are cured by specific treatment — 
namely, quinine. Neuralgia is often seen during the course, or as a result, of 
typhoid fever, small-pox, and similar acute infectious diseases, and in the second- 
ary stage of syphilis. Among toxic substances we may mention especially alcohol, 
lead, arsenic, mercury, and perhaps nicotine, as those which have a relation to the 
development of neuralgia. Yet in these cases it is usually not neuralgia but pain 
of some other kind — the arthralgia of lead poisoning, the polyneuritic pains of 
alcoholic subjects, etc. 4. Symptomatic neuralgia is also found in many con- 
stitutional diseases, in gout, and very often in diabetes mellitus. It is supposed 
that in such cases abnormal chemical influences act on the sensory nerves. 5. 
Finally, there was formerly much said about " reflex neuralgia," where, for exam- 
ple, disease of the sexual organs was thought to cause neuralgia in distant nerves. 
Such observations, however, can not endure strict criticism. Most of these cases 
are hysterical. 

[Although the reflex origin of neuralgia and other nervous disturbances is 
very doubtful, it is well known that pain due to disease of a given organ may be 
referred to another part of the body. A familiar example is the reference of the 
pain from hip disease to the knee. This reference of pain to distant parts is 
probably dependent upon the anatomical distribution of the nerves. Head has 
made an exhaustive study of the distribution of the visceral nerves in the spinal 
cord, and has found that, in disease of the internal organs, the pain is apt to be 
referred to certain areas of the skin whose sensory nerves go to the correspond- 
ing spinal segments. The internal organs are represented in the spinal cord as 
follows : Heart, 1-3 D ; * lungs, 1-5 D ; stomach, 6-9 D (cardiac end, 6-7 D ; 
pylorus, 9 D) ; intestines, 9-12 D ; rectum, 2-4 S ; liver and gall-bladder, 7-10 
D ; kidney and ureter, 10-12 D ; bladder, mucous membrane, and neck, 1-4 S ; 
over-distention of bladder, 11 D-l L; prostate, 10-12 D; 1-3 S; 5 L; epididymis, 
11 D-l L; testicle and ovary, 10 D; appendages, 11 D-l L; uterus, in contraction, 
10 D-l L; os uteri, 1-4 S. For the cutaneous areas corresponding to these seg- 



* D, dorsal segment; L, lumbar; S, sacral. 



806 



DISEASES OF THE NERVOUS SYSTEM 



merits of the cord see the colored plate (page 924). Disease of the internal organs 
may also cause referred pains in the head, perhaps through the connections of the 
vagus nerve. Disease of the lungs causes referred pain in the fronto-nasal, mid- 
orbital, and fronto-temporal areas; of the heart in the mid-orbital, fronto-tem- 
poral, and temporal areas; of the stomach and intestines in the temporal, verti- 
cal, and parietal areas; of the liver in the vertical and occipital areas; and of 
the ovaries and testicles in the occipital area. Diseases of the uterus, Eallopian 
tubes, and bladder do not give rise to referred pain in the head. Affections in the 
head itself also give rise to referred pains in the head. Refraction errors cause 
pain in the mid-orbital region ; disease of the cornea or anterior chamber of the 
eye, pain in the fronto-nasal area ; of the iris, in the temporal area ; farther back in 
the eye, in the temporal, fronto-temporal, and maxillary areas ; of the membrana 
tympani and middle ear, in the hyoid area ; elevation of tension in the middle ear, 
in the vertical and parietal areas; disease of the tongue, in the mental, hyoid, 
and superior laryngeal areas. Dana had previously represented the regions of 
referred pain in visceral disturbances in much the same way.] 

General Symptomatology of Neuralgia. — The neuralgic paroxysm begins 
either quite suddenly, or, more frequently, after certain prodromata, such as cold 
feelings, prickling, slight painful sensations, etc., have preceded it for some time. 
The pain during the attack is usually of the greatest severity, and is described 
as either burning and boring, or as shooting and tearing like lightning. There are 
frequently short temporary remissions of the pain. The location of the pain usu- 
ally corresponds precisely to the distribution of the affected nerve, so that the 
patient can often point out quite definitely the anatomical course of the nerve. 
At the height of the attack there is often an " irradiation " or shooting of the pain 
into the territory of neighboring nerves. External irritants, such as cold air, 
mental excitement, and especially movements of the affected part, often produce 
an increase of the pain. 

On physical examination, we notice, first, certain disturbances of sensibility. 
The skin in the neuralgic part often shows more or less anaesthesia, which is most 
apparent in the intervals between the separate attacks and immediately after 
them. Much more frequently, however, both during the attack and during the 
time when the patient is free from pain, there is hyperesthesia of the skin and 
the parts beneath. There are certain definite points which are often very sensi- 
tive and tender even to light pressure. These are called painful points (points 
douloureux). They were first fully described for the different forms of neuralgia 
by Valleix, in 1841, although in much too schematic a way, but they have con- 
siderable diagnostic importance, since they may often be found, not only during 
the attack itself, but also during the free intervals, although then they are less 
marked. The painful points always correspond to certain places in the course of 
the trunk or the larger branches of the affected nerve, and are found especially 
where, in marked and deep pressure on the nerve, we can press on some firm part 
beneath. They are probably always due to an abnormal sensitiveness to pressure 
in the affected nerve itself. In many cases of neuralgia they may of course be 
wholly wanting. 

Motor symptoms as well as sensory are not infrequent in neuralgia. Co-exist- 
ing symptoms of paralysis must always be regarded as a complication caused by 
some coarse lesion of the motor nerves ; hence in pure idiopathic neuralgia they 
are entirely absent. The co-existing symptoms of motor irritation, which are 
often seen, are usually directly dependent upon the neuralgia, however, and 
hence are to be regarded chiefly as reflex contractions, due to the gTeat irritation 
of the sensory nerves. 

Yaso-motor symptoms are often seen in neuralgia. In the face especially, in 
trigeminal neuralgia, we often see a marked pallor or a decided reddening of the 



NEURALGIA IX GENERAL 



807 



skin and conjunctiva. Abnormal secretions, of tears or sweat, may also be seen 
during- the attack or at the end of it. We do not know whether all these symp- 
toms arise from direct or reflex nervous irritation. Trophic disturbances are 
noticed in various ways. During the attack we see eruptions of urticaria, or still 
more frequently of herpes vesicles, along the course of the affected nerves, as in 
herpes zoster. In severe and protracted neuralgias permanent changes in the 
tissues have been repeatedly seen in the parts supplied by the affected nerves. 
Among these are a falling out or a whitening of the hair, or more rarely an 
abnormally great growth of hair, thickening or atrophy of the skin, staining or 
pigmentation of the skin, atrophy of the deeper parts, etc. Lastly we may men- 
tion that during the neuralgic attack we sometimes find a diminished frequency 
of the pulse. 

The general nutrition of the body often does not suffer at all in neuralgia, but 
in many cases, especially when sleeping and eating are constantly disturbed by 
the attacks of pain, the disease gradually has a noticeable action on the whole 
constitution. The patient becomes pale and emaciated, and often the persistent 
and distressing pain is not without influence on his mental condition. He be- 
comes irritable and inclined to melancholy. Patients have, in repeated instances, 
even committed suicide as a result of severe and incurable neuralgia. 

The whole course of neuralgia shows the greatest diversity. As has been said 
repeatedly, the onset of the disease in separate attacks is the chief characteristic 
feature. The precise pathogenesis of these attacks is, of course, entirely unknown 
to us. These attacks usually come on every day or several times a day, or some- 
times at longer regular or irregular intervals. They may last only a few minutes 
or several hours. During the period between the attacks many patients feel quite 
well, but some have still a certain sensitiveness of the skin. The disease as a 
whole sometimes lasts only a few days or weeks, but sometimes it persists with 
manifold variations for years and years, and, in a word, is not capable of im- 
provement; although, on the other hand, there are recoveries after the disease 
has lasted for years. In many cases, of course, the disease depends upon the pres- 
ence of some definite anatomical cause, such as a tumor, a disease of the bone, or 
an aneurism. 

Many details will be spoken of in the following chapter. 

General Treatment of Neuralgia. — Prophylaxis of neuralgia is possible in 
this way, that certain constitutional anomalies, such as anaemia or a general nerv- 
ous predisposition, favor its appearance, as we have seen; and in attacking these 
conditions, we may recognize ? factor which, can prevent to a certain degree any 
subsequent development of neuralgia. It is still more important, in people who 
have already suffered from neuralgia, to prevent the return of the affection if we 
can. For this object we must first consider the strengthening of the whole body, 
in order to make it better resist the action of any causes of disease. The meas- 
ures to be chiefly employed for this purpose are proper food, good air, baths, sea- 
bathing, cold bathing, gymnastics, etc. Of course, we must also particularly 
guard the part of the body that has once been attacked from any irritation, such 
as cold, mechanical and toxic irritants, or over-exertion, 

In treating neuralgia itself we must always look first with great care for some 
causal factor, which may be accessible to treatment. This fulfillment of the 
causal indication is often possible in neuralgias which are due to mechanical 
causes. The extirpation of tumors, the excision of cicatrices, the removal of for- 
eign bodies, the treatment of inflammatory new growths, of syphilitic affections, 
of aneurisms, etc., is in many cases attended by brilliant success, but, of course, in 
many other cases the underlying disease is unfortunately not amenable to suc- 
cessful treatment. We should also carry out a causal treatment in the neuralgias 
which are to be referred to general anaemia, to a general neuropathic constitution, 



808 



DISEASES OF THE KEKVOUS SYSTEM 



to hysteria, etc. In such cases we must always ascribe great value to the general 
treatment, such as diet, manner of life, psychical treatment, baths, iron, and 
nervines, as well as to the special treatment directed against the neuralgia ; and 
the same holds true, of course, in the neuralgias occurring- in diabetes, gout, and 
syphilis. We must always bear particularly in mind the possibility of syphilitic 
neuralgia, since in such cases iodide of potassium may often have a marked 
curative action. We may also fulfill the causal indication in the malarial neu- 
ralgias. If neuralgia comes on at approximately regular intervals in persons 
who come from a malarial district, and who perhaps have already suffered from 
other malarial affections, the exhibition of quinine in large doses, twenty to forty- 
five grains (grammes 1.5-3.0) at once, will usually speedily cut short the attack. 
In obstinate cases in which quinine does no good, we should try arsenic, in the 
form of Fowler's solution. In many apparently toxic neuralgias, too, from lead, 
mercury, or alcohol, our first endeavor in treatment should be to remove the cause 
of the disease. 

In all cases where the causal treatment can not be carried out, or where it 
alone is not sufficient, we must consider those numerous remedies and methods of 
treatment which correspond to the indicatio morbi and to the symptomatic indica- 
tions. Starting with the hypothesis of an inflammatory condition of the nerve, 
we have often tried to exert a favorable influence on the disease by local deriva- 
tives, mustard plasters, irritating embrocations, such as spirit of mustard, vera- 
trine ointment (two and a half per cent.), or tincture of iodine, or by blisters, or 
even by the cautery. The remedies first mentioned are used only in mild cases. 
Vesicatories, placed along the course of the affected nerve, or behind the ear in 
facial neuralgia, sometimes act very well in fresh cases, especially in fresh 
" rheumatic " cases of sciatica. We resort to the hot iron chiefly in old and very 
severe cases, in which, indeed, especially in sciatica, some very favorable results 
have been thus obtained. 

The local electrical treatment of neuralgia is sometimes of undoubted benefit. 
We many times secure an improvement in the symptoms, which is of course 
temporary, even in those cases where the special cause of the disease is not influ- 
enced by the electricity, although in idiopathic neuralgias in fresh, and some- 
times even in old cases, we can often obtain a complete cure. There are no gen- 
eral rules with regard to the methods to be employed, since different specialists 
have their own favorite methods. The following forms of application are most in 
use and are most to be recommended : 1. Stabile action of the anode of a constant 
current on the affected nerve-trunk over as great an extent as possible, e^vecially 
on any painful points. We must entirely avoid any great variations in the cur- 
rent or interruptions of it. We gradually increase the intensity of the current 
up to medium strength. The sittings should last three to six minutes, and some- 
times even longer, and they must be repeated daily. 2. In neuralgia of the larger 
nerves we should use a stabile descending (sometimes ascending) constant cur- 
rent, in which the anode is placed on the most central point of the nerve-trunk 
available, or on the vertebral column, and the cathode on different peripheral 
points. 3. The faradic current also frequently acts very well. We faradize the 
nerve either with a moderately strong " increasing " current, or we apply the wire 
brush to the skin over the affected nerves. The latter method is very painful, 
but it is often attended with excellent results. 4. Some electro-therapeutists, 
like Moritz Meyer, lay stress upon the stabile application of the anode of the 
constant current to any painful points on the vertebral column, such as have been 
found in many cases of neuralgia by Trousseau. 

As a general rule, it is always well to begin with a mild and very cautious use 
of electricity, and not to go on to the stronger currents until later. Electricity 
often acts brilliantly at once, during the attack of pain, but sometimes no im- 



NEURALGIA IN GENERAL 



809 



provenient is seen until after several sittings. If, after two or three weeks, we 
obtain no result at all, after employing different methods of applying electri- 
city, it is the best plan to give up electrical treatment entirely as not suited to 
the case. 

In the treatment of neuralgia we must consider a number of internal rem- 
edies, as well as electricity; some of these act symptomaticaUy, like the narcotics, 
while others have obtained the reputation of having a specific action. Among the 
latter, quinine has decidedly the greatest value. In , severe cases quinine may 
do excellent service, not only in malarial neuralgias, although most surely in 
those, but also in " idiopathic " neuralgias. It is in these cases that the remedy 
is given in large doses. We begin with fifteen to thirty grains (grammes 1-2) a 
day, best given in one dose, and in severe cases we may increase to sixty or sev- 
enty-five grains (grammes 4—5) or more. We see the best results from quinine in 
trigeminal neuralgia, while in other forms, as in sciatica, it is much less efficient. 
Beside quinine, salicylate of sodium is sometimes beneficial, especially in the 
rheumatic forms of neuralgia. Antipyrine, in fifteen- to thirty-grain (grammes 
1-2) doses, antifebrine, in three- to seven-grain (gramme 0.25-0.5) doses, phe- 
nacetine, in seven- to fifteen-grain (gramme 0.5-1) doses, salipyrine, in twenty- 
to thirty-grain doses (grammes 1.5-2.0), and similar remedies, have lately been 
very often used. Next in rank, for continued use, come arsenic and bromide of 
potassium. The former is given in pill form or as Eowler's solution, five drops 
three times a day, increasing gradually. Bromide of potassium acts only in large 
doses, forty-five to seventy-five or a hundred and fifty grains a day (grammes 3-5- 
10). Among the many other remedies which have been recommended in the past, 
but which at present are seldom used, we may mention here ergotine, internally 
and subcutaneously, oil of turpentine, oxide of zinc, valerianate of zinc, tincture 
of gelsemium, aconitine, phosphorus, subcutaneous injections of osmic acid, ten to 
fifteen minims (gramme 0.5-1) of a one-per-cent. solution, etc. 

In all severe neuralgias the use of narcotics, especially of morphine, is un- 
avoidable. Morphine is used almost exclusively during the attack, and is best 
given as a subcutaneous injection of one twelfth to one sixth of a grain (gramme 
0.005-0.01) in the vicinity of the painful part. The anodyne effect almost invari- 
ably follows, but in obstinate and protracted cases the patient gradually becomes 
accustomed to the remedy. We must then resort to still larger doses, and these, 
too, finally fail in their effect. Among the victims of the morphine habit we find 
many patients who have suffered or who still suffer from severe neuralgia, so that 
we must always be very cautious and conservative in the protracted use of mor- 
phine. We should be especially cautious before deciding to put the hypodermic 
syringe into the patient's own hand. Many physicians ascribe not only a pallia- 
tive but a permanent benefit to injections of morphine in neuralgia. We some- 
times see., in fact, that mild neuralgias recover under the exclusive use of mor- 
phine injections; but these are probably cases of spontaneous recovery. The 
internal use of morphine and opium preparations is decidedly inferior to the sub- 
cutaneous administration in certainty and rapidity of action. The external appli- 
cation of narcotic ointments, or embrocations, is much employed in practice, but 
it appears to be of advantage only in milder cases. We prescribe ointments with 
extract of opium (one to ten), extract of belladonna (two to ten), extract of 
opium and veratfine (one part of each to twenty of simple ointment), etc. We 
may also use chloroform, by applying blotting-paper wet with chloroform, or 
embrocations of chloroform oil, and ether as a spray. Chloral and also paralde- 
hyde are often prescribed in chronic neuralgias for their hypnotic effect. Croton 
chloral has been especially recommended in neuralgia. Other hypnotics, sul- 
phonal, etc., are also used. Finally, we must add that some physicians have 
praised the anodyne effect of subcutaneous injections of atropine, grain to 



810 



DISEASES OF THE NEKVOUS SYSTEM 



to to ! (grammes 0.0005-0.001-0.003 !) at a dose, sometimes even in cases where 
morphine does not act. 

In severe cases the surgical treatment of neuralgia is often of great impor- 
tance — the section of nerves, neurotomy, or the excision of a portion of the nerve, 
neurectomy — in order to prevent the union of the divided nerve, or, finally, the 
drawing out of the nerve — so-called exairesis. A detailed account of the meth- 
ods of operation is to be found in the text-books of surgery. We may state here 
merely that the surgical treatment of neuralgia, especially of severe trigeminal 
neuralgia, often has excellent results. The explanation of this success, however, 
is by no means easy. There is probably not only a break in conduction from the 
pain-exciting spot to the center, but an immediate or secondary change in the 
whole sensory neurone, by which the neuralgic change is made to cease. Of 
course a cure is not obtained in all cases. In any event, we should advise an 
operation only in severe cases, where all other remedies have been tried in vain, 
and the patient may be promised the possibility, or even the probability, of suc- 
cess, but never the certainty of it. Besides section of the nerves, nerve stretch- 
ing has lately been frequently tried in neuralgia. We will return to this method 
of treatment in speaking of sciatica. 

The chief question as to the use of baths arises only in the treatment of neu- 
ralgias in the domain of the nerves of the extremities, especially in sciatica, and 
therefore these and massage will be spoken of more in detail in connection with 
the separate forms of neuralgia. 

We see, then, that a large number of remedies are at our command in the treat- 
ment of neuralgia, and that the choice among them is not always easy. In any 
given case we look for the causal indication, and try to fulfill it if possible. In 
the many cases, however, where we fail to find this, we must first of all try to 
alleviate the pain, for which purpose, if external derivatives do not suffice, our 
most effective remedy is morphine. We must then lay out a special plan of treat- 
ment. We try electricity, or, if this be not practicable, one of the other remedies 
mentioned above. We put most trust in quinine and antipyrine, especially in 
fresh cases; among other remedies, in anaemic persons, arsenic, and, in more 
robust persons, bromide of potassium are of service. If all these and similar rem- 
edies give no aid, in proper cases we may still hope for success from operative in- 
terference, or else we must confine ourselves simply to a purely symptomatic 
treatment with narcotics. 



CHAPTER IV 
THE INDIVIDUAL FORMS OF NEURALGIA 

1. Neuralgia of the Trigeminus 

(Prosopalgia. Tic douloureux. FothergUVs Face-ache) 

JEtiology. — Trigeminal neuralgia is one of the commonest and most impor- 
tant neuralgias. In its origin many causes and predisposing factors of all sorts 
play a part, as was stated in detail in the preceding chapter. Many mild forms, 
especially neuralgia in the first branch, apparently are of acute origin and have 
no discoverable cause. In such cases some unknown infectious or auto-toxic 
influences may play a part. Not infrequently, especially in mild neuralgias of the 
first branch, we can not overlook the influence of exposure to cold (wind, wet) 
as a possible cause. Neuralgias after acute infectious diseases (influenza, 
typhoid), and especially malarial neuralgias, are situated most frequently in the 



THE INDIVIDUAL FORMS OF NEURALGIA 



811 



first branch of the trigeminus, more rarely in the second, and only exceptionally 
in the third. Trigeminal neuralgia may also be due to diseases of the cranial 
bones and periosteum, very often to diseases of the teeth (caries, exostoses, anom- 
alies of development and position of the teeth), and also to diseases of the nasal 
and frontal cavities and diseases of the middle ear and of the eye (inflammation 
and also strain of the eyes). Romberg found an aneurism of the internal carotid, 
pressing on the Gasserian ganglion, as the cause in a severe and incurable case. 
We have seen a precisely analogous case. Finally, the severe trigeminal neural- 
gias, which last for years, are of very great practical importance ; for these we can 
usually find no cause at all, or at most a general nervous predisposition. This 
form, which is the prototype of the genuine, severe, idiopathic neuralgias, comes 
on usually in somewhat advanced life, and is perhaps somewhat more frequent in 
women than in men. The special form of disease of the nerve in these cases is 
still wholly obscure. The few anatomical reports as to resected nerve branches 
and extirpated Gasserian ganglions (vide infra) are contradictory and capable 
of no positive interpretation. [Dana, Putnam, and others have found degenera- 
tive neuritis in the peripheral fibers of the excised nerve in these severe cases, 
sometimes associated with obliterating endarteritis in the blood-vessels supplying 
the nerves. Spiller has found extensive degenerative changes in the nerve-cells of 
the Gasserian ganglion, but these may be secondary to the changes in the nerve- 
fibers. — K.] 

Symptoms and Course. — The attacks of pain in neuralgia of the fifth pair are 
usually quite intense, and in severe cases they may attain a most distressing and 
terrible severity. They arise either entirely without cause, or from some slight 
influence, such as washing the face [making the slightest movement of the face in 
eating or talking. — K.], taking physical exercise, or mental excitement. They 
often come on quite regularly at definite hours, especially in the forenoon, but in 
other cases they follow no rule. There are sometimes long, painless intervals 
between the separate attacks, and sometimes the attacks follow one another in 
an almost uninterrupted series. The lightning-like, cutting pains extend to the 
distribution of the affected branch of the trigeminus, but they sometimes shoot 
into the occiput, the back of the neck, the shoulders, etc. We can often perceive 
reflex twitchings in the face, especially blepharospasm, and twitching of the 
corners of the mouth. The vaso-motor disturbances are noticed at first as abnor- 
mal pallor, but later usually as quite an abnormal redness of the face and con- 
junctiva. In neuralgia of the upper two branches we often see, during the attack, 
an unusually great secretion of tears. An excessive flow of saliva and an in- 
creased secretion from the nasal mucous membrane are more rare. Sometimes, 
but still quite rarely, we see herpetic eruptions in the course of the affected 
nerve, zoster frontalis, herpes of the conjunctiva, etc. In some cases, too, more 
severe diseases of the eyes, belonging to the category of neuroparalytic ophthalmia, 
have been observed, and also paralysis of the ocular muscles. Such complications 
always point to some gross organic lesion of the trigeminus and its neighborhood. 
In neuralgias that have lasted longer, we often see still further trophic disturb- 
ances : changes (thickening or atrophy) in the skin and subcutaneous cellular tis- 
sue, the hair turning gray or falling out in the frontal region, etc. 

Most trigeminal neuralgias are situated, not in the whole distribution of the 
nerve, but only in one or more of its branches (see Figs. 92 and 93, page 803). 
We accordingly distinguish: 1. Neuralgia of the first branch (ophthalmic neural- 
gia) which is especially frequent as supra-orbital or frontal neuralgia. The pain 
shoots chiefly from the supra-orbital foramen upward into the forehead, and 
sometimes to the region of the internal angle of the eye and the bridge of the 
nose (ethmoidal nerve) or into the zygomatic region (lachrymal nerve). In this 
we find, as a rule, that pressure on the point of exit of the nerve at the supra- 



812 



DISEASES OF THE [NERVOUS SYSTEM 



orbital foramen is more or less painful. More rarely we find painful points also 
on the nose, at the inner angle of the eye, or the parietal eminence, etc. 2. 
Neuralgia of the second branch (supra-maxillary neuralgia) is most frequent in 
the distribution of the infra-orbital nerve (infra-orbital neuralgia), with the chief 
painful point at the infra-orbital foramen, and others on the zygoma, on the 
upper lid, etc. The chief pain usually starts from the infra-orbital foramen, and 
is situated in the lower eyelid, the cheek, the upper jaw, the upper lip, and in part 
also in the temporal region. During the attack of pain tears are often seen in 
the eye. 3. Neuralgia of the third branch (infra-maxillary neuralgia) is situ- 
ated chiefly in the branches of the mandibular nerve (inferior alveolar and men- 
tal nerves). The pain affects the region of the lower jaw and the chin; but some- 
times the pain occurs in the temporal region, in the auriculotemporal nerve, and 
in some cases it is especially distressing in the tongue, in the lingual nerve. The 
chief painful points are at the mental foramen and the lower temporal region. 

The general course of neuralgia of the fifth pair differs very much in different 
cases. We see all forms, from the mildest, which rapidly passes off, to the sever- 
est and incurable types, which may drive the patient to despair. In general, 
neuralgia of the first branch usually belongs to the relatively milder forms ; neu- 
ralgia of the second, and especially of the third branch to the severer forms. 
The above-mentioned a epileptiform " neuralgia (the true tic douloureux) may 
last for years with slight interruptions; this occurs chiefly in the second and 
third branches. 

Diagnosis. — The diagnosis of trigeminal neuralgia is in general not difficult 
if only we consider the character and distribution of the pain, its occurrence in 
separate paroxysms, and the presence of any painful pressure points. Of course a 
careful local examination is always necessary to exclude the existence of inflam- 
matory or other diseases of the bones, periosteum, and teeth., Neuralgia of the 
first branch may be confounded with other forms of headache, and especially with 
true migraine (vide infra), since in the latter the pain is often located in the re- 
gion of the supra-orbital nerve. Only by a careful consideration of accompanying 
symptoms (scotoma, vomiting) can we avoid a mistake. In the severe neuralgias 
of the second and third branches the reflex muscular twitchings are very marked, 
so that, on very superficial observation, trigeminal neuralgia may be mistaken for 
clonic facial spasm ("tic douloureux" for "tic conv ulsif "). 

Prognosis. — The prognosis is never to be made with complete certainty. It is 
most favorable in fresh cases of supra-orbital neuralgia which have a manifest 
cause, which may be removed, as a basis ; but if the affection is due to a coarse 
anatomical cause which can not be removed, or if we are dealing with chronic 
cases, especially of the second or third branch, the prognosis, unfortunately, is 
often very doubtful or utterly unfavorable. 

Treatment. — The treatment of trigeminal neuralgia rests entirely upon the 
principles given in the preceding chapter. In searching for the causal indications 
we must look chiefly, in neuralgia of the second and third branches, for diseased 
teeth, and also in all cases for any affections of the nose, of the frontal sinuses, or 
of the middle ear. If such affections exist they should be treated in the appro- 
priate way. Carious teeth, which are painful and which seem to have any relation 
to the neuralgia, should always be removed; but we must warn patients against 
permitting in their despair all their sound teeth to be extracted by unskillful 
dentists without any benefit — a thing which we have frequently known to happen. 
If there be a suspicion of syphilis or malaria, we should prescribe iodide of potas- 
sium or quinine. [Even in non-syphilitic cases of the severer type large doses 
of iodide of potassium (grammes 2.0-6.0, grain 30-90, thrice daily) combined 
with mercury may act very beneficially. Aconitine is of some benefit. The 
application of the positive pole of the galvanic battery, wet with a ten- to twenty- 



THE INDIVIDUAL FORMS OF NEURALGIA 813 



per-cent. solution of cocaine, may give temporary relief (electrical cataphoresis). 
Dana has obtained good results from absolute rest in bed and daily injections of 
strychnine (grammes 0.001-0.004, grain -eVrV) f° r several weeks. — K.] 

In addition, in fresh " rheumatic " neuralgias, we should first try quinine, in 
doses of fifteen to forty-five grains (grammes 1.0-3.0) or more, or one of the many 
new " nervines " — antipyrine, antifebrine, phenaeetine, salipyrine, exalgine, etc. 
They sometimes act very favorabh T , but in other cases the action is uncertain. 
Mixtures of the above-mentioned drugs (antipyrine with phenaeetine, etc.) often 
act better than a single drug. Many other remedies, which were formerly often 
used in neuralgia, are at present only rarely prescribed; as, for example, butyl 
(croton) chloral, tincture of gelsemium, aconitine, etc. Arsenic is more fre- 
quently prescribed at present, with somewhat more prospect of benefit. 

Besides internal remedies, electricity is also to be considered. It is best given 
by applying the anode to the painful points of exit of the affected nerve and to any 
other painful points, while the cathode is held on the back of the neck. We 
should use weak currents and avoid any sudden variations in the current. Other 
methods (faradic brush) may also be tried. Massage has also been recommended 
for trigeminal neuralgia ; but in really severe cases neither massage nor electric- 
ity is of any permanent benefit. 

If a severe neuralgia persists in spite of rational treatment by electricity or 
drugs, we should not delay too long in proposing to the patient operative treat- 
ment if possible. In frontal and infra-orbital neuralgia especially neurectomy is 
a comparatively slight operation, which has many excellent results to show. 
Even in the severe and otherwise incurable neuralgias of the third branch neurec- 
tomy is sometimes attended with the best results. The full description of the 
technicalities of the operation, as well as the description of nerve-stretching 
(which is much less to be recommended), must be left to the text-books on sur- 
gery. We may add that Krause and others in very severe cases have extirpated 
the Gasserian ganglion successfully and with benefit. 

If we have to limit ourselves to a purely symptomatic treatment, injections of 
morphine become unavoidable in severe cases, but we should restrict their use 
as much as possible. The above-mentioned nervines have sometimes a symptom- 
atic action. We can sometimes lessen or shorten the paroxysm of pain by pres- 
sure on the nerve or by compression of the carotid. 

2. Occipital Neuralgia 

Of the neuralgias involving the sensory region of the upper four cervical 
nerves, neuralgia of the occipitalis major (Eigs. 92, 93) is relatively the most 
frequent and practically the most important. Besides the factors to be considered 
in all neuralgias, we must pay particular attention, in regard to aetiology, to dis- 
eases of the upper cervical vertebras — caries and new growths. The painful par- 
oxysms may attain the greatest severity. They are usually located in the two 
occipital nerves at once, although often more severe on one side than on the 
other. Painful points are most frequently found midway between the mastoid 
process and the upper cervical vertebras. Vaso-motor disturbances, falling out of 
the hair, etc., have been often observed. 

The prognosis depends upon the variety of the disease. In primary neuralgic 
affections it is generally favorable. In such cases, if fresh, a rapid recovery may 
often be brought about by salicylate of sodium, antipyrine, the constant current, 
or sometimes by strong cutaneous irritants to the back of the neck (blisters). In 
other cases, of course, which are due to some severe disease (vertebral caries, 
tumors, etc.), the prognosis is often utterly unfavorable, and treatment can be 
only symptomatic (morphine, etc.). 

Other neuralgias in the distribution of the cervical plexus are rare. They 



814 



DISEASES OF THE NERVOUS SYSTEM 



occur in the distribution of the occipitalis minor, when, according to Seeligmiil- 
ler, they are quite frequently due to syphilis, and are easily cured by iodide of 
potassium, and in the distribution of the great auricular and the supra-clavicular 
nerves. A phrenic neuralgia even has been described, in which the pain extends 
along the course of the phrenic nerve to the insertion of the diaphragm ; but this 
is at all events very rare. In these cases, as in many of the so-called visceral 
neuralgias, we probably mistake quite different forms of disease or hysterical 
symptoms for neuralgia. 

3. Neuralgia in the Region of the Brachial Plexus , 

{Cervico-brachial Neuralgia) 

Brachial neuralgia is, on the whole, rare, and it is hardly ever limited strictly 
to the distribution of a single nerve. In general, the radial and ulnar nerves are 
rather more frequently affected than the median. We also see at times neuralgia 
of the internal cutaneous nerve and other cutaneous branches, and neuralgia of 
the sensory branches of the axillary (circumflex) nerve. In regard to aetiology, 
we have to mention first wounds and contusions of the nerves, and also cicatrices 
and foreign bodies. The amputation neuralgias also belong to this class. Severe 
neuralgia in which the pain may extend over a greater part of the whole arm is 
sometimes seen after injury of the fingers (crushing, cuts, etc.). In some of 
these cases we may have to do with an ascending neuritis, starting from injury 
of a small nerve branch ; in other cases there are probably cicatricial contractions, 
thickenings of the neurilemma, or small neuromata developing after the injury, 
which excite the pains. The " amputation neuralgias," which are often very 
severe in amputation stumps, are due to neuromata which form on the cut ends 
of nerves. Severe neuralgia often arises from pressure on the brachial nerves, 
as in cases of tumors in the axilla or neck (cancer, etc.), aneurisms of the aorta, 
etc. Double brachial neuralgia should always excite suspicion of disease in the 
neighborhood of the upper posterior nerve-roots, especially of cervical pachy- 
meningitis, spondylitis of the lower cervical vertebra?, etc. 

If we except the neuralgias secondary to trauma and compression already 
described, true primary neuralgia in the region of the brachial nerves is very 
rare. We may sometimes, and most frequently, speak of neuralgia coming on 
after exposure to cold, although the distinction between this form of neuralgia 
and true neuritis (q. v.) is often very slight. If we hold less strictly to the con- 
ception of neuralgia and include also the " nervous " pains not limited to the 
region of one special nerve and not due to any other discoverable local disease, 
we may find such " brachialgias " more frequently. They come on chiefly as one 
symptom of hysteria or neurasthenia in persons with a nervous predisposition, 
and are often very obstinate and apparently severe. We must also pay especial 
attention to the patient's calling and occupation. In seamstresses, piano-players, 
persons who write much or do much other work with the arms supported, etc., 
we sometimes see quite severe brachialgia for which we can find no other cause — 
the so-called " occupation neuralgias." A general nervous predisposition also 
comes into play not infrequently in such cases. 

We must mention finally those brachialgias which are dependent upon arterio- 
sclerosis. In the true stenocardiac attack (vide page 343) the pain often shoots 
into the left arm. Many brachialgias, apparently associated with gout or diabetes 
mellitus, may also be dependent upon such vascular changes and the disturb- 
ances of nutrition caused by them in the peripheral nerves. 

We have little to add concerning the special symptomatology of brachial neu- 
ralgia. The pain, as we have stated, is usually ascribed to the whole course of the 
nerves without being very exactly localized. It is greater either in the upper arm 



THE INDIVIDUAL FOKMS OF NEURALGIA 



815 



or in the forearm and fingers. Painful points are sometimes found over the bra- 
chial plexus, over the radial nerve on the external surface of the upper arm, over 
the ulnar nerve in the sulcus at the internal condyle, over the median nerve at the 
inner border of the biceps, and where the cutaneous nerves emerge from the f asciae. 
Yaso-motor and trophic disturbances, such as " glossy ringers," a peculiar, shiny, 
atrophic condition of the skin of the fingers, eruptions of herpes, etc., are often 
seen in true organic neuralgias, and sometimes we also see a pronounced atrophy 
of the whole arm. The diagnosis of neuralgia as such is usually easy ; we must 
bear in mind only the risk of confusion with articular affections, and especially 
with beginning arthritis deformans. It is sometimes much harder to determine 
the cause of the neuralgia. This always requires a careful general investigation 
and close attention to all the conditions which may be involved. 

The treatment of brachial neuralgia is often no easy task, since we frequently 
have to do with protracted and obstinate diseases. The causal indications should 
be met if possible ; besides these we should make use chiefly of electricity (the de- 
scending galvanic current along the affected nerves). To relieve the pain we may 
also use salicylate of sodium, antipyrine, phenacetine, etc., and finally local 
warm packs, peat-baths, sand-baths, etc. We should be very guarded in using 
narcotics (morphine). If the brachialgia be associated with neurasthenia or 
hysteria, we can obtain success only by an appropriate general treatment with a 
psychical suggestive influence. In some severe cases of true neuralgia we must 
consider the possibility of surgical interference, such as nerve-stretching, the 
extirpation of cicatrices, etc. 

4. Intercostal Neuralgia 

(Dorso-inter costal Neuralgia) 

The neuralgias of this class are almost always pure intercostal neuralgias, 
since the posterior dorsal branches of the thoracic nerves are only exceptionally 
involved. The middle intercostal nerves, from the fifth to the ninth, are usually 
affected, one or more of them being attacked at the same time. The affection is 
much more frequent on the left side than on the right. 

In regard to aetiology, it is important to remember that obstinate intercostal 
neuralgias are often a symptom, and for a long time the only symptom, of severe 
organic disease, especially affections of the ribs ; diseases of the vertebras, such 
as caries, carcinoma, and actinomycosis ; diseases of the cord, such as tabes, me- 
ningeal tumors, syphilis, and aneurism of the aorta. Genuine idiopathic inter- 
costal neuralgia, however, is also met with, as well as these symptomatic forms, 
but, according to our own experience, less often than we might imagine from 
many of the statements. Intercostal neuralgia has been reported, especially in 
anaemic and nervous women, both in youth and middle age. Traumatic lesions 
of the intercostal nerves and taking cold also play a part in the aetiology. 

The pain in intercostal neuralgia may attain a remarkable severity, and it is 
usually increased by any considerable movement of the thorax. Hence the pa- 
tient avoids deep inspirations, coughing, loud talking, etc., as much as possible. 
We usually find three painful points — one near the vertebral column, one some- 
where in the middle of the nerve, and a third near the sternum or over the rectus 
abdominis. We may mention, among the trophic disturbances, the comparatively 
frequent occurrence of herpes zoster. In such cases we probably always have an 
actual neuritis of one or more nerves. The pain precedes the eruption of zoster, 
or comes on at the same time with it. It often lasts for a long time after the 
cutaneous affection has healed. The special method of origin of the zoster ves- 
icles is still obscure. Recent careful anatomical investigations (A. Dubler) 
favor the hypothesis that the formation of vesicles arises simply from a direct 



816 



DISEASES OF THE NERVOUS SYSTEM 



extension of the inflammatory process from the terminal branches of the nerves 
to the skin. The hypothesis of special trophic disturbances would therefore be 
unnecessary. It is worthy of note that the attacks of zoster often exhibit a cer- 
tain epidemic and sometimes even an endemic distribution, so as to suggest an 
infectious agency. The almost constant swelling of the neighboring lymph- 
glands, in the axillae, at the lower border of the pectoral muscle, etc., also favors 
the theory of the existence of a true inflammatory neuritis in herpes zoster. We 
can often find a slight diminution of sensibility on the skin between the individ- 
ual vesicles. 

The course of intercostal neuralgia depends chiefly upon the aetiology of the 
affection. Primary neuralgias are often quite obstinate, but on the whole they 
usually give a favorable prognosis. This is especially true of the intercostal neu- 
ritis associated with herpes zoster. The differential diagnosis between genuine 
intercostal neuralgia and rheumatic affections of the muscles, incipient pleurisy, 
etc., is not always easy. In these cases a careful physical examination, a con- 
sideration of the localization of the pain, of the presence of painful points, and of 
the whole course of the disease, are needed to protect us from errors. Steno- 
cardiac attacks (see page 343) are sometimes falsely regarded as intercostal neu- 
ralgia, and we must also remember that severe diseases of the vertebrae or the 
spinal meninges may at first assume the aspect of intercostal neuralgia. 

The treatment is governed by the general rules given in the previous chapter. 
Cutaneous irritants, mustard plasters, or blisters often act very well in fresh 
cases. Local anaesthesia (chloroform, ether), especially a spray of methyl or 
ethyl chloride, may occasionally be of benefit. Electricity is given by the faradic 
brush or the constant current ; with the latter, the cathode is placed on the verte- 
bral column, and the anode on the lateral and anterior painful points, using quite 
a strong stabile current. All the usual anti-neuralgics (antipyrine, phenacetine, 
exalgine, etc.) may be used internally. In severe cases we can not avoid injec- 
tions of morphine. Herpes zoster heals by simple treatment with lanoline or by 
dusting on powders, such as one part of zinc oxide to two of starch. 

Mastodynia {Neuralgia of the Mammary Gland). — Mastodynia ("irritable 
breast " of Astley Cooper) is to be considered as a special form of nerve pain 
in the distribution of the intercostal nerves. It occurs almost solely in women, 
after the age of puberty, although it may occur in men, and is a very painful, 
distressing, and obstinate affection. The pain is either continuous, or it comes on 
in separate paroxysms, sometimes accompanied by vomiting. The whole breast, 
or more frequently different parts of it, is extremely sensitive to the touch. We 
know little that is definite as to its aetiology. Anaemia, hysteria, and traumatic 
action seem to have some influence on it. We sometimes feel little nodules in the 
breast, which are very painful (tubercula dolorosa, neuromata?), and which may 
sometimes give rise to the suspicion that a carcinoma is developing. 

The disease may last for years. Treatment is difficult. Warm packs to the 
breast, bandaging the breast, and especially narcotics, may afford relief. Elec- 
tricity may be of decided service. In the worst cases operative interference has 
been attempted — amputation of the breast, or extirpation of the painful nodules 
— but its results are uncertain. Nageli highly recommends stretching of the 
whole breast en masse', the breast is seized with both hands and stretched and 
extended for several minutes with special regard to the tenderest points. 

5. Neuralgia in the Region of the Lumbar Plexus 
As the neuralgias of this class are rare, and show few peculiarities, we will 

content ourselves with a brief account of the most important forms. 

Lumbo-abdominal neuralgia causes pain in the lumbar region, which shoots 

into the buttocks, the hypogastrium, and the genitals. Crural neuralgia is seated, 



THE INDIVIDUAL FORMS OF NEURALGIA 



817 



in part, in the region of the external anterior cutaneous nerve of the thigh, and in 
part in the region of the cutaneous branches of the crural nerve, the internal and 
middle cutaneous. Its distribution over the cutaneous distribution of the great 
saphenous nerve, the inner portion of the calves,, and the inner border of the foot, 
is especially characteristic. In obturator neuralgia the pain extends along the 
inside of the thigh, down to the vicinity of the knee-joint (see Figs. 90 and 91, 
page 802). 

In their individual characteristics, all these neuralgias agree with what has 
been said in the previous chapter. The diagnosis is not always easy, and we must 
pay special attention to avoid confusing them with affections of the bones and 
joints, with lumbago, renal colic, etc. 

We must mention here a special symptom-complex, meralgia ■paraesthetica 
(Bernhardt, Roth), the chief symptoms of which are pain, paresthesia, and par- 
tial anaesthesia on the outer side of one or both thighs — that is, in the territory 
of the external cutaneous femoral nerve. Mechanical factors in particular (long- 
continued walking, the pressure of articles of clothing, hard work), or in some 
cases exposure to cold or acute infectious diseases, seem to excite this trouble, 
which is sometimes very persistent. The treatment consists of embrocations, 
electricity, baths, etc. 

6. Sciatica 

(Ischiatic Neuralgia. Ischialgia. Malum Coturinii) 

iEtiology. — Xext to trigeminal neuralgia, sciatica is by far the most fre- 
quent, and practically the most important form of neuralgia. The anatomical 
course of the sciatic nerve renders it especially exposed to mechanical injuries 
and the influence of cold. Many cases of sciatica are certainly due to such 
causes as over-exertion of the leg in hard work, sitting for a long time on an 
uncomfortable seat, exposure to wet and cold, etc. ; and this is why sciatica is in 
general far commoner in men than in women, and also much commoner in the 
laboring classes than in the higher classes. Certain ^etiological conditions may 
•of course provoke sciatica in women also, especially the pressure of the gravid 
uterus on the sacral plexus or mechanical injury of the plexus in difficult labor 
(forceps, etc.). Venous stasis in the pelvic veins (hemorrhoids) and habitual 
constipation more rarely seem to give rise to the development of sciatica. 

The relations of sciatica to certain constitutional and toxic general diseases 
are of practical importance. Thus a simple or even a double sciatica is not very 
Tare in diabetes mellitus, and it is sometimes seen in true gout (arthritis urica), 
in articular rheumatism, following syphilis or gonorrhoea, in alcoholic subjects, 
etc. We must also bear in mind the occurrence of apparently pure sciatic pain 
in tabes dorsalis. 

Symptomatic neuralgia in the region of the sciatic nerve is also seen in pelvic 
tumors, caries of the sacrum, and similar diseases. 

Symptoms and Course. — Sciatica takes a somewhat different position from 
the other forms of neuralgia, since the sciatic pain does not usually show the 
special characteristics of true neuralgia in a fully pronounced fashion. In par- 
ticular, the individual paroxysms of pain are rarely so pronounced and so inter- 
rupted by free intervals in sciatica as is the case, for example, in many trigem- 
inal neuralgias. Although an increase or a diminution of the pain is common in 
sciatica, the pain on the whole gives us more definitely the impression of a per- 
sistent neuritic pain, and we can therefore scarcely be mistaken if we consider 
the anatomical cause of most cases of ordinary sciatica to be an actual sciatic 
neuritis. 

The pain usually begins in the lumbar and sacral regions and then gradually 
passes downward, following the course of the sciatic nerve, through the gluteal 
52 



818 



DISEASES OE THE NEKVOUS SYSTEM 



region and the posterior surface of the thigh to the hollow of the knee, and then 
down to the peroneal region (outer part of the leg, outer edge of the foot, and 
back of the foot), or more rarely to the tibial region (sole of the foot). The 
accuracy with which many patients point out with the finger the distribution of 
the pain, corresponding accurately to the anatomical course of the nerve, is a most 
characteristic feature for the diagnosis of sciatica. Individual cases, however, 
differ considerably, since at times the pain is felt to a marked degree only in the 
upper portion and hardly extends at all to the lower leg, while in other cases the 
severest pain is felt below the knee. This is probably due to the fact that the 
neuritis, which is the cause of the pain, affects one or another part of the nerve,, 
being chiefly either in the upper root portion or in the terminal branches. The 
pains themselves are rarely described by the patients as " darting," but more com- 
monly as " burning,*' " boring," etc. The pain is 
often worse at night than during the day. It is in- 
creased by different movements of the leg, by an 
uncomfortable position, by pressure, by cold, etc. 
Patients with severe sciatica are therefore almost 
completely bedridden, and they can take a few un- 
aided steps only with the greatest pain. If we make 
the patient stand, there is often, but of course not 
always, a very characteristic way of holding the 
body. In order to take the weight of the body off 
the affected, tender leg, the trunk is bent over to 
the opposite side, and the spine thus becomes 
scoliotic, the convexity being usually toward the 
healthy side (sciatic scoliosis, see Fig. 94). 

If we examine the affected leg more closely, 
we shall notice first the sensitiveness of the sciatic 
nerve to direct pressure. This is often not so great 
as we might expect, probably because the upper part 
of the nerve, which is not so easily accessible to 
pressure, is chiefly affected; but we frequently find 
the nerve itself quite sensitive to pressure in the 
middle of the gluteus or at its lower border, in the 
hollow of the knee, or at the head of the fibula and 
elsewhere. If the patient be in a lying or sitting 
position and the thigh be strongly flexed, passively, 
on the trunk, while the lower leg is at the same 
time kept extended, the procedure gives rise to a 
gluteal pain which is characteristic. By this ma- 
neuver the sciatic nerve is apparently irritated by 
being stretched so much. Among the other nervous 
disturbances we may mention an actual paresis of 
the muscles supplied by the sciatic nerve (for ex- 
ample, the flexors of the lower leg) ; this is rare, 
and, as a rule, indicates more deeply-seated disease. 
The muscular hypertonicity (in part of reflex ori- 
gin) is more striking; it sometimes takes the form 
of actual tremor or twitching of the painful leg. A peculiar muscle-wave (the 
so-called "myokymia") is also seen in sciatica. The patellar reflex is usually 
unchanged ; but in severe sciatica we have quite frequently, although, of course, 
not always, seen the gastrocnemius reflex, obtained by striking the Achilles ten- 
don, absent on the affected side ; this is of value in diagnosis. [The patellar reflex 
is often somewhat exaggerated on the affected side in the early stages of sciatica,. 




Fig. 94. — Sciatic sc< 
sciatica, (Personal observation.) 



THE IXDIYIDUAL FOBMS OF KEUKALGIA 



819 



and diminished in the later stages. — K.] On careful examination we sometimes 
find a slight disturbance of sensibility, but it is very rarely marked. In long-con- 
tinued cases there is almost always a very noticeable atrophy of the affected leg. 
The circumference of both the thigh and calf is usually several centimetres less 
on the affected side than on the healthy side. This atrophy is possibly connected 
with vaso-motor disturbances, for the skin of the affected leg often feels decidedly 
cooler than that of the healthy side. The atrophy, however, is due mainly to the 
inactivity of the painful leg. [In a considerable number of cases quantitative 
or qualitative changes in the electrical reactions are found on the affected side. 
This would indicate that the atrophy was degenerative in character, due to neu- 
ritic changes in the nerve. — K.] 

Sciatica rarely lasts less than several weeks, and in many cases months or 
even years may elapse before the pain entirely disappears and the leg completely 
regains its normal usefulness. The course, however, often shows very marked 
variations. In simple sciatica (not due to some other underlying disease) the 
final outcome is usually favorable. We must bear in mind, however, that the 
disease has a marked tendency to recur, so that any one who has once had sciatica 
must avoid with special care all exposure which may cause a return of the suffer- 
ing. The general course of symptomatic sciatica is of course dependent mainly 
upon the nature of the underlying disease. 

Diagnosis. — The diagnosis of sciatica is easy in the majority of typical cases, 
but it may sometimes be quite difficult. It is chiefly confused with lumbago, an 
acute coxitis, nervous coxalgia (vide infra), and psoas abscess. Even when the 
diagnosis of sciatica as such is definite, we must always consider with care the 
patient's general condition to determine whether we are dealing with a simple 
primary sciatica (primary sciatic neuritis) or with a symptomatic sciatica fol- 
lowing some other underlying disease. In the section on setiology above we 
have mentioned the possibilities which the physician must especially bear in mind. 
In cases where there is a suspicion of simulation (as in accident cases), we must 
note the accurate localization oi the pain and the tender points, and especially 
the objective symptoms, the almost invariable wasting of the affected leg, and the 
frequent absence of the Achilles tendon reflex. 

Treatment. — In ordinary primary sciatica and in fresh cases we usually begin 
with " anti-rheumatic " treatment. The patient should be put to bed and kept 
warm. We ourselves have treated many cases of sciatica with very good results 
by methodical sweating (hot-packs, hot-air baths). Internally, we would first 
prescribe salicylate of sodium, antipyrine, salipyrine, or phenacetine, from which 
we often obtain at least an improvement in the symptoms. We have never seen 
any good effect from oil of turpentine, which is often used in England. We have 
as little faith in the injections of osmic acid which are recommended (vide page 
809). "Local derivatives," especially blisters along the nerve, are at present 
somewhat out of fashion, but we have often seen decided benefit from blisters, 
and we therefore use them quite frequently in obstinate cases. Warm fomenta- 
tions, a Priessnitz's bandage about the entire leg, etc., usually give relief, and 
also embrocations with chloroform oil, a spray of chloride of methyl, etc. If the 
pain is very severe, so that sleep is constantly disturbed, we must use narcotics, 
especially subcutaneous injections of morphine. The author has not been able to 
bring himself to employ methodical treatment by morphine injections, as has been 
recommended from many sides. 

Of other methods of treatment, besides those already mentioned, we may con- 
sider electricity, massage, nerve-stretching, and baths. 

In electrical treatment we usually employ quite strong descending currents, 
with large electrodes, which we let act on the nerve for five or ten minutes a day, 
while we include one portion of the nerve after another in the current. Where 



820 



DISEASES OF THE NERVOUS SYSTEM 



there is muck stiffness in the leg-, we open and close the current a few times, in 
order to excite muscular contraction. Many cases are suitable for the use of the 
faradic current, especially for the wire brush. Besides electricity, massage has 
often given excellent results in sciatica. Details of the technique to be employed 
may be found in the special treatises on this important method of treatment.* 

Baths (douches, rubbing) are beneficial in most cases of persistent sciatica. 
The regular use of simple warm baths (half an hour daily at a temperature of 
27°-28° B. [93°-95° E.]) is of benefit, especially when combined with massage 
or electrical treatment. We see still more favorable results at certain bath cures, 
especially in Wiesbaden and also in Wildbad, Teplitz, etc. Peat-baths, and espe- 
cially hot sand-baths (Kostritz, Blasewitz), may have a good effect. 

Operative nerve-stretching may be tried only in very old and very obstinate 
cases. In some cases it has been attended by benefit. We have repeatedly em- 
ployed bloodless nerve-stretching with satisfactory results. This is done by put- 
ting the patient on the back and then passively flexing the thigh against the trunk 
as much as possible, and keeping it there for two or three minutes each day. 
[This may be done, if necessary, under ether. If the lower leg be kept extended 
the stretching is greater. — K.] 

It is very important always to pay attention to the general as well as the 
local treatment, in order to remove any active causative conditions. A change 
in the mode of life, avoidance of rheumatic, toxic, and mechanical injuries, regu- 
lation of the bowels, etc., are sometimes attended by visible results. Any under- 
lying diseases must of course be especially treated (iodide of potassium in syphi- 
lis, anti-diabetic treatment, etc.). 

[Mention should be made here of a method of treatment advocated by Weir 
Mitchell, which is occasionally useful in other forms of neuralgia as well as in 
sciatica. It consists in absolute rest of the affected limb by application of a splint. 
With this he combines the application of cold, by an ice-bag over the length of the 
nerve, which may be continued for a number of hours. — K.] 

7. Neuralgia of the Genitals and the Bectal Begion 

Neuralgic affections of the parts named are not frequent, but still a number of 
cases have been described by different observers. Of course most of these obser- 
vations are of ancient date and many of them are at present perhaps to be ex- 
plained in some other way. 

The pain in these cases has its seat either in the external genitals, or in the 
urethra, or in the anal and perineal region. The most frequent form is spermatic 
neuralgia ("irritable testis" of Astley Cooper), in which there is the most in- 
tense pain in the spermatic cord and the testicles, which is almost always asso- 
ciated with an extreme hyperesthesia of the affected parts. The treatment of 
this form of neuralgia by narcotics and electricity is often unsuccessful, so that 
in severe cases resort has sometimes been had even to castration. In women, 
genuine uterine and ovarian neuralgia does occur, but most cases are either symp- 
tomatic neuralgia or a manifestation of hysteria. 

Coccygodynia is the name of a form of severe pain in the coccygeal region, 
seen usually in women, which is much increased by walking, defecation, etc. The 
affection is so distressing that operations have been repeatedly performed on ac- 



* Busch, " Allgemeine Orthopadie, Gymnastik u. Massage," Leipsic, Vogel, 1882 ; Schreiber, 
"Praktische Anleitung zur Behandlung durch Massage," Vienna, 1883 [translated by Mendelson, 
Philadelphia, 1887] ; Reibmayr, "Die Massage und ihre Verwerthung in der prakt. Medicin," Vienna, 
1883; Hunerfauth, " Handbuch der Massage," Leipsie, 1887, etc. [Graham, "A Treatise on Massage," 
New York, 1890 ; Eccles, " The Practice of Massage," London, 1895 ; Kleen, " Handbook of Massage " 
(translated by .Hartwell), Philadelphia, 1892]. 



THE INDIVIDUAL FORMS OF NEURALGIA 



821 



count of it to remove or to cut around the coccyx. We have twice seen this same 
symptom as a complication of tabes. 

8. ACHILLODYNIA. TALALGIA. TARSALGIA. METATARSALGIA 

For practical reasons we will mention briefly here a number of peculiar and 
often very painful affections of the feet. 

Achillodynia is the name given to a pain at the insertion of the Achilles 
tendon, which is often very obstinate and a hindrance to walking. The trouble 
often seems to be connected with gonorrhoea, in other cases with gout, injury, 
over-exertion, hysteria, etc. We can sometimes make out a slight local swelling, 
but often there is no objective change. The treatment consists of rest, inunction 
of mercurial ointment, warm baths and packs, attention to any existing under- 
lying disease, etc. 

Pain in the heel is called talalgia or tarsalgia. Mechanical causes (long- 
continued standing or walking, the pressure of boots, etc.) often seem to be of 
significance, but sometimes we can not discover any cause. We must of course 
always consider inflammatory changes, flat-foot, etc. Baths, massage, and gal- 
vanism are most to be recommended. 

Metatarsalgia (nevralgie metatarsienne, Morton's disease) is an extremely 
distressing and severe pain, chiefly in the neighborhood of the fourth and fifth 
metatarso-phalangeal joints. The trouble is observed especially in women in mid- 
dle life, and it may be sometimes connected with wearing ill-fitting shoes. In 
other cases injury, gout, etc., are regarded as causes. [It is often due to the pres- 
sure upon the nerve between the two phalangeal ends of the metatarsal bones, and 
it may be relieved by pressure upon the tarsal ends, which causes the phalangeal 
ends to separate. — K.] The treatment consists of prescribing proper shoes, rest, 
local fomentations, baths, etc. In some severe cases the painful bones have been 
resected with success. 

There are also other forms of pain in the feet besides these mentioned, which 
are usually hard to explain. Hysterical conditions certainly play a part in some 
cases, and are to be taken into account in treatment, but in other cases we often 
have to deal with mechanical and inflammatory conditions which are hard to 
remove. 

9. The so-called Articular Neuralgias (Articular Neuroses) 

Neuralgia of the joints, first described by the English physician Brodie, was 
first generally known in Germany after Esmarch proved, by publishing many 
observations, that apparently severe and very painful diseases of the joints are 
often found, which are due to no discoverable anatomical disease of the joint, and 
which we are therefore justified in regarding as nervous affections. Since the 
localized pain in the joint is the chief symptom in most of the cases of this class, 
the somewhat unfit term " neuralgia of the joints " has been chosen, although we 
do not find here, as a rule, such typical and paroxysmal attacks of pain as in gen- 
uine neuralgia, and although, too, a number of other symptoms are usually pres- 
ent, which do not occur in genuine neuralgia. 

We see neuralgia of the joints chiefly in nervous persons disposed to hysteria, 
and therefore more frequently in women and girls than in men, but it is also quite 
common in children. We can very often make out a psychical cause for the 
origin of the disease. The affection is often caused by injuries which affect the 
joint, and which would be in themselves without significance, if they were not 
associated with a decided fright, and did not direct the patient's thoughts to the 
affected limb. Articular neuralgias do not, therefore, belong to the pure neural- 
gias, but are symptoms of hysteria (traumatic hysteria). 



822 



DISEASES OF THE NEKVOUS SYSTEM 



Either immediately after such an occurrence, or often only some weeks later, 
the patient begins to complain of pain. The knee- or hip-joint is almost always 
affected, only rarely the joints of the upper extremity. The pain is continuous, 
but it is more severe at times, especially on motion, or mental excitement. At 
other times, especially if the patient's attention be diverted from the trouble, it 
seems to diminish to a considerable extent. It is localized mainly in the joint, but 
the whole leg is often painful. The patient is usually very sensitive to pressure or 
jarring, and sometimes we may even discover some painful points on pressure 
over the joints. The patient can not walk at all, or at least walking is very pain- 
ful, and she limps badly. In severe cases, especially if the excessive sympathy of 
those about her reduces the patient's power to resist her suffering, she becomes 
completely bedridden for weeks or months. There is usually a decided weakness 
in the affected leg, which is almost always associated with great muscular rigidity 
and tension. The leg is extended, or flexed, and rotated inward, in just the same 
way as in genuine coxitis. 

The diagnosis of articular neurosis is often quite difficult, but it is almost 
always possible, with long observation of the case. At first, of course, the disease 
often seems to be a severe affection of the joint, on account of the great pain, the 
rigid position, and the complete inability to use the leg. The experienced physi- 
cian, however, is usually struck by the absence of any definite physical changes in 
the joint, especially of swelling, and also by the changes in the intensity of the 
complaint, by the influence of mental emotion on the suffering, and finally by the 
general impression he gets from the patients, the way they behave, and the con- 
trast between their evidently exaggerated complaint and their usual (though, of 
course, not invariable) good appearance, appetite, and undisturbed sleep. If the 
patient's attention be diverted, the same pressure on the joint, which before was 
unendurable, is not even felt. In doubtful cases an examination under chloro- 
form is very advisable. With this, contractures apparently the most severe van- 
ish, and the normal character and mobility of the joint become plainly manifest. 

As soon as the diagnosis of an articular neurosis is made the treatment has 
quite definite indications. All embrocations, poultices, bandages, .etc., are to be 
laid aside. The patient is to be brought to the conviction that the pain is de- 
pendent only upon the morbid anxiety, and that walking is indeed quite possible if 
she will only first learn to will to walk again. We therefore make the patient 
practice walking methodically ; these attempts at first prove very poor and appar- 
ently distressing to the patient, but they often lead very speedily to better results. 
These exercises are very much aided by electrical treatment of the joint, passing a 
strong current through it or using the faradic brush, and also by local cold 
douches and massage. Under some circumstances the use of internal remedies 
may be indicated, in many cases with regard only to the mental condition. We 
give iron to anaemic patients, and also the nervines. (See the chapters on hys- 
teria and traumatic neuroses.) 

10. Acroparesthesia 

Certain symptoms of sensory irritation, to which F. Schultze has given the 
name of " acroparesthesia," have only of late years aroused general attention 
(Laquer and others), although they have long been familiar to all experienced 
physicians and have been repeatedly described in medical literature. It is, in fact, 
quite a common complaint, the chief symptom of which consists of an unpleasant 
and often even very painful sensation at the tips (aKpa) of the extremities, 
especially in the hands, finger-tips, feet, and toes. This sensation is almost 
constant, or at least it recurs very frequently. 

The trouble usually appears in middle life, and it is said to be somewhat more 
frequent in women than in men. In many cases we can find no special cause, but 



THE INDIVIDUAL FOEMS OF NEUEALGIA 



823 



sometimes we can discover certain injurious influences which have affected the 
hands or feet, such as past exposure to cold, freezing, much washing in cold 
water, fatiguing mechanical occupations, chemical irritants, etc. 

The abnormal sensations are usually described as darting, prickling, tearing, 
etc. Their chief seat is, as has been said, in the fingers and finger-tips. Both 
hands are usually affected, but the trouble is often more pronounced upon one 
side than upon the other, and certain fingers of the same hand are sometimes 
more painful than others. The feet (toes) are more rarely affected than the 
hands; in such cases venous stasis (varicose veins) seems to us to have a certain 
significance in the aetiology. We must also consider arterio-sclerotic changes in 
the vessels (see page 373). The pain is not equally severe at all times; it is 
often worse at night and toward morning, ceasing during the day. 

If we examine the hands or feet closely we can sometimes detect no objective 
abnormality, but in many cases certain " vaso-motor " phenomena are first of all 
manifest. The painful parts are cooler and more cyanotic than under normal 
conditions, but we have also seen very obstinate cases in which the hands usually 
felt hot and sweated constantly and profusely. The sensibility is normal, or there 
may be in some parts a very slight blunting of tactile sensibility, or more rarely 
a marked hyperesthesia to touch. Motion, as a rule, is undisturbed, but many 
patients complain of a certain stiffness of the hands. In general, however, it is 
the pain, often very severe, which limits the usefulness of the hands, and often 
.greatly disturbs the patient's work. There are no special changes in the reflexes. 
In some cases we have seen very marked trophic changes, especially a manifest 
smallness and tapering of the terminal phalanges, marked curving of the nails, 
a shininess of the skin (glossy skin), etc. A short time ago in a very obstinate 
case, which had lasted for years, we saw torpid ulcers develop on the toes without 
any external cause ; they were very painful and showed no tendency at all to heal. 

The course of the disease is in some cases benign, recovery taking place after 
several months ; but in many other cases acroparesthesia is a very obstinate, 
chronic condition, lasting for years, and, in spite of its lack of danger, causing 
the patient great discomfort and distress. 

Nothing definite is known as yet as to the nature and special origin of the 
disease. It is generally assumed that it is an irritative condition of the sensory 
terminal nerve-fibers and terminal apparatus — that is, that it is a purely periph- 
eral trouble ; but it is still uncertain whether we have to do with a primary dis- 
ease of the nerves themselves or with a disease of the smallest terminal arteries 
and consequent circulatory disturbances with their sequelae. 

The diagnosis of acroparesthesia is in general easy, since the picture of the 
disease is in fact very characteristic ; but we must always bear in mind that such 
paraesthesiae sometimes occur as symptoms or precursors of organic central dis- 
eases (for example, as precursors of apoplexy, in other brain diseases, in tabes, 
diabetes, etc.). 

Symptomatic treatment is all that is possible, and in this regard the local use 
of electricity, especially the faradic brush, seems to give the best results; but the 
constant current, electrical hand-baths, etc., are sometimes of benefit. Experi- 
ence must decide in the individual case as to the influence of thermic procedures 
(warm and cold hand-baths, cold douches, the Scotch douche, etc.). Besides local 
treatment, we must also pay attention to the patient's general condition (iron, 
quinine, arsenic in anaemia, etc.). [Drugs which act upon the blood-vessels, such 
as ergot, nitroglycerine, or the nitrites, are sometimes of service. — K.] 



824 



DISEASES OF THE NERVOUS SYSTEM 



CHAPTER V 

HABITUAL HEADACHE 

( Cephalcm. Cephalalgia) 

In addition to the neuralgias, we must speak here of habitual or " nervous " 
headache, an affection which is very often met with in practice, but in regard to 
whose precise causes or whose special nature our knowledge is still in many re- 
spects very unsatisfactory. 

We do not term the symptomatic headaches, so often observed, " nervous head- 
aches." The former come on in acute febrile infectious diseases, in pronounced 
general anaemia, in the different anatomical diseases of the brain and its mem- 
branes, of the skull, the frontal sinuses, etc. Just as little ought we to confuse 
habitual headache with other painful and well-characterized affections, especially 
typical neuralgia in the frontal branch of the trigeminus, or in the occipital 
nerves, or with genuine migraine or hemicrania {vide infra). The cases which 
belong to this class are rather those in which the headache forms to a certain de- 
gree a disease in itself, and is the sole, or at least the chief, symptom of which 
the patient complains, and for which he seeks aid. We know no definite ana- 
tomical basis for them. We usually assume disturbances of circulation and of 
the fine nutrition as the special causes of headache ; but the nature of these 
changes is still wholly unknown. We can also state little that is definite as to 
the special place where these pains arise. We do not know positively whether 
painful irritations may arise in the brain-substance itself. In case pain should 
be produced by irritation of the sensory parts of the brain, it would probably not 
be felt in the head, but it would be projected toward the periphery of the body. 
The cerebral meninges, however, especially the dura mater, are decidedly sensi- 
tive, and hence they may usually be regarded as the special seat of headache. 

The manifold character of the circumstances under which headaches arise 
renders it probable that the causes of headache are very different in different 
cases. We have to do either with persons who seem perfectly healthy in other re- 
spects, or with weak and anaemic people, or again with robust, very well nour- 
ished, " full-blooded " persons with red faces. Hence we look for the cause of the 
pain, according to the general constitution of the patient, either in an abnormal 
hyperaemia or in an anaemia of the brain and its membranes — hyperaemic or anae- 
mic cephalalgia. We very often find headache, too, as the chief symptom in nerv- 
ous, neurasthenic people — neurasthenic cephalalgia. To this class belong espe- 
cially people who are overworked physically and mentally — scholars, officials, 
students before an examination, etc. If we believe that we can make out " rheu- 
matic " influences, such as taking cold, or toxic influences, such as alcohol, nico- 
tine, or chronic lead poisoning, we speak of a rheumatic or a toxic cephalalgia ; 
but, strictly speaking, " rheumatic " headache is probably not a nervous headache 
at all, since it seems to be in many cases, at least, a slight rheumatic inflammation 
of the external soft parts of the head. Patients with habitual headache often 
suffer at the same time from chronic gastric disturbances or habitual constipa- 
tion, so that the latter disorders, in many cases, stand perhaps in a causal rela- 
tion (toxic influences?) to the headaches. Finally, it is a very important point 
that headache is sometimes associated with chronic diseases of neighboring 
organs, especially of the nose, the naso-pharynx, and the ear. In very many 
cases, however, we can find no definite cause at all for the affection, so that we 
have to do with a genuine idiopathic disease. Habitual headache, existing from 
childhood, is certainly in most cases the expression of a general " nervous con- 
stitution," which is due to congenital conditions which of course are still wholly 



HABITUAL HEADACHE 



825 



unknown in their details. Habitual headache, therefore, is often an hereditary 
disease. [One of the frequent causes of persistent hea-dache is eye-strain, due 
to the persistent unconscious effort of the muscles of accommodation to over- 
come some error of refraction, such as astigmatism or hypermetropia. The pain 
is often referred to the frontal region, and it is brought on or made worse by 
using the eyes for near work. In some cases this eye-strain may be associated 
with insufficiency of some of the external muscles of the eye. This condition may 
be associated with normal visual power, so that the patient often maintains that 
there can be no trouble with the eyes ; this is especially true where the refractive 
error is slight, less than one dioptric. It is therefore essential, in every case of 
persistent headache, to have a thorough examination of the eyes, in order to 
determine whether there is astigmatism or hypermetropia. The adjustment of 
proper glasses, or, in rare cases, tenotomy of some of the external muscles, will 
often give marked relief, although even in these cases attention must also be 
paid to the general condition. In many cases the error of refraction is but one 
out of many causes which give rise to the headache, so that we should never be too 
confident in our prognosis of cure, and we should also never be content with find- 
ing a single cause, but we should search for all possible causes. Referred pains in 
the head from disease elsewhere have been spoken of on page 806. — K.] 

Habitual headache is always a chronic disease. It may last for months or 
years, or even through the whole life, either being present continually, or, what 
is more frequent, coming on in separate attacks and lasting several hours or days. 
These attacks sometimes come without any evident cause, but they may often 
be referred to definite influences, to mental excitement, physical exertion, errors 
of diet, etc. The pain is felt either in the forehead or in the occiput, or some- 
times over the whole head. It is sometimes limited to a definite and quite sharply 
defined part of the head. The precise form of the pain is described in different 
ways, either as boring, or tearing, or as if the head were pressed together from 
without, or as if it would split open. In many cases the intensity of the pain is 
not great ; there is merely a dizziness and a feeling of " pressure " in the head, 
but in other cases the pain is very severe. In such cases there is also at times a 
pronounced hyperesthesia of the skin of the head, so that it may cause pain even 
to touch the hair. 

The general health is almost always disturbed in headache. The patient can 
not work, he is often ill-tempered and irritable, and he loses his appetite. We 
sometimes see more marked gastric symptoms, especially nausea and vomiting 
(transition forms to migraine, q. v.), and sometimes copious perspiration. Severe 
cases of the disease are of great importance, since by an attack the patient is 
rendered almost wholly unable to attend to his business. For many women, espe- 
cially, habitual headache is a factor which dominates their whole life as a re- 
straint and disturbance. 

The treatment of headache is a very difficult and usually a thankless task. In 
the first place, of course, we should try to adapt our treatment to the aetiology of 
the disease if it is evident. We should therefore never neglect to make a thor- 
ough examination of all the organs which are to be considered (nose, ear, stom- 
ach, heart, kidneys, [eyes], etc.), and pay especial attention to any existing under- 
lying diseases (syphilis, gout, alcoholism, organic nervous disease, etc.). The 
general physical constitution also requires the greatest attention. For anaemic 
patients we prescribe iron, arsenic, a country residence, strengthening diet, etc. 
We order full-blooded persons, especially if they also suffer from indigestion, to 
follow a restricted diet, to have gymnastic treatment, or to drink bitter waters, 
or we send them to such health-resorts as Marienbad or Carlsbad. Nervous head- 
aches in hysterical and neurasthenic patients require, above all, a rational gen- 
eral treatment : mental treatment, a regulation of their mode of life, cold-water 



826 



DISEASES OF THE NERVOUS SYSTEM 



cures, electricity, general faradization, galvanism to the head or to the sympa- 
thetic, etc. Eor persons who suffer from nervous headache in consequence of 
excessive mental strain and excitement, we most urgently advise complete physi- 
cal and mental rest for a long time. We send them to the country or make a trial 
of sea-bathing. 

The number of symptomatic remedies recommended to relieve headache is 
very considerable. In most of the tedious cases the patient himself has learned 
to know his disease perfectly well. Many know that there is no remedy for 
" their old headaches," and they merely desire to rest, waiting until the pain 
ceases of itself. Others have become accustomed to employ certain domestic 
remedies : they put poultices on the head, take a cold or a hot foot-bath, put a 
mustard plaster to the back of the neck, bathe the forehead with cologne-water, 
use a menthol pencil, bind a towel tightly about the head, drink strong tea, 
smell ammonia or " smelling-salts," etc. We sometimes see good results, although 
frequently we do not, from the internal remedies. These may be used, either 
during the attack or for a longer period, to prevent the return of the pain. A new 
remedy often works well, but the benefit is not lasting. There are no special 
indications for the different remedies, so that we must try to see which one is 
the most efficacious. Antipyrine is most used of late in doses of seven to twenty 
grains (gramme 0.5-1.5). Its efficacy in migraine is undoubted, but it sometimes 
gives distinct relief in other forms of headache. We may also use antifebrine, in 
doses of three to seven grains (gramme 0.25-0.5), phenacetine, seven to fifteen 
grains (gramme 0.5-1), and quinine, five to twelve grains (gramme 0.3-0.75). In 
" rheumatic " headaches which come on after exposure to cold, draughts, etc., 
we may try sodic salicylate, half a drachm to a drachm (grammes 2-4). It is of 
practical importance that a mixture of these remedies (for instance, equal parts of 
antipyrine and phenacetine) is often more efficient than a single remedy by itself. 
Of other drugs we may mention paullinia serbilis (guarana, which contains caf- 
feine), in seven- to thirty-grain powders (grammes 0.5-2), three to six one-grain 
ergotine pills (gramme 0.05) a day in hypersemic headache, potassic bromide half 
a drachm to a drachm (grammes 2-4), arsenic, [cannabis indica, caffeine], etc. 

Electrical treatment (vide supra) has given decidedly good results in many 
cases, although the mental factor perhaps plays the chief part here. We must 
always begin electrical treatment with great caution, and try first what method 
is best borne. Cold-water cures, too, are sometimes beneficial, as we have said 
above, or residence in the country, at the seashore, or in the mountains. 

We can sometimes do the patient good service with the remedies mentioned, 
but in other cases the evil obstinately defies all attempts at cure. Then, however, 
the patient has still the encouragement left that the disease often ceases at last 
spontaneously in advanced age, after lasting years and years. 



CHAPTER VI 
ANOMALIES OF THE SENSE OF SMELL 

Anomalies of smell, which depend upon a disease of the olfactory nerve itself, 
of its terminal apparatus, or of its central termination, are not infrequently 
observed, but they have no great practical interest. It is well known that only 
the upper two turbinated bones and the upper part of the septum of the nares, the 
olfactory region, are supplied by fibers of the olfactory nerve. The odors excite 
the special olfactory cells which lie between the epithelial cells. The processes 



ANOMALIES OF THE SENSE OF TASTE 



827 



of these cells — that is, the olfactory nerves — pass through the openings of the 
lamina cribrosa to the olfactory bulbs in which they split up. The ganglion cells 
of the bulb form neurones of the second order for the olfactory tract. Their 
nerve-fibers pass through the olfactory tract to the brain. The fibers for smell 
either enter into relation with the optic thalamus or terminate in the cortex of 
the uncinate gyrus and the cornu Ammonis. A part of the olfactory fibers, how- 
ever, undergo a decussation in the anterior commissure. The fornix and the 
corpora albicantia have also relations with the olfactory apparatus, which in 
man is only a poorly developed organ, while in many animals it has a very de- 
cided morphological development. 

In testing the sense of smell, we use substances which do not at the same time 
irritate the sensory fibers of the trigeminus in the nasal cavity. The best sub- 
stances to use are cologne-water, ethereal oils, such as oil of cloves or oil of berga- 
mot, oil of turpentine, camphor, musk, valerian, asafoetida, etc. 

Hyperesthesia of the sense of smell (hyperosmia) makes itself manifest either 
by a remarkably fine perception of odors, or by an abnormal sensitiveness to 
them. The latter symptom is often noticed, especially in the hysterical. Patients 
have headaches, or attacks of fainting, from slight odors, which healthy persons 
notice but little. Subjective sensations of smell (hallucinations of smell) are 
quite frequent among the insane, and sometimes during the aura of an epi- 
leptic attack. 

A diminution of the power of smell (olfactory ansesthesia, anosmia) is not 
infrequently seen in the different diseases of the nose — coryza, severe inflamma- 
tion, etc. ; also in affections of the base of the skull, such as tumors, and acute 
and chronic meningitis, which involve the trunk of the olfactory sympathetically, 
and also in cerebral disease, tumors, etc. In right hemiplegia and aphasia, for 
example, co-existing anosmia of the left nasal cavity has sometimes been ob- 
served. In far-advanced tabes dorsalis we have sometimes found pronounced 
anosmia, dependent, perhaps, upon an atrophy of the olfactory nerve. Complete 
or unilateral anosmia, however, is most frequently observed in the hysterical 
(hysterical hemiangesthesia, traumatic hysteria, etc.). It is important to state 
that in every marked enfeeblement of the smell the " taste " for many forms of 
food suffers, since it is well known that their " aroma," as in roast meats, wines, 
and the different sorts of cheese, is due chiefly to the co-existing sensations 
of smell. 

The treatment of anomalies of smell almost always coincides with the treat- 
ment of the primary disease. In case the disturbance of smell makes special 
interference desirable, we can try electrization of the nasal mucous membrane, 
or painting it with very irritating or very odorous solutions. 



CHAPTER YII 
ANOMALIES OF THE SENSE OF TASTE 

Sensations of taste are obtained from two nerves — the glosso-pharyngeal, and 
the lingual nerve from the third branch of the trigeminus. The glosso-pharyn- 
geal is the nerve of taste for the posterior third of the tongue and the palate, the 
lingual for the anterior two thirds of the tongue. The gustatory fibers of the lin- 
gual, all, or at least a great part of them, pass over to the chorda tympani, and 
reach with this the trunk of the facial; they do not remain in the facial, how- 
ever, as many pathological observations have most plainly shown, but they finally 



828 



DISEASES OF THE NEKVOUS SYSTEM 



come back to the trigeminus, and, as has been believed up to the present time,, 
probably chiefly by the great superficial petrosal nerve and the Vidian nerve to 
the spheno-palatine ganglion, in this way passing to the second branch of the 
trigeminus; or, as is rendered probable by more recent investigations, they pass 
by means of the otic ganglion to the third branch of the trigeminus and to the 
Gasserian ganglion (vide page 802). We know nothing definite as to their 
further course and their central termination. 

Hyperaasthesia of taste is rare, and it has been seen almost exclusively in the 
hysterical. Paresthesia of taste is sometimes found in patients with facial 
paralysis, who complain of an abnormal taste in their mouths. In the insane,, 
too, subjective sensations of taste (hallucinations of taste) may occur. Anaes- 
thesia of the gustatory nerves (gustatory anaesthesia, ageusia) is, however, quite 
frequent. As follows from what has gone before, this may be seen : (1) In affec- 
tions of the peripheral terminal organs of the gustatory nerves, as in disease of 
the mucous membrane of the tongue; (2) in affections of the glosso-pharyngeal,. 
such as compression; (3) in affections of the lingual nerve, and of the trigem- 
inus within the cranial cavity; (4) in affections of the chorda tympani, from 
diseases of the middle ear; (5) in affections of the facial nerve between the 
entrance of the chorda tympani and the geniculate ganglion; but we know from 
experience that any obstacle to conduction in this nerve, above or below the points 
named, causes no disturbance of the sense of taste. Central disturbances of 
taste are said to have been observed in affections of the posterior portion of the 
internal capsule. Disturbances of taste are very common in hysteria and allied 
conditions (traumatic neuroses, etc.). 

The test of the sense of taste must be made separately for all the different 
varieties of the sensation of taste, since partial paralyses of taste are not infre- 
quent. The test is performed by putting small amounts of the substance to be 
tasted in solution on the tongue with a glass rod or a brush. The anterior and 
posterior parts are to be tested separately. A solution of quinine or tincture of 
nux vomica serves as a test for bitter, a solution of sugar for sweet, vinegar or 
dilute muriatic acid for sour, and a solution of common salt for salt. We may 
also use as a test for taste the well-known galvanic taste, which is strongest at 
the anode, but is also detected at the cathode in even very weak currents, and 
hence is so often noticed from by-currents in galvanizing the head, neck, etc. 

An accurate diagnosis as to the seat and cause of disturbances of taste can be 
made only by considering the other symptoms which are also present. Direct 
treatment may best be employed by the aid of electricity. 



EEMAEKS UPON THE DISTUKBAlsrCES OF MOTILITY 829 



SECTION II 

Diseases of the Motor Nerves 
CHAPTER I 

GENERAL REMARKS UPON THE DISTURBANCES OF MOTILITY 

1. Paralysis 

General Classification of Paralyses. — By " paralysis " we mean the loss of vol- 
untary motion in the muscles of the body controlled by the will. We usually dis- 
tinguish between the complete loss of the power of active motion (paralysis) and 
the mere weakening of it (paresis). In complete paralysis of any part of the 
oody, or of a single muscle, the slightest voluntary motion can not be produced 
in it; while in paresis of a diseased part certain 
movements are still possible, but they are more 
or less below the normal in strength, extent, and 
duration. 

In every portion of the tract that leads from the 
motor portions of the cortical gray matter of the 
I)rain to the muscles — that is, in every part of the 
so-called great " cortico-muscular conduction- 
path " or " pyramidal tract " — disease may lead to 
paralysis if it takes away from the part affected its 
power to conduct voluntary motor excitations. 
Every destruction or inhibition of function of the 
motor centers in the cerebral cortex, with whose 
integrity the initiation of voluntary innervation 
is associated, must also lead to a paralysis in the 
corresponding muscular region. Finally, diseases 
of the muscles even may cause paralysis, since 
the muscles may either have their contractile 
substance injured, or lose their power to respond 
by a contraction to any nervous excitation that 
reaches them ("myopathic paralyses"). 

If we represent to ourselves briefly the precise 
course of the chief tract for exciting voluntary 
movements, so far as it is now known, we must put 
the beginning of this tract, according to all recent 
experiments, in the region of the central convolu- 
tions of the cerebrum and of the paracentral lobule. 
Here we find the so-called psycho-motor centers 
(see the details in the chapter on cerebral localiza- 
tion), from which the motor fibers in the corona 
radiata converge and pass downward. The lat- 
ter, after they have united into quite a compact 
bundle, enter the internal capsule, which they traverse obliquely. As we see in a 
horizontal section through the cerebral hemispheres (see Pig. 95), the internal 
capsule consists of two limbs — an anterior, between the lenticular and the caudate 
nuclei, and a posterior, between the lenticular nucleus and the optic thalamus. 
The two limbs form an obtuse angle, opening outward, whose top — that is, the 
junction of the anterior and posterior limbs of the internal capsule — is termed 
the " knee of the capsule." The motor tract (Py) lies in the posterior limb of the 




Fig. 95.— Horizontal section through 
the right cerebral hemisphere. 
NC. Caudate nucleus. Th. Optic 
thalamus. LK. Lenticular nu- 
cleus (first, second, and third di- 
visions). vS. Anterior limb of 
the internal capsule. hS. Poste- 
rior limb of the internal capsule. 
Fa. Fibers belonging to the facial 
nerve. Py. Pyramidal tract (mo- 
tor). S. Sensory tract (probably 
cutaneous nerves and those of 
special sense). O. Occipital lobe. 



830 



DISEASES OE THE NERVOUS SYSTEM 




Fig. 96.— Transverse section through the crura 
cerebri in secondary degeneration of the 
right pyramidal tract. (From Charcot.) 
sn. Substantia nigra, p. The degenerated 
and therefore translucent pyramidal tract. 
III. Oculo-motor nerve. AS. Aqueduct of 
Sylvius. 



internal capsule about the posterior end of its middle third. The fibers for the 
cranial motor nerves (facial, hypoglossus) lie farther forward than the fibers for 

the extremities. The tract runs downward 
rather obliquely, so that in the upper part 
of the internal capsule it lies somewhat 
farther forward than in the lower. Erom 
the internal capsule the pyramidal tract 
enters the crusta. It lies first in the third 
quarter, counting from the inside, then 
farther down in the middle third of the 
crusta (see Fig. 96). The fibers for the 
cranial motor nerves here lie nearer the 
median line than the fibers for the extrem- 
ities. Farther downward the tract passes 
into the anterior half of the pons. In 
the pons the fibers of the pyramidal 
tract are somewhat separated, but they 
come together below it into the compact 
bundle of the pyramids on the anterior 
surface of the medulla. In this course 
from the internal capsule to the medulla 
oblongata all the nerve tracts for the muscles of the head branch off laterally, 
and, after they have decussated in the median line, they go to the nuclei of their 

respective nerves (oculo-motor nuclei 
under the aqueduct of Sylvius, facial nu- 
clei in the pons, hypoglossal nuclei in the 
medulla, etc.). The motor fibers for the 
trunk and extremities remain in the 
pyramids, at the lower end of which the 
decussation of these fibers (motor decus- 
sation of the pyramids, decussatio pyram- 
idum), takes place. The fibers of each 
pyramid pass over, for the most part, into 
the lateral column of the opposite half 
of the spinal cord, and here from the dis- 
tinct bundle of the lateral pyramidal 
tract (PyS, see Figs. 97 and 98). A small 
part of the pyramids, which sometimes 
seems to be entirely wanting, remains uncrossed, and passes downward as the 
so-called anterior pyramidal tract (PyV, Fig. 97) in the anterior column of 

the cord on the same side. From the lat- 
eral column, or the anterior column of the 
cord, the motor fibers pass into the ante- 
rior gray columns of the cord, and are 
here connected with the large motor gan- 
glion-cells of the ariterior cornua. We 
now know that this connection does not 
take place in the sense of a direct pas- 
sage of the lateral tract fibers into the 
cells of the anterior cornua, but that each 
fiber breaks up into a " nervous terminal 
Fig. 98.-Transverse section through the lumbar arborization," which surrounds the proto- 

enlargement. PyS. Lateral pyramidal tract. p l asm i c processes of a ganglion-cell of the 
(The anterior tract is no longer present in * . . *L , . ?. . , 

the lumbar portion of the cord.) anterior horn and m this way enters into 




Fig. 97.—' 



Transverse section through the cervi- 
cal enlargement of the spinal cord. PyS. 
Lateral pyramidal tract. PyV. Anterior 
pyramidal tract (in this case present only on 
one side). 




REMARKS UPON THE DISTURBANCES OF MOTILITY 831 



the closest relation with it. From the ganglion-cell of the anterior horn its axis- 
cylinder process passes off directly as the anterior root-fiber, and the anterior 
spinal roots are further continued as the peripheral motor nerves. In the muscle, 
as we know, the nerve-fiber again breaks up into a terminal arborization (" motor 
end plate"), which finally transmits the irritation coming from the cerebrum to 
the contractile muscular fiber. 

The long motor tract, just described, the cortico-muscular path or the pyram- 
idal tract, whose course has been quite accurately determined in its details by 
the results of pathological observations (Tiirck, Charcot) and investigations into 
the history of its development (Flechsig), is composed of two neurones connected 
with each other: the first (central) motor neurone extends from the cell of origin 
in the cerebral cortex to the terminal arborization of the fiber in the motor nuclei 
(nuclei of the cranial motor nerves, motor ganglion cells in the anterior cornua) ; 
the second (peripheral neurone) extends from the above-mentioned ganglion cells 
to the muscles, and is accordingly formed essentially by the ganglion cell and the 
peripheral nerve-fiber. It forms, at all events, the chief path for the conduction 
of voluntary innervation. It is possible that there are other motor paths of con- 
duction besides this tract, but we know nothing definite concerning them. 

If we pay attention to the course of the motor tracts described, we shall easily 
understand certain peculiarities in the distribution of motor paralyses, which are 
of great importance in diagnosis. Since the motor centers for separate parts of 
the body, such as the face, the arm, or the leg, are separated from one another in 
the cerebral cortex, and are distributed over a comparatively large surface, as we 
shall see more fully later on, it is easily explained why affections of the cortex, if 
they are not very extensive, may lead to paralysis of only a single part of the 
body. We call such an isolated paralysis of one part of the body monoplegia, and 
thus we speak of a cortical facial or brachial monoplegia. Farther downward in 
the brain, in the internal capsule and the crus cerebri, however, as we have seen, 
all the motor fibers are collected into one bundle, whose diameter takes up com- 
paratively little space. Hence we perceive that any disease of the brain, which 
is situated in this part of the motor tract, may easily make this tract incapable 
of conduction throughout its whole extent, or at least throughout the great- 
est part of it. The result must be, then, a more or less complete paralysis of the 
facial muscles, the arm, and the leg at the same time — that is, of the entire half 
of the body — a form of paralysis which is termed hemiplegia or unilateral paraly- 
sis. We may note here that, as a result of the passage of the motor fibers to 
the other half of the cord in the decussation of the pyramids, the paralysis must 
develop on the side of the body opposite to the focus of disease in the brain. 
Farther down in the medulla and the cord the fibers coming from both hemi- 
spheres, and belonging to the two sides of the body, lie quite near each other. Since 
many diseases of the cord have a tendency to affect the two halves of the cord at 
once, or gradually to extend over the whole transverse section of the cord, a simul- 
taneous paralysis of the corresponding portion of the two sides of the body will 
be apt to arise as a result of this. This form of paralysis we call paraplegia. Dis- 
eases in the cervical cord may have as a result a paralysis of all four extremities 
or of the two arms — cervical, brachial, or superior paraplegia; diseases in the 
dorsal and lumbar cord a paraplegia of the two legs — inferior paraplegia, often 
called simply " paraplegia," without further prefix. In diseases of the peripheral 
nerves we have, of course, again a limitation of the paralysis to the region of the 
affected nerve. The paralysis may be quite extensive in diseases of a nervous 
plexus — paralysis of a peripheral plexus; or it may confine itself wholly to the 
region of a single nerve, or even of a single branch of the nerve — paralysis of a 
peripheral nerve. 

We will have to add many more details to what has just been said, but as a 



832 



DISEASES OF THE NERVOUS SYSTEM 



fundamental principle we may now note that hemiplegia is the chief form of 
cerebral paralysis, while paraplegia is the chief form of spinal paralysis. Mono- 
plegias are usually either cortical cerebral paralyses, or peripheral paralyses. 

General ^Etiology of Paralysis. — The kind of lesion which leads to paralysis 
may, in the different cases, be very diverse. From easily understood reasons we 
-can very rarely decide as to the kind of lesion from the intensity and extent of 
the paralysis, but only from the manifest serological factors, from the develop- 
ment and course of the paralysis, from other morbid symptoms that are also 
present, etc. In general, we may divide the paralyses into two groups, according 
to the nature of their cause: into paralyses from causes that can be discovered 
anatomically, and into the so-called functional paralyses, in which no anatomical 
cause for the paralysis can be found ; but since our anatomical, and especially our 
histological, methods of investigation have become better developed and are more 
employed, the domain of functional paralyses has become gradually more and 
more restricted, and a definite anatomical cause has now been found for many 
paralyses which were once regarded as functional. 

All the diseases of the nervous system may be anatomical causes of paralysis, 
if they lie in a spot where they damage or destroy the paths of motor conduction. 
Inflammation, degeneration, new growths, hsemorrhages, and severe disturbances 
of circulation, with their results, especially embolic and thrombotic softening, are 
found in the brain, the cord, and the peripheral nerves, and under some circum- 
stances give rise to the phenomenon of paralysis. Mechanical lesions of the nerv- 
ous system also play a great part in the pathogenesis of paralysis, especially in- 
juries, and compression of the brain, the cord, and the peripheral nerves by swell- 
ings, new growths, and other diseases in their vicinity. 

We also know certain toxic substances which cause direct injury (degenera- 
tion) of the motor-nerve territory (chiefly the peripheral motor nerves), and con- 
sequent paralysis. Of these toxic paralyses, alcoholic paralysis (vide infra) and 
lead paralysis (vide infra) are the most important in their clinical relations; but 
other poisonous substances, such as copper, arsenic, and certain vegetable alka- 
loids, may also cause paralysis. 

We may group a large number of paralyses together under the term of " paraly- 
sis after acute diseases." Since in these cases we always have to do with acute 
infectious diseases, we may assume, as their most probable cause, certain changes 
in the nervous system, sometimes in the brain or cord, but much more frequently 
in the peripheral nerves, which stand in direct relation to the specific infectious 
material. There seem to be chemical poisons (" ptomaines ") which form in the 
body in infectious disease, and cause degeneration of certain nerve-fibers, in the 
same way, for example, as lead. We most frequently see paralysis appear after 
diphtheria, diphtheritic paralysis (vide infra), or more rarely after typhoid fever, 
small-pox, dysentery, the acute exanthemata, etc. The paralyses which may 
arise in certain chronic infectious diseases, especially in syphilis and tubercu- 
losis, usually have another origin. Here we usually have to do with the specific 
morbid product itself (gumma, tubercle), which may invade various parts of the 
nervous system, but, on the other hand, we must under some circumstances con- 
sider the action of toxines even in paralyses in syphilis and tuberculosis. Final- 
ly, certain paralyses which occur in certain general constitutional diseases, such 
as diabetes and gout, are also due probably to toxic influences. 

Those paralyses which come on most manifestly because of exposure to cold 
are termed paralyses from exposure to cold, or " refrigeratory," or frequently 
" rheumatic " paralyses. Although many spinal diseases, such as myelitis, may 
perhaps be referred to exposure to wet or cold, we usually reckon among rheu- 
matic paralyses only certain peripheral paralyses, such as that in the domain of 
the facial nerve. The functional disturbance of the nerves in these cases probably 



REMARKS UPON THE DISTUKBA3TCES OF MOTILITY 833 



depends "upon mild inflammatory changes in them produced by cold, and is accord- 
ingly of an anatomical and not merely of a functional nature. 

There are, however, quite a comprehensive group of paralyses which we must 
to-day still term functional paralyses. To this class belong the hysterical paraly- 
ses, the paralyses from psychical causes, such as paralysis from fright, the " pa- 
ralyses from imagination," etc. We shall learn to recognize these more fully in 
the chapter on hysteria. 

In conclusion, we must bear in mind the so-called " reflex paralyses," whose 
setiology is not yet fully explained — that is, paralyses which may come on in the 
course of diseases of certain internal organs, especially of the intestine, and of 
the urinary and sexual organs, as a result of centripetal irritations acting reflexly. 
An attempt has been made to explain their origin, from analogy with well-known 
physiological experiments, by the idea that a " reflex inhibition " is excited in 
certain motor regions by a sensory irritation arising in the diseased organs, a 
theory which has not yet been fully confirmed. Leyden's hypothesis is scarcely 
more probable, and it is by no means proved. According to it the paralyses of this 
class are explained by an ascending neuritis, arising from the organs originally 
affected (see the chapter on neuritis). Generally speaking, the whole conception 
of " reflex paralyses " is still far from clear, and we will do well to be extremely 
guarded in their diagnosis. Many cases which were formerly regarded as reflex 
paralyses are to be classed as hysteria, especially as traumatic hysteria (q. v.). 
Lepine has also regarded the paralysis of the arm of the affected side, seen in 
some cases of empyema, especially after operative interference, as a " reflex pa- 
ralysis," an explanation which may be proper in some cases, but in regard to 
which we should be the more cautious, as metastatic abscesses of the brain are 
not very infrequently found in empyema (see the chapters on purulent menin- 
gitis and cerebral abscess). 

General Symptomatology of Paralyses. — We can recognize the existence of a 
paralysis, independently of the patient's statements as to the impossibility of per- 
forming certain motions and functions, only by a careful and thorough physical 
examination of the power of voluntary motion. This examination in patients 
with nervous disease must extend to all parts of the body, and demands an accu- 
rate knowledge of all the movements that can normally be executed by the differ- 
ent joints, and of the muscles and nerves requisite to produce them (see the tables 
at the end of this chapter). 

In each individual case of paralysis some other symptoms must be considered 
besides immobility — first the condition of the paralyzed muscles, and then certain 
accompanying symptoms that are often present with the paralysis. 

In regard to the first point, the trophic condition of the paralyzed muscle is of 
the greatest diagnostic and practical importance. In comparing a large number 
of paralyses, a very evident difference in this respect strikes us at once. We see 
on the one hand paralyses where the paralyzed muscles retain their normal vol- 
ume for a comparatively long time and only gradually waste as a consequence of 
disease and the lack of the normal influences of innervation, although this atro- 
phy never goes beyond a certain degree. On the other hand, however, we also see 
cases in which there is a considerable atrophy in the paralyzed muscles in a few 
weeks or months, finally progressing to an almost complete disappearance of the 
muscles. This distinction is so comprehensive that all the last-named paralyses 
have been classed together under the name of " atrophic paralyses." 

If we once more represent to ourselves the whole course of the motor tracts, 
from the cerebral cortex to the voluntary muscles, we shall remember that these 
tracts are composed of two connected yet independent neurones. The peripheral 
neurone directly innervating the muscle has its ganglion-cell in the anterior 
cornua of the spinal cord. Clinical and anatomical experience teaches us that, 
53 



834 



DISEASES OF THE NERVOUS SYSTEM 



in all those paralyses where the cause — that is, the break in conduction of the 
motor fibers — lies in the first (central) neurone from the cortex up to, but exclud- 
ing the cells in the anterior cornua, there is, as a rule, only a slow and relatively 
slight amount of atrophy in the paralyzed muscles, while in those paralyses where 
the cause is situated in the second (peripheral) neurone — that is, in these gan- 
glion-cells themselves, or in the motor nerves peripheral to them — a pronounced 
muscular atrophy rapidly develops. The only possible interpretation of this fact 
is, that the large motor ganglion-cells of the anterior cornua have, as we express 
it, a trophic influence on the muscles innervated by them. As we have seen above, 
the peripheral motor-nerve fiber is nothing but the direct, long cellular process 
of a motor ganglion-cell in the anterior horn. It is therefore easy to under- 
stand that this process atrophies when it is separated from the cell-body and its 
cell nucleus, or when the cell itself is destroyed. If, however, the motor nerve 
degenerates, the muscle belonging to it is entirely separated from all influences of 
innervation; neither voluntary nor reflex nerve irritations can act upon it any 
longer. This lack of innervation apparently causes such a change in the trophic 
conditions of the paralyzed muscle that its fibers disappear one after the other, 
until finally, in long-continued paralyses, only a slight trace of muscular tissue is 
left. We can therefore consider the peripheral motor neurone and the muscular 
fiber as, in a certain degree, a trophic unit. 

It has been generally believed that the anatomico-histological processes in the 
rapidly atrophying muscles were also different in diseases of the peripheral motor 
neurones from the processes of slow and slighter atrophy in paralyses from dis- 
ease of the central motor neurones. In the first case we were dealing with a 
so-called " degenerative " atrophy of the fibers — that is, with an atrophy asso- 
ciated with granular and fatty destruction of the fibers — and in the second case 
only with a " simple 99 atrophy. Such a histological difference, however, can not 
be strictly maintained. We are always dealing, essentially, with a diminution in 
the size of the fibers, where, however, the transverse striation of the muscle re- 
mains plainly visible. We also find a great increase in the nuclei of the muscle, 
and, finally, we often see an increase of the interstitial connective and fatty 
tissue. 

We observe a further distinction in the condition of the paralyzed muscles if 
we perform passive motion in the paralyzed parts. There are paralyses where we 
can perform passive motion of the paralyzed parts at any joint with perfect ease 
and freedom, and without perceiving the slightest resistance. We term such 
paralyses " flaccid paralyses," but there are also paralyses where passive motion 
meets with considerable muscular resistance, so that it can be performed only with 
a certain greater or less amount of exertion, or not at all, or only within certain 
limits : spastic paralyses. This distinction is dependent upon the state of mus- 
cular tonus in the paralyzed muscles. If this tonus be increased (hypertonia of 
the muscles) and the muscles be found in a state of marked and permanent con- 
traction, the paralyzed parts show a peculiar stiffness, or even an almost com- 
plete spastic rigidity. If the muscular tonus be diminished or wholly lost (hypo- 
tonia of the muscles), the paralyzed limbs are flaccid and sometimes even "flap- 
ping." Since the muscular tonus is in all probability of reflex origin, it is not 
remarkable that spastic paralyses are usually associated with an increase, and 
flaccid paralyses often with a loss of the reflexes, especially the tendon reflexes 
(vide infra). States of marked permanent shortening of the muscles, whereby 
certain parts are fixed in an abnormal position, are called muscular contractures. 
The cause of their development will be spoken of later. 

Finally, in every case of paralysis, we must consider the other nervous symp- 
toms which accompany it, since these may also be of great importance in judging 
of the cause of the paralysis. We must first of all investigate the condition of 



REMARKS UPON THE DISTURBANCES OF MOTILITY 835 



tlie reflexes (vide infra) in the paralyzed parts, already mentioned, from which 
many conclusions can be drawn as to the seat of the lesion which causes the 
paralysis. We must also test the state of the sensibility, both in the skin and in 
the muscles themselves. Certain attendant trophic and vaso-motor symptoms 
are also to be regarded. The skin over the paralyzed parts sometimes appears 
cyanotic, or marble-like ; it feels cool, is oedematous, and sometimes is peculiarly 
dry, hard, and scaly. The examination of the electrical excitability of the 
paralyzed nerves and muscles is of especial importance. The phenomena oc- 
curring in these conditions will be particularly described below. 

2. Symptoms of Motor Irritation 

As we have termed the symptoms of motor deficiency "paralysis," we group 
the symptoms of motor irritation in general together under the name of " spasm." 
We mean by this all the morbid movements occurring in the muscles involunta- 
rily and even against the will. Although we may find spasm in the smooth mus- 
cles, which generally are not controlled by the will, as in spasm of the bronchial 
muscles, spasm of the vessels, etc., we will concern ourselves here only with the 
spasmodic movements in the voluntary muscles. We must look for the cause of 
these in abnormal irritation exerted in some way on the motor tracts, but we 
know very little of the precise nature and character of this irritation in most 
cases. The abnormal irritation often acts directly on the motor nervous region, 
especially in the frequent spasms in affections in the neighborhood of the cortical 
motor centers; but the motor irritations often seem to be excited secondarily 
through some reflex channel — reflex spasms. 

Eor a long time two kinds of spasm have been distinguished symptomatically.. 
We term those spasms clonic where the abnormal muscular contraction lasts 
only a short time, and then is interrupted by a short period of relaxation, to come 
on again afresh. The affected parts of the body are thus put in a constant con- 
vulsive motion. In distinction from this we term those abnormal muscular con- 
tractions tonic spasms where the muscle remains spasmodically contracted for a 
longer time — minutes, hours, or days. The affected part of the body is thus kept 
motionless in some abnormal position. Both forms of spasm, however, show 
many transitions and combinations, so that we must often speak of " tonic-clonic " 
spasms. 

A more careful examination of the symptoms of motor irritation, however, 
gives a still greater number of different forms. We will here group together the 
most important varieties of morbid involuntary movements. 

1. Epileptiform convulsions are severe, and usually clonic spasms, at times 
tonic-clonic, either involving the whole body, and then always associated with dis- 
turbances of consciousness, or limited to one half or one portion of the body. By 
them the whole body or the affected part is put into violent motion, usually 
thrashing and shaking movements. The pure epileptic spasm in epilepsy is the 
type of this form of spasm, but precisely analogous spasms, "epileptiform" 
spasms, are seen in organic diseases of the brain, in uraemia, etc. 

2. Persistent rhythmical contractions in single groups of muscles are some- 
times seen in certain cerebral diseases, such as apoplexy and sclerosis, and also, 
as we have observed, after acute myelitis. In these the part of the body affected 
is put in motion by continuous, separate, weaker or stronger thrusts, which follow 
one another in a regular rhythm. Rhythmical contractions are also seen as pre- 
cursors or at the end of epileptiform spasms. 

3. Trembling motions, or tremor, as we say in ordinary parlance, are moderate 
motions, rapidly following one another, with a not very marked excursion. If the 
tremor is more pronounced, we term it " shaking." Tremor is an important symp- 
tom, almost pathognomonic in many nervous diseases, such as paralysis agitans, 



836 



DISEASES OF THE NEEVOUS SYSTEM 



but we know almost nothing* in regard to the more intimate manner of its origin. 
We often see pronounced tremor, especially in the hands, in exophthalmic goitre. 
We know that tremor is often present in old people — senile tremor ; and in alco- 
holic subjects — alcoholic tremor. Tremor sometimes appears in muscles at rest, 
that is, not innervated by the will, and sometimes only in those which are moved 
voluntarily. This latter form of tremor, which is seen most frequently in multi- 
ple sclerosis (vide infra), is- termed " intention tremor." Very marked intention 
tremor, which is increased by any mental excitement, is also seen as a symptom 
of chronic mercurial poisoning (mercurial tremor), particularly in mirror-mak- 
ers, etc. 

We may mention here the so-called essential tremor, that is, a condition where 
the tremor, which is most marked in the hands, is the only morbid symptom and 
can be referred to no known cause. On energetic voluntary innervation of the 
muscles the tremor, as a rule, ceases. This form of tremor is sometimes seen in 
comparatively young people, and even in children. A distinct hereditary pre- 
disposition is often present, so that several " tremblers " are found in the same 
family (hereditary tremor). 

We very often find trembling in " nervous " persons, which is at once increased 
by any emotion (nervous, neurasthenic tremor). Marked tremor is also frequent 
in hysteria, especially in traumatic hysteria. 

4. Single contractions, either sudden twitchings, or in the form of a slow con- 
traction of the muscle, are seen with especial frequency in diseases of the cord. 
They are either single, or frequent and persistent. Their mode of origin is not 
always plain. They may depend on direct motor irritation or they may have a 
reflex origin. In the latter case each twitching is sometimes associated with a 
sudden feeling of pain (symptoms of irritation of the posterior roots?). 

5. Fascicular and fibrillary muscular contractions are little contractions in the 
separate muscular bundles, which may be seen on a close examination of the mus- 
cles, but which do not have any special influence on motion. If the fibrillary con- 
tractions in a muscle are very pronounced, there may develop an actual " wave " 
in the muscular substance. We see this symptom especially in atrophied muscles, 
particularly in spinal progressive muscular atrophy (vide infra) and other spinal 
amyotrophies, but there also seem to be independent forms of diseases of the 
muscles, in which we may see for a long time a persistent and extensive muscular 
wave, associated with pain, profuse sweating, etc. — the so-called myokymia of 
F. Schultze. 

6. Choreic movements are either slight contractions or quite complicated and 
extensive, but brief and involuntary movements, which usually appear in the face, 
in one limb, or sometimes over the whole body, without regard to rule. In severe 
cases they are almost continuous, but in milder cases they are interrupted by 
shorter or longer pauses. They form the chief symptom of chorea proper, but they 
are also present in other cerebral affections, such as symptomatic chorea, post- 
hemiplegic chorea, etc. 

7. Movements of athetosis is the name we give to peculiar involuntary and 
usually quite slow movements, which are seen especially in the arms and hands, 
but also in the head, trunk, etc. The fingers make slow 1 but often very exten- 
sive movements, are extended, spread apart, flexed, and moved over and around 
one another in the most remarkable way. This form of motor irritation occurs as 
a special disease, " athetosis" or as a symptom in certain central nervous diseases, 
especially the cerebral paralysis of children (vide infra). 

8. Constant or co-ordinated spasms are symptoms of motor irritation in which 
the patient performs complicated movements by compulsion — forced movements. 
Among these are classed the compulsory going forward or moving in a circle, the 
turning about the axis of the body (forced attitudes), and also certain peculiar 



KEMAEKS UPON THE DISTURBANCES OF MOTILITY 837 



complicated forms of spasm, such as spasms of jumping, laughing, screaming, 
with all sorts of spasms of the respiratory, pharyngeal,' and laryngeal muscles, 
associated with hiccoughing and belching sounds, etc. They are seen most fre- 
quently in severe cases of hysteria, but epilepsy may also occur exceptionally in 
the form of co-ordinated spasms. The forced movements and attitudes men- 
tioned above are seen chiefly in affections of the cerebellum and the cerebellar 
peduncles. 

9. Tonic spasm, as has been said, is the name for all morbid muscular contrac- 
tions that continue for a long time. Tonic spasm in the muscles of mastication, 
the masseters, is termed trismus. Tonic spasm in the muscles of the back and 
neck, by which the whole body is drawn backward, and the vertebral column is 
bent into an arch with the convexity in front, is called opisthotonos. Tonic 
rigidity of the whole body is termed tetanus. Tonic spasms are seen not infre- 
quently as an idiopathic condition, but also in tetanus, tetany, hysteria, etc. 

10. Cataleptic rigidity is the name of that tonic condition of the muscles in 
which the limbs are deprived of the influence of the will, but are held in position 
by the muscles in any position given to them passively. It is seen chiefly in cer- 
tain cases of hysteria, but cataleptic states are also present in other cerebral dis- 
eases, especially if associated with general mental stupor, such as tumors, menin- 
gitis, etc. (see the chapter on catalepsy). 

11. Associated movements are abnormal movements which appear, while mak- 
ing voluntary movements, in muscles which have no connection with the move- 
ment willed. Thus in hemiplegia associated movements sometimes take place 
in the arm when the patient wills to move the leg alone. In spinal cases the 
movement of one leg is sometimes accompanied also by an unintentional move- 
ment of the other leg. Associated movements are commonest in the muscles of 
the same limb. Thus we often see in hemiplegia or in spastic spinal paralysis 
that patients can not flex the leg up toward the body without at the same time pro- 
ducing a marked dorsal extension of the foot as an associated movement. In 
old peripheral facial paralysis (q. v.) we very often see associated movements in 
the facial muscles. 

Besides the conditions of motor irritation, other attendant nervous symptoms 
often occur at the same time. Symptoms of motor paralysis and irritation are 
very often combined with each other, since the different forms of spasm may 
appear not only in groups of muscles whose motion is otherwise normal, but also 
in paretic or paralyzed muscles. In general convulsions the state of the con- 
sciousness deserves special attention. Genuine general epileptic attacks are asso- 
ciated with complete loss of consciousness, hysterical attacks are often associated 
with clouding of consciousness, but in most of the other forms of spasm the con- 
sciousness is unaffected. Finally, it is worthy of mention that tonic spasms espe- 
cially are attended by a feeling of decided pain, which is probably due to an irrita- 
tion of the intra-muscular sensory nerves. Such painful tonic muscular contrac- 
tions are termed cramps. Among them are the well-known painful spasms in the 
calves, etc. 

3, Ataxia 

In executing all normal complicated movements we need the simultaneous 
action of several muscles. Consider the numerous muscles which must be put in 
activity in walking, in grasping, and in all the manifold employments of the 
hands. Hence, in order to perform such movements correctly, it is not only 
necessary that all the muscles concerned should be innervated by the will — that 
is, that they be not paralyzed — but that we should also be able so to modify the 
innervation of each individual muscle that its contraction corresponds precisely 
to the special part of the work belonging to it. A prescribed voluntary motion 



838 



DISEASES OE THE NERVOUS SYSTEM 



can take place only when, first, all the muscles requisite for it come into no less 
but also no greater action ; second, when each individual muscle contracts only so 
far and so much as its special task requires; and, third, when the conditions in 
the time of innervation take their normal course — that is, when all the muscles 
involved contract at the same time or in the proper order one after another. A 
movement which is executed in such a prescribed manner we call a co-ordinated 
movement, and the process of modifying properly the innervation of the different 
muscles necessary for a complicated movement we call the co-ordination of motion. 
We must especially bear in mind that the simultaneous action of several muscles 
is so far necessary, even for what seem to be the simplest movements, that muscles 
antagonistic to those moved must also come into activity. Only by the aid of the 
ever-ready antagonistic muscles can we grade our movements as finely, or check 
or hasten them as rapidly, as is demanded for the execution of almost all compli- 
cated movements. 

Nervous pathology is rich in facts which can make the idea and the necessity 
of the co-ordination of motion clear to us. We often see disturbances of motility 
which make the patient incapable of any fine motor acts, and yet which do not 
depend at all upon any motor weakness or paralysis, but only upon a disturbance 
in the co-ordination of motion. Such a disturbance we call ataxia, and we speak 
of an ataxia of the arms, of the legs, etc., when the parts named can perform all 
the motions and often even retain their full strength, but these movements show, 
usually at once, a striking, disordered, uncertain " ataxic " character. 

Many theories have been advanced as to the precise cause of ataxia. In gen- 
eral, however, there can be hardly a doubt that ataxia depends upon a disturbance 
of centripetal influences. We must suppose that our movements are constantly 
kept in order and control (co-ordinated) by centripetal excitations coming from 
the skin, muscles, and joints, although they are not all by any means consciously 
perceived. By such excitations the child learns gradually to change his original 
uncontrolled and unregulated movements into orderly movements. In the adult 
most movements have already been so long practiced as to be sure and steady. 
The learning of a new movement, a new dexterity, however, takes place in pre- 
cisely the same way. Even a long-practiced movement (walking, grasping) 
needs the constant control and regulation exerted by centripetal excitations. 
If these controlling influences are lacking by reason of any disease of their 
corresponding centripetal tracts, ataxia is the necessary result. Ataxia may occur 
both in peripheral nervous diseases and also in diseases of the spinal cord, cere- 
bellum, and cerebrum. It is therefore evident that the special circumstances 
which give rise to ataxia may be very diverse. We will return to this point in 
the description of the individual diseases which lead to ataxia. (See especially 
the chapters on tabes dorsalis, multiple neuritis, and affections of the cerebellum.) 

4. General Remarks upon testing the Reflexes and upon the Condition 

of THEM 

In testing the reflexes, which should never be omitted in any case of nervous 
disease on account of its frequent great diagnostic importance, we must distin- 
guish the two chief groups of reflexes from each other: the cutaneous reflexes, 
and the " tendon reflexes." 

Cutaneous Reflexes. — We term the muscular contractions, excited reflexly by 
irritation of the sensory centripetal cutaneous nerves, cutaneous reflexes. These 
are usually present only to a slight degree in the upper extremities ; but we can 
sometimes excite reflexes even here by pricking or pinching the skin, especially 
the skin of the fingers. The very marked reflex in many people caused by tickling 
the axilla is well known. The test of the cutaneous reflexes in the lower extrem- 
ities is much more important. The soles of the feet are the most sensitive parts 



EEMAKKS UPON THE DISTURBANCES OF MOTILITY 839 



for exciting a reflex, whose arc lies in the first and second sacral segments of 
the spinal cord. Simply tickling the soles with the finger, is a sufficient irritation 
(the tickling reflex), and so is the prick of a pin (the prick reflex), or stroking 
the skin hard with a blunt object, usually the handle of a percussion-hammer (xhe 
stroking reflex). Thermal irritants are also very suitable for exciting a reflex, 
especially bits of ice held to the skin (cold reflex). It is often advisable to try all 
these methods, since with diminished reflex irritability a reflex contraction in the 
leg can often be excited by some one of them, alone. We should also examine the 
reflex irritability of the rest of the skin, as well as the soles of the feet, by a pin- 
prick, by pinching a fold of the skin, etc. We should especially remember that 
in nervous diseases there is often a delay in the reflex, so that the reflex contrac- 
tion appears only when the irritation has lasted for a certain time. Thus in many 
diseases of the cord, as we have often seen, the reflex follows only after we have 
kept a needle sticking into the skin for some time or have pinched a fold of skin 
continuously for several (ten or fifteen) seconds, a delay which has a connection 
with the fact of the " time summation of reflex irritation " known from physiol- 
ogy. The summation of reflex irritation not infrequently coincides with the 
summation of irritation from the sensation of pain (vide supra, page 793), so 
that, after the irritation has acted for a certain length of time, the sensation 
of pain and the reflex contraction occur at the same time. In the stroking reflex 
(a rapid, vigorous stroking of the sole of the foot or of other parts of the skin 
with the handle of a percussion hammer) we have a local summation of reflex 
irritation, since many different parts of the skin are rapidly irritated one after 
another. In the tickling reflex the local and the time summation of reflex irrita- 
tion are united. All parts of the skin do not show the same " reflex sensibility." 
The reflexes are usually set free more readily from the sole of the foot than from 
the skin of the leg or thigh. The reflex contraction in such cases consists usually 
of a dorsal extension of the foot and a coincident flexion of the knee and hip. 
In the toes, stroking the sole usually causes in healthy persons a flexor reflex, cut- 
in the paralyzed there is often a dorsal extension of the great toe. After irritat- 
ing the skin of the thigh we sometimes see reflex contractions in the extensors 
of the lower leg. The stronger and more persistent the irritation, the more ener- 
getic and widespread is the reflex contraction. Where the reflex irritability is 
actively increased, sticking a needle into the sole will often produce a vigorous 
flexor contraction in the irritated leg, and also a weaker contraction at the same 
time in the other leg. 

[The researches of Babinski, confirmed by many other observers, have shown 
that dorsal extension of the great toe, following stroking of the sole, is in adults 
a valuable sign as indicating disturbance of the central motor neurones, the 
pyramidal tract. It is rarely, if ever, obtained in health, except in young chil- 
dren, but it is found in the majority of cases of old hemiplegia, spastic paralysis, 
etc., where there is degeneration of the pyramidal tract, and it may occur before 
there is any notable increase in the tendon reflexes. The first response on irri- 
tating the sole of the foot in health is usually a plantar flexion of the great or 
small toes ; in some instances there is only a contraction of the tensor vaginaa 
femoris muscle, which may readily escape observation. In other cases, still, 
the irritation at once causes a sudden withdrawal of the leg. We rarely, if 
ever, fail to elicit some form of response, which is equal on the two sides, in 
health. — K] 

We must also mention two special forms of cutaneous reflex which are often 
examined : the abdominal reflex and the cremaster reflex. The abdominal reflex 
is best excited by stroking the abdominal wall rapidly and with some force with 
the handle of a percussion hammer. If we stroke from without inward on the 
linea alba, we can distinguish, according to the level of the irritation, an upper, 



840 



DISEASES OF THE NERVOUS SYSTEM 



middle, and lower abdominal reflex. On stroking from above downward, these 
contractions unite. In health the abdominal reflex is only very rarely absent, 
chiefly in persons with a very lax abdominal wall and in the corpulent. In cere- 
bral hemiplegia the absence of the reflex on the paralyzed side is an important 
sign. In spinal diseases the reflex may be absent on one or both sides, which 
should lead us to bear in mind that the centripetal portion of the reflex arc of the 
lower and middle abdominal reflex enters the spinal cord through the posterior 
roots of the tenth to twelfth intercostal nerves, and of the upper abdominal 
[epigastric] reflex through the posterior roots of the ninth intercostal nerve 
(Dinkier). The cremaster reflex is a reflex ascent of the testicle when the inner 
side of the thigh is forcibly stroked or when sudden deep pressure is exerted by 
the hand a hand's breadth above the internal condyle. This reflex is almost 
always present in healthy boys and men, although in varying strength. We 
must take care not to confuse the cremaster reflex with the contraction of the 
dartos. The clinical significance of the cremaster reflex is similar to that of the 
abdominal reflex. The reflex arc of the cremaster reflex is at the level of the 
first and second lumbar nerves. Other cutaneous reflexes — the gluteal, the mam- 
mill a ry, etc. — have at present no special practical significance. 

Tendon Reflexes. — Of almost greater practical importance than the investiga- 
tion of the cutaneous reflexes is the test of the phenomena classed under the 
name of the " tendon reflexes," and first carefully investigated and described by 
Erb and Westphal in the year 1875. We understand by these those muscular con- 
tractions which arise from the brief mechanical irritation of the tendons and 
analogous parts, such as the periosteum and fasciae. Westphal originally held 
that these contractions were the result of direct mechanical irritation, but later 
accurate clinical and experimental work has shown that the " tendon reflexes," as 
Erb had maintained from the beginning, are true reflex phenomena, starting 
from the mechanical irritation of the sensory nerves in the tendons, periosteum, 
etc. The tendon reflex of most practical importance is the patellar reflex, " knee 
phenomenon" (Westphal) [or "knee-jerk" (Mitchell)] — that is, a contraction 
occurring in the quadriceps after mechanical irritation of the ligamentum patellae 
by a quick blow with a percussion hammer. In order to evoke this reflex it is 
especially necessary for the person examined to avoid all active muscular tension 
in the leg, especially in the extensor. If we examine patients who are not in bed, 
we can test the patellar reflex by making the patient while sitting cross the leg 
to be tested over the other, and by striking the patellar tendon as the leg hangs 
loose ; but it seems to us more convenient to direct the patient to extend the leg 
until it forms an obtuse angle with the thigh with the opening of the angle below. 
If the sole be set fully on the floor the extensor cruris is made tense in this posi- 
tion, and we can very easily and plainly excite the contraction of the quadriceps 
by striking the patellar tendon. When the patient is in bed it is best to raise the 
leg to be tested into a semi-flexed position by putting the left hand under the 
hollow of the knee; the foot remains lying on the bed, and the patient should 
avoid any active muscular tension. If the patellar reflex be weak and hard to 
detect, we should try the proceeding advised by Jendrassik, which consists in 
testing the reflex while the patient grips the two hands together, and tries with 
all his strength to pull them apart. By this or any other vigorous tension of the 
muscles of the upper extremities the muscles of the legs are probably greatly re- 
laxed, while any voluntary innervation is avoided, and thus is explained the in- 
crease of the reflex, which is often pronounced. If by the help of this " Jendras- 
sik' s test " no reflex is to be elicited, we may regard it as absent, a condition 
which is almost always of pathological significance, since complete absence of the 
patellar reflex practically never occurs in health. The reflex arc in the cord for 
the patellar reflex is found in the second lumbar segment. 



BEMABKS UPON THE DISTURBANCES OF MOTILITY 841 



The second important tendon reflex to be provoked in the lower extremity is 
the Achilles tendon reflex. If we give to the foot of the person examined (who 
should lie on his side in bed) a passive position of slight dorsal extension, so that 
the tendo Achillis is a little tense, and then strike the tendon a quick blow, a 
marked contraction of the gastrocnemius follows. Precisely the same reflex is 
usually to be elicited by striking the plantar fascia. The Achilles tendon reflex is 
not quite so constant in healthy persons as the patellar reflex, but it is usually 
present and well marked. Its reflex arc in the cord lies at the level of the third 
to the fifth sacral segments. Where the tendon reflexes are abnormally increased, 
however, the Achilles tendon reflex is very vigorous, and then we can very often 
produce it in the following especially characteristic manner. If we make a sud- 
den, short, vigorous, passive, dorsal extension of the foot, the tendo Achillis is 
suddenly made tense, and thus is irritated mechanically. As a result of this, 
there is a reflex plantar flexion of the foot. If now, by persistent passive dorsal 
extension of the foot, the tendo Achillis is again made tense, there follow by 
turns new plantar and dorsal movements of the foot, so that the foot is thus 
put into a vigorous tremor. This symptom, which can only exceptionally be pro- 
voked in healthy persons, is termed ankle clonus (foot clonus), or "foot phenom- 
enon" (Westphal). Where there is a very great increase of the tendon reflexes 
the tremor is sometimes not confined to the foot, but the whole leg falls into a 
vigorous clonus, a symptom which was once given the unsuitable name of spinal 
epilepsy, since it apparently came on spontaneously as a result of some tension of 
the tendons. We can also obtain the patellar reflex in the form of a clonus if we 
pull the patella firmly down with the finger and force it downward by a sudden 
blow on the finger. 

The two symptoms described — the patellar reflex, and the Achilles tendon re- 
flex or foot phenomenon — are practically the most important, and are the most 
often tested, but they are by no means the only reflexes in the lower extremity. 
Besides the reflexes from the special tendons, we also frequently obtain muscular 
contractions by striking the periosteum and the fasciae, which have been termed 
the periosteal and fascia reflexes. Thus a contraction in the quadriceps often 
follows a blow on the anterior surface of the tibia when the reflex excitability is 
increased. We also see contractions frequently in the adductors of the thigh on 
striking the internal condyle of the femur, contractions in the muscles of the 
posterior aspect of the thigh in striking the calves, etc. 

Under normal conditions the tendon reflexes in the upper extremities are 
sometimes quite weak or entirely absent, but where the irritability is abnormally 
increased we see even here the most various and vigorous reflexes. The most 
important and most constant are the periosteal reflexes, from striking on the 
lower end of the radius and ulna. As a rule, in our observations, we have usually 
obtained a contraction in the supinator longus and biceps from a blow on the 
head of the radius, and a weaker contraction in the same muscles from the head 
of the ulna, and also, very frequently, pronation of the forearm and flexion of the 
wrist and fingers. The deltoid also contracts not infrequently from a blow on the 
lower end of the ulna. Direct tendon reflexes in the biceps and triceps on strik- 
ing their own tendons are also almost always to be obtained. [The triceps reflex 
seems the most constant of all the reflexes of the upper extremity. — K.] We may 
also not infrequently obtain a contraction in the biceps by a blow on the clavicle. 
A persistent clonus in the hand upon passive volar flexion sometimes occurs, but it 
is rare. 

A more detailed account of the behavior of the cutaneous and tendon reflexes 
in the individual diseases of the nervous system will be given later in the special 
chapters, where we shall also learn the present theories as to the course of the 
reflex tracts and the influence of other nerve tracts upon them. 



842 



DISEASES OE THE NEKVOUS SYSTEM 



Mechanical Muscular Irritability and Paradoxical Contraction. — "Direct 
mechanical irritability of the muscles " is shown by the occurrence of energetic 
brief contractions of single muscular bundles or of the whole muscle from a direct 
blow on the belly of the muscle with a percussion hammer. In such cases, how- 
ever, we are dealing, in my opinion, not with a direct muscular irritation, but with 
a mechanical irritation of the nerves which enter the muscle, since the muscular 
contractions are always strongest when we strike the corresponding point of 
entrance of the nerves, precisely the same as faradic irritation of the muscle. 
The ensuing muscular contraction, however, may sometimes be a reflex, evoked 
by mechanical irritation of the fascia stretched over the muscle. These contrac- 
tions just described are to be distinguished from the so-called idiomuscular con- 
tractions. We see these most plainly if we give a vigorous blow with the ulnar 
side of the hand or with a percussion hammer to the belly of a muscle, such as the 
biceps. A small transverse, circumscribed muscular swelling forms at the point 
struck, and gradually disappears again. The test for mechanical muscular irrita- 
bility has not yet attained any special practical importance. 

" Paradoxical contraction " is the name which Westphal has given to a symp- 
tom seen especially in the tibialis anticus, and rarely also in the flexors of the leg 
and forearm. It is when the foot, after being put in passive dorsal extension, re- 
mains in this position even after the expiration of a considerable time (several 
minutes), and a marked prominence of the tendon of the tibialis anticus is usu- 
ally visible. We can not at the present time give a definite explanation of this 
phenomenon, which so far has been observed in various spinal and cerebral dis- 
eases, multiple sclerosis, paralysis agitans, etc. 

5. General Remarks upon the Changes of Electrical Excitability in 
the Motor Nerves and Muscles* 

Electricity, since the investigations of Duchenne, Kemak, Benedikt, Moritz 
Meyer, von Ziemssen, Brenner, Erb, and others, has become not only one of the 
most prominent therapeutic aids in the treatment of nervous diseases, but it also 
plays an extremely important part in the examination of nervous patients, since 
the test of the electrical excitability of diseased nerves and muscles gives us a 
large amount of valuable information in regard to diagnosis and prognosis. 

Every complete electrical examination must be made with both currents — the 
faradic or induction current (usually the secondary current), and the galvanic or 
constant current. One " indifferent " pole is usually put on the sternum or the 
back of the neck, and the other " testing " pole on the nerve or muscle to be 
tested. For the indifferent pole we use a large electrode (about twelve centi- 
metres long), and as a testing pole a smaller electrode, the best being Erb's 
" normal electrode," with a surface of ten square centimetres. The excitement 
of the muscle from the nerve is called indirect; the excitement from placing 
the electrode on the muscle itself (where, of course, the excitement of the intra- 
muscular nerves can not be excluded) is called direct. Those points on the human 
body where the different nerves and muscles are most easily accessible to the elec- 
trical excitement are to be found in Figs. 99 to 104, taken from Erb's handbook. 

In faradic examination the normal condition is that we can provoke marked 
muscular contractions both from the nerves and from direct excitement of the 
muscles at the points generally accessible to excitement. As von Ziemssen has 
found, the points at which the muscle can most easily be made to contract by 



* In regard to all the details of electrical diagnosis and electro-therapeutics we would refer to Erb's 
" Handbuch der Elektrotherapie." Leipsic, Vogel, 1886. [Translated by De Watteville. New York : 
Win. Wood & Co., 1887.] E. Kemak's " Grundriss der Elektrodiagnostik und Elektrotherapie." 
Vienna, 1895, etc. 



KEMARKS UPON THE DISTURBANCES OF MOTILITY 843 



" direct " excitement correspond exactly to the points where the motor nerves 
enter the muscle. The direct faradic muscular excitation is therefore always a 
nerve excitation. In order to determine the excitability quantitatively we meas- 
ure the distance between the two coils of the induction apparatus (coil distance, 



Frontalis. 

Facial 
(upper branch). 

Corrugator supercilii, 



Orbicul. palpebrarum 
Nasal muscles. < 



Zygomatici. 



Orbicularis oris. 



Facial (middle br'ch), 
Masseter, 

Levator menti. 
Quadratus menti. 
Triangularis menti. 

Hypoglossals. 
Facial {lower branch). 

Platysma myoides. 

Kyoid muscles. \ 



Omo-hyoid. 



Anterior thoracic 
(Pectoralis major). 




Region of the central 
convolutions. 



Region of the third 
frontal convolution 
and the insula 
(speech center;. 

Temporalis. 

Facial {upper) in 
front of ear. 

Facial (trunk). 
Posterior auricular. 
Facial (middle brch). 
Facial (lower branch). 
Splenius. 

Sterno-cleido-mastoid . 

Spinal accessory. 
Levator ariguli 

scapulae. 
Trapezius. 

Dorsalis scapulae. 
Axillary (circumflex). 

Long thoracic (serra- 
tus magnusj. 



Phrenic. Supraclavicular point. 

(Erb 1 s point. Deltoid, 
biceps, brachialis amicus, 
and supinator longus.) 

Fig. 99. 



Brachial plexus. 



Rollenabstand) at which the first minimal contraction of the muscle occurs. On 
increasing the current, the minimal contraction gradually passes into a vigorous 
tetanic contraction of the muscles. 

Galvanic examination is performed by the aid of a "current reverser," by 
which the current at any desired strength can be rapidly opened and closed and 
the testing pole can be made either the negative pole (the cathode or zinc pole) 
or the positive pole (the anode or copper or carbon pole). 

The nerves and muscles are excited not by the continuous flow of the elec- 
trical current, but only by its variations and the sudden opening and closing of 
the current. 

By the help of this " polar method of investigation " (Brenner) we can easily 
determine the law of contraction, which holds equally for the normal motor nerves 
and for the muscles. 

With a very weak current no noticeable excitement takes place. If we grad- 
ually increase the strength of the current, the first weak contraction of the muscle 
occurs at the closure of the cathode — that is, when the current is closed so that 
the cathode is made the testing pole. On opening the cathode, or on closing or 
opening the anode, nothing follows. If we increase the strength of the current 
still more, the cathodic closure contractions become stronger, and the anodic 



844 



DISEASES OF THE NERVOUS SYSTEM 



closure and anodic opening contractions appear, now the one being earlier and 
stronger, and now the other. Opening of the cathode has still no effect. Only 
with a very strong current, in which the cathodic closure contractions have 
already become tetanic — that is, they still persist after the closure of the current 
— can we provoke weak cathodic opening contractions. Expressed in the abbrevia- 



Triceps (long head) 



Triceps (internal head) 



Ulnar. 



Flexor carpi ulnaris 
Flexor profundus digitorum, 



Flexor sublimis digitorum 
(II and IU). 



Flexor sublimis digitorum 
a and IV). 

Ulnar. 

Palmaris brevis. 
Abductor minimi digiti. 
Flexor brevis minimi digiti. 
Opponens minimi digiti. 

Lumbricales. < 




Deltoid (anterior 
half). 



Musculo-cutaneous 
Biceps. 

Brachialis anticus 



Supinator longus. 
Pronator radii teres. 
Flexor carpi radialis. 



Flexor sublimis digitorum. 

Flexor longus pollicis. 
Median. 

Abductor pollicis. 
Opponens pollicis. 
Flexor brevis pollicis. 
Adductor pollicis. 



Fig. 100. 

tions now in general use in electrical diagnosis, the law of contraction for normal 
muscles and nerves in man is as follows : * 

* Ka signifies cathode, An = anode, S = closure, O = opening, z (Zuckung) — weak contraction, 
Z = stronger contraction, Te = tetanus. Sometimes the increasing strength of the contractions is 
abbreviated by the signs Z, Z' and Z". [Many English and American writers on electricity use letters 



KEMARKS UPON THE DISTURBANCES OF MOTILITY 845 



1. Lowest degree with weak currents : XaSz, KaO — , AnS — , AnO — . 

2. Middle degree with stronger currents : KaSZ, KaO — , AnSz, AnOz. 

3. Highest degree with very strong currents : KaSTe, KaOz, AnSZ, AnOZ. 

The variations from the normal state seen under pathological conditions con- 
sist of quantitative and also of qualitative changes in the law of contraction. We 
term the simple increase or diminution of the electrical excitability in nerves or 
muscles, without simultaneous changes in the quality and order of the occurrence 
of muscular contractions, quantitative changes. The discovery of increased or 
diminished excitability of nerve and muscle can be made most easily in unilateral 
diseases, where we can compare the strengths of current required to obtain the 
minimal contraction on the diseased and healthy sides with each other. This is 
now determined without any special difficulty, since the general introduction of 



Deltoid (posterior half). 





Triceps (long head). 



Radial (musculo-spiral). 
Brachialis anticus. 

Supinator longus. 
Extensor carpi radialis longior. 
Extensor carpi radialis brevior. 

Extensor communis digitorum. -j 
Extensor indicis. 

Extensor ossis metacarpi pollicis. 
Extensor primi internodii pollicis. 



Dorsal interossei, I and II. \ 



Fig. 101. 

the absolute galvanometer. With the galvanometer thrown out of circuit we find 
with how many cells or at what position of the rheostat the first distinct cathodic 

derived from the English names. Thus C stands for cathode, closure, and contraction. A and have 
the same meaning. It seems to us clearer and conducive to greater harmony to retain the German 
abbreviations, which are simple and definite. — Trans.] 




Triceps (external head). 



®-—-.:?-7, ( — Extensor carpi ulnaris. 
'•• y Supinator brevis. 

— Exteusor minimi digiti. 
Extensor indicis. 



Extensor secundi internodii 
pollicis. 



-Abductor minimi digiti. 

/ Dorsal interossei, 
j" III and IV. 



DISEASES OF THE NERVOUS SYSTEM 



846 



closure contraction (KaSZ) occurs. Then the galvanometer is put into the cir- 
cuit and the strength of the current in milliamperes is read off directly. By 




extensive investigations on healthy persons Stintzing has found certain limits 
within which the normal excitability of the different nerves varies. Deviations 
from these figures above or below normal accordingly permit us to recognize an 
increase or a diminution of the galvanic excitability. It is to be borne in mind 
that Stintzing uses a small " normal electrode " with a surface of three square 
centimetres. Some of the most important averages found by Stintzing are shown 
in the following table : 

Facial nerve. . . . 
Accessory nerve 
Ulnar nerve. . . . 
Median nerve. . 
Radial nerve . . . 
Crural nerve. . . 
Peroneal nerve. 
Tibial nerve . . . 

An accurate measurement of the absolute strength of the faradic current is 
possible, but it has as yet been but little introduced into practice. We usually 
content ourselves, as we have said, with the statement of the coil distance at 
which the first perceptible contraction occurs. Stintzing found as an average 
position for the frontal nerve, 128.5 millimetres ; for the accessory nerve, 137 milli- 
metres ; for the radial nerve, 105 millimetres ; for the median nerve, 122.5 milli- 



1.0-2.5 milliamperes. 

0.1-0.4 " 

0.2-0.9 " 

0.3-1.5 " 

0.9-2.7 " 

0.4-1.7 " 

0.2-2.0 " 

0.4-2.0 " 



REMARKS UPON THE DISTURBANCES OP MOTILITY 847 



metres; for the ulnar nerve, 130 millimetres; for the crural nerve, 111.5 milli- 
metres; for the peroneal nerve, 115 millimetres; and for the tibial nerve, 107.5 
millimetres. We must refer to the special works for further details. 

Changes in the quantitative electrical excitability are not uncommon in patho- 
logical conditions, but they have no very great practical diagnostic significance. 
A pathological increase of electrical excitability is seen especially in tetany, a 
diminution in many cases of neuritis, and sometimes also in myelitis, pressure 
paralyses, etc. The apparent diminution of excitability is often due only to 
increased resistance (dry, thick skin, thick layer of fat, etc.). 

Much more important, however, than the simple quantitative changes of elec- 
trical excitability are those not merely quantitative but also qualitative devia- 



Sciatic 



Biceps femoris (long head), 



Biceps femoris (short head) [ 



Peroneal. 

Gastrocnemius (external head). 

Soleus. 

Flexor longus hallucis 




Gluteus maximus. 



Adductor magnus. 
Semitendinosus. 
Semimembranosus. 



Posterior tibial. 



Gastrocnemius (internal head). 



Soleus. 



Flexor longus digitorum. 



Tibial. 



Fig. 103. 

tions from the normal law of contraction, which were first discovered in certain 
forms of paralysis by Baierlacher in 1859, and were soon generally confirmed. 
Erb has given these the name of the " reaction of degeneration," because they are 
closely connected with the progress of certain anatomical changes in the para- 
lyzed muscles and nerves. 

In order to make the relations of the reaction of degeneration clear, let us 
select as an example any fresh peripheral paralysis and follow the changes in 
excitability to the two currents in the nerves and muscles. In a short time (two 



848 DISEASES OP THE NERVOUS SYSTEM 

or three days) after the onset of the paralysis a gradually increasing decline in 
the faradic and galvanic excitability in the nerve begins. After one or two 
weeks the excitability is completely lost, so that from the nerve we can no longer 
provoke any trace of muscular contraction with the strongest faradic or con- 
stant current. During this time the excitability of the paralyzed muscles to 
the faradic current has also rapidly diminished, and finally has wholly disap- 
peared. The case is quite different with galvanic excitement of the muscles. 
Here we find at first a slight diminution, which in the second week passes to a 
decided increase of the galvanic muscular excitability. We now obtain marked 
muscular contractions with relatively very weak currents. Besides that, two 
other very important peculiarities are to be noted : 1. The muscular contractions 
are first of all not short and lightning-like, as under normal conditions, but they 




Fig. 104. 



seem quite sluggish, protracted, " worm-like," and often persist during the whole 
duration of the closure of the current. 2. The muscular contractions occur not 
only chiefly at cathodic closure (KaS), as under normal conditions, but the anodic 
closure contractions (AnSZ) are as strong as the cathodic closure contractions 
(KaSZ), or even plainly exceed them. With stronger currents anodic closure 
tetanus (AnSTe) is readily obtained. The cathodic opening contraction (KaOZ) 
is also frequently stronger. 3. It may finally be mentioned here that the mechan- 
ical irritability of the muscles in such cases is usually increased, and the muscles 
when struck also show a slow, worm-like contraction. 

This second degree of the reaction of degeneration lasts from four to eight 
weeks. If the paralysis be severe and long continued, or incurable, at the end of 
this period comes a decline of the galvanic muscular excitability. The contrac- 



BE1IARKS UPOX THE DISTURBANCES OF MOTILITY 849 



tions become weaker, the strength of current necessary to produce them greater, 
and, finally, in incurable cases, even with the strongest currents, we can obtain 
only a little slow anodic closure contraction (AnSZ), or none at all. It is differ- 
ent, however, in the milder, curable cases. In these the passage to the normal con- 
dition gradually follows either the increase of the galvanic muscular excitability, 
or, in more protracted cases, its secondary decline. The contractions become more 
vigorous and shorter, the cathodic closure contraction (KaSZ) again pre- 
dominates, the faradic muscular excitability and the faradic and galvanic excita- 
bility of the nerves finally return, and with them the old normal conditions are 
restored. A fact to be observed in these cases is of great interest, namely, that 
the voluntary motion in such cases often returns decidedly earlier than the elec- 
trical excitability of the peripheral nerves. We see, then, that a diseased nerve 
may be capable of conducting excitations coming from the brain, while the taking 
up of excitation, its direct excitability, is still completely lost. In such cases we 
can obtain a muscular contraction by electrical excitation of the nerve above the 
point of lesion. 

Besides the complete reaction of degeneration just described, there is also a so- 
called partial reaction of degeneration, which is not infrequent in milder cases. 
This may show itself in several forms, but it is chiefly when the diminution 
of the faradic and galvanic excitability in the nerves and the diminution of 
faradic excitability in the muscles is only of a slight degree, while the character- 
istic changes in the direct galvanic excitement of the muscles — ready appearance 
of anodic closure contractions (AnSZ), and especially the noticeably slow charac- 
ter of the ensuing muscular contractions — are fully developed. In general the 
slow muscular contraction on direct galvanic irritation of the muscles is practi- 
cally the most important symptom of reaction of degeneration. "We sometimes 
see the occurrence of slow contractions on faradic excitement of nerves and mus- 
cles — " faradic reaction of degeneration," and in some cases we even see slow 
muscular contractions on indirect galvanic irritation of the nerve (partial reac- 
tion of degeneration with indirect slowness of contraction). In the course of 
atrophic paralyses we often see that the different varieties of reaction of degen- 
eration pass into one another as the process advances or improves (Stintzing). 

Anatomical Changes of the Nerves and Muscles in the Reaction of Degen- 
eration; its Significance in Diagnosis and Prognosis. — As we have previously 
seen, all paralyses may be divided into two great groups — into atrophic paralyses, 
and paralyses without marked atrophy of the affected muscles. We have learned 
to recognize the necessary hypothesis of the " trophic " influence of the ganglion- , 
cells in the anterior comua of the spinal cord as the foundation of this distinction, 
an influence which is easily to be understood when we consider that ganglion-cell 
and peripheral motor nerve-fiber form an anatomical unit with which the muscu- 
lar fiber is directly connected as a terminal organ. In all cases where the disease 
affects these ganglion-cells, or is situated in the peripheral nerves, so that the 
trophic influence of the ganglion-cells on the muscles can no longer be of influ- 
ence, we have a degenerative atrophy of the peripheral portion of the nerve, and 
also a relatively rapid atrophy of the muscle belonging to it. This secondary de- 
generation of the peripheral nerves and the consequent atrophy of the muscles 
are the anatomical causes of the phenomena of electrical reaction of degeneration. 

If we have to do with a peripheral paralysis, such as a traumatic lesion of a 
nerve-trunk, the portion of the nerve peripheral to the point of lesion is separated 
from its cell of origin in the cord, and begins to undergo secondary degeneration. 
The first anatomical sign of the degeneration is a breaking down of the medullary 
sheath at first into large and gradually into smaller flakes and drops. The axis 
cylinder is also soon destroyed, so that the sheath of Schwann finally incloses only 
approximately homogeneous fluid contents, which are in great part rapidly ab- 
54 



850 



DISEASES OF THE NERVOUS SYSTEM 



sorbed. At the same time there is an increase of the nuclei in the sheath of 
Schwann, and this increase, when the process is long continued, leads to a de- 
cided increase of the interstitial connective tissue in the nerve. The diminution 
and final loss of electrical irritability in the nerve are perfectly parallel to these 
anatomical changes, for we can readily understand that such a completely de- 
stroyed nerve can be excited neither by the f aradic nor by the g-alvanic current. 

The degeneration of the nerve involves its finest terminal branches in the 
muscles ; but the muscle itself, as we have said, does not remain unchanged. The 
muscular fibers undergo a marked atrophy. They become much smaller, their 
transverse striation may be preserved for a long time, but it often becomes some- 
what less distinct. Some muscular fibers show a peculiar yellow homogeneous 
consistency which is called " waxy degeneration." Fatty or marked granular de- 
generation of the fibers occurs only in the later stages. The motor end-plates of 
the nerves in the muscles are spared for a comparatively long time, and they dis- 
appear only when the degeneration of the muscles has reached the highest degree. 
There is also a considerable increase in the muscle nuclei and in the later stages 
a considerable new formation of interstitial connective tissue, often associated 
with an abundant deposit of fat. Muscles thus altered react only to the galvanic 
current and in the slow manner described above. We recognize from this that 
the muscle deprived of its nerve still retains a certain trophic independence. The 
slow galvanic contraction is the expression of the purely muscular irritability 
which is still retained by itself in the muscle deprived of its nerve and conse- 
quently atrophied, while the faradic irritability is lost because the faradic irrita- 
tion of the muscle can be accomplished only by means of the terminal branches of 
the nerve in the muscle. 

In the incurable cases the processes of degeneration just described gradually 
advance, but, in the cases that recover, a number of processes of regeneration 
begin sooner or later. We can not here go into the finer details. We would men- 
tion merely that the " regeneration " in all probability takes place only from the 
central nerve-stump; that it consists, therefore, essentially of a new outgrowth 
from the maimed neurones. The old nerve-sheaths of the cut-off or degenerated 
peripheral portion serve as conduction tubes. The axis cylinders grow out first, 
and then new medullary sheaths are formed. The end-plates of the nerves are 
restored very early, according to Gessler, even before the nerve-fibers. The mus- 
cular fibers also increase in volume at the same time. 

Voluntary motion in the previously paralyzed muscle returns hand in hand 
with the processes of regeneration. It appears, as has been already mentioned, 
sooner than the normal electrical excitability of the nerves and muscles, because 
it can take place as soon as the axis cylinders are again formed, while the normal 
electrical excitability of nerves and muscles can take place only after the restora- 
tion of the medullary sheaths. We usually express this fact by saying that the 
reception of peripheral irritations depends upon the persistence of the medullary 
sheath. The destroyed medullary sheaths perhaps form a sort of isolating layer 
about the axis cylinders, which is only a poor conductor of the electrical current. 
This is the reason why in diseases of the peripheral nerves we sometimes find re- 
action of degeneration in muscles and nerves which have lost none of their vol- 
untary motility. In such cases there is probably disease of the medullary sheaths 
without much degeneration of the axis cylinders. 

The same anatomical changes, which we have just described as a secondary 
degeneration in lesions of the peripheral motor nerves, also develop, if the pri- 
mary disease has its seat in the anterior cornua of the gray matter of the spinal 
cord — that is, in the trophic centers themselves. In these cases, of course, the 
form of the disease has nothing to do with it. Both in the different forms of 
inflammation and of primary atrophy, and also in new growths, which affect the 



REMARKS UPON THE DISTURBANCES OF MOTILITY -51 



anterior gray matter of the cord, a secondary degeneration, with pronounced reac- 
tion of degeneration, develops from the anterior roots of that portion of the cord 
affected to the ends of the peripheral nerves, and even to the corresponding mus- 
cles. We shall also learn to recognize a number of primary degenerations of the 
peripheral nerves, such as primary neuritis, diphtheritic and toxic paralyses, etc. 
In such cases we find almost precisely the same anatomical changes as in sec- 
ondary degenerations, and, in consequence of these changes, there is also elec- 
trical reaction of degeneration in the paralyzed nerves and muscles. In all cere- 
bral paralyses, however, and in those spinal paralyses where the cause of the 
paralysis is situated above the part of the anterior gray cornua concerned, the 
degeneration of the peripheral nerves, and also the reaction of degeneration, are 
entirely wanting. 

We thus see that the reaction of degeneration, in regard to diagnosis, at once 
permits us to decide that the disease is situated in the anterior gray cornua, in 
the anterior roots, or in the peripheral nerves. It does not permit any further 
distinction. In regard to prognosis, it teaches us that anatomical changes have 
taken place in the nerves and muscles, from which, under some circumstances 
(that is, if the ganglion-cell bodies are still preserved), a restoration is still very 
possible, but at all events it can take place only after the lapse of a considerable 
time, at least two or three months. We shall soon learn to recognize a number of 
mild peripheral paralyses in which there is generally no reaction of degeneration. 
From the absence of reaction of degeneration we can then draw the conclusion, 
with certainty, that no coarse anatomical changes are present in the nerve, and 
that we may expect a much more rapid recovery from the trouble, perhaps in 
three or four weeks. The partial reaction of degeneration, above mentioned, is 
also an important symptom in regard to prognosis. It shows probably that slight 
changes have occurred only in the terminal branches of the muscle nerves, while 
the larger nerve-trunks have remained approximately normal. The latter have 
therefore retained their electrical excitability while the terminal branches of the 
nerves have lost it. The partial reaction of degeneration therefore always permits 
a more favorable prognosis in regard to time than the complete reaction of degen- 
eration. 



6. Table of the Different Forms of Voluntary AIotiox and the Muscles 
and Xerves coxcerxed Therelx 

In order to obtain an accurate knowledge of the extent of the paralysis in 
complicated paralytic conditions (hemiplegia, paraplegia, muscular atrophy, etc.), 
it is imperatively necessary to test all the muscle groups in order. The perform- 
ance of these tests and their diagnostic value and significance will be materially 
aided by the use of the following table, arranged according to movements. 

I. MUSCLES OF THE HEAD AND TRUNK 

1. Facial Muscles and Muscles of Mastication 

1. Wrinkling the forehead transversely (Mm. frontalis et occipitalis. X. 
facialis). 

2. TVrinkling the forehead longitudinally (M. corrugator supercilii. X. 
facialis). 

3. Closing the eyes (M. orbicularis palpebrarum. X. facialis). 

4. Dilating the nostrils (M. compressor nasi et M levator ala? nasi. X. 
facialis). 

5. Drawing the mouth outward and upward (Aim levator labii superioris. 
zygomatici, risorius, X. facialis). 



852 



DISEASES OF THE NERVOUS SYSTEM 



6. Drawing the mouth downward (M. depressor anguli oris et labii superioris, 
1ST. facialis). 

7. Kaising the lower lip (M. levator menti, N. facialis). 

8. Protruding the lips and whistling (M. orbicularis oris, N. facialis). 

9. Chewing (Mm. masseter et temporalis, motor branch of N. trigeminus). 

10. Lateral and forward movements of the lower jaw (Mm. pterygoidei externi 
et interni, N. trigeminus). 

2. Ocular Muscles 

1. Kaising the upper lid (M. levator palpebrse superioris, N. oculomotorius). 

2. Looking upward and inward (M. rectus superior) and upward and outward 
(M. obliquus inferior, 1ST. oculomotorius). 

3. Looking inward (M. rectus internus, M. oculomotorius). 

4. Looking outward (M. rectus externus, N. abducens). 

5. Looking downward and inward (M. rectus inferior, "N". oculomotorius). 

6. Looking downward and outward (M. obliquus superior, 1ST. trochlearis). 

7. Contraction of the pupil (sphincter iridis, 1ST. oculomotorius). 

8. Accommodation (M. ciliaris, ~N. oculomotorius). 

3. Tongue. Soft Palate. Pharynx. Larynx 

1. Tongue movements (N. hypoglossus). 

2. Soft palate (N. vago-accessorius). 

3. Swallowing (N. vago-accessorius). 

4. Epiglottis (Mm. thyreo-epiglotticus et ary-epiglotticus, 1ST. laryngeus supe- 
rior). 

5. Vocal cords (N~. recurrens). 

4. Head and Trunk 

1. Elexion of the head and cervical vertebras forward (Mm. recti capitis antici, 
longus colli rectus, cervicales 1-3), M. sterno-cleido-mastoideus (N. acces- 
sorius). 

2. Movement of the head and cervical vertebras backward (Mm. splenius capi- 
tis et colli, biventer complexus, recti capitis postici, spinalis et semispinalis cervi- 
cis, 1ST. cervicales 1-4). 

3. Turning the head (M. sterno-cleido-mastoideus, N". accessorius, M. obliquus 
capitis inferior et obliquus colli). 

4. Lateral flexion of the head (Mm. recti capitis laterales, M. spinalis cer- 
vicis). 

5. Extension of the vertebral column (Mm. sacro-lumbalis et longissimus 
dorsi, M. spinalis dorsi). 

6. Flexion of the vertebral column forward (abdominal muscles). 

7. Torsion of the vertebral column (M. semispinalis dorsi). 

8. Lateral flexion of the vertebral column (M. quadratus lumborum, inner- 
vated from the crural plexus), Mm. intertransversarii. 

9. Diaphragm (N. phrenicus from !N". cervicales 4 and 5). 

i 

II. SHOULDER-BLADE AND UPPER EXTREMITY 

1. Movements of the Shoulder-blade 
1. Raising the shoulder-blade (M. trapezius, N". accessorius, M. levator anguli 
scapulas, 3 and 4 C. !N".*). 



* C. N. = cervical nerve, L. N. = lumbar nerve, S. N. = saeral nerve, that is, the several anterior 
roots arising from the corresponding segment of the spinal cord. 



KEMAEKS UPON THE DISTURBANCES OF MOTILITY 853 



2. Drawing the shoulder-blade toward the median line (Mm. rhomboidei, Mm. 
thoracici posteriores from 4 and 5 C. N.). 

3. Fixation and rotation of the shoulder-blade in raising the upper arm to a 
vertical position (M. serratus anticus major, N. thoracicus major from 5 C. N.). 

2. Movements at the Shoulder 

1. Raising the arm forward and outward (M. deltoideus, N. axillaris * [cir- 
cumflex] from 4 and 5 C. N.). 

2. Adduction and drawing downward (Mm. pectorales major et minor, N. 
thoracici anteriores from 6 C. 1ST., M. latissimus dorsi, N. subscapularis longus 
from 5 and 6 C. N.). 

3. Outward rotation (Mm. supraspinalis, infraspinalis, teres minor, N. supra- 
scapularis from 4 C. N.). 

4. Inward rotation (Mm. subscapularis et teres major, N. subscapularis from 
6 C.N.). 

3. Movements at the Elbow 

1. Flexion (Mm. biceps et brachialis anticus, N. musculo-cutaneus ; 5 and 
6 C. N., M. supinator longus, N. radialis [musculo-spiralis] ; 6 and 7 C. N.). 

2. Extension (M. triceps, N. radialis, 6 and 7 C. N.). 

3. Pronation (Mm. pronator teres et pronator quadratus, N. medianus; 
6 C. N.). 

4. Supination (M. biceps, 1ST. musculo-cutaneous, M. supinator brevis, N. 
radialis; 5 C. N.). 

4. Movements at the Wrist 

' 1. Dorsal extension (Mm. extensor carpi radialis longus et brevis, extensor 
carpi ulnaris, N. radialis; 6 and 7 C. N.). 

2. Volar flexion (Flexor carpi radialis, N. medianus. Flexor carpi ulnaris, 
N. ulnaris; 7 and 8 C.N.). 

3. Padial flexion (M. extensor carpi radialis longus). 

4. Ulnar flexion (Mm. flexor et extensor carpi ulnaris). 

5. Movements of the Fingers 

1. Extension of the proximal phalanges (Mm. extensor digitorum communis, 
extensor indicis, extensor minimi digiti, N. radialis; 6 and 7 C. N.). 

2. Extension of the distal phalanges [phalangines and phalangettes] (M. in- 
terossei, 1ST. ulnaris). 

3. Flexion of the proximal phalanges (Mm. interossei et lumbricales, Nn. 
ulnaris et medianus; 7 and 8 C. N.). 

4. Flexion of the distal phalanges (Mm. flexor digitorum sublimis et pro- 
fundus, the latter for the third phalanx [phalangettes], N. medianus; 7 and 
8 C.N.). 

5. Spreading the fingers, abduction (Mm. interossei externi [dorsales], N. 
ulnaris; 8 C.N.). 

6. Adduction of the fingers (Mm. interossei interni [palmares], N. ulnaris). 

7. Flexion of the proximal phalanx and abduction of the little finger (Mm. 
flexor brevis et abductor digiti minimi in the hypothenar eminence, N. ulnaris). 

6. Movements, of the Thumb 

1. Extension of the metacarpal and both phalanges (Mm. extensor pollicis 
brevis et longus, the latter for the second phalanx, N. radialis; 8 C. N.). 

2. Abduction of the metacarpus (M. abductor pollicis longus, N. radialis). 



* We have followed Henle's nomenclature for the peripheral nerves. — K. 



854 



DISEASES OE THE NERVOUS SYSTEM 



3. Adduction of the metacarpus (M. adductor et caput profundurn flexoris 
brevis, X. ulnaris). 

4. Elexion and opposition of the metacarpus, flexion of the first phalanx with 
simultaneous extension of the distal phalanx (Thenar muscles: Mm. opponens, 
abductor brevis et caput superficiale flexoris brevis. X. medianus; 8 C. X.). 

5. Elexion of the second phalanx (M. flexor pollicis longus, X. medianus). 

III. LOWER EXTREMITY 

1. Move ments at the Hip 

1. Elexion (Mm. ilio-psoas, sartorius, X. cruralis. M. tensor vagina? femoris, 
X. glutaeus superior; 2 and 3 L. X.). 

2. Extension (AL glutteus maximus, X. glutaeus inferior from the sciatic 
plexus ; 1 S. X.). 

3. Abduction (M. glutaeus medius et minimus, X. glutseus superior ; 1 S. X.). 

4. Adduction (Mm. adductor brevis. adductor longus, adductor magnus. 
pectineus, gracilis, X. obturatorius from lumbar plexus; 3 L. X.). 

5. Outward rotation (Mm. pyrifonnis. obturatur interims, gemelli. quadratus 
femoris, X. ischiadicus, M. obturator extemus, X. obturatorius from lumbar 
plexus; 5 L. X.). 

6. Inward rotation (Mm. glutaeus medius et minimus, X. glutaeus superior : 
1 S. X.). 

2. Movements at the Knee 

1. Extension (M. extensor cruris quadriceps. X. cruralis; 3 and 4 L.X.). 

2. Elexion (Mm. biceps, semimembranosus et semitendinosus. X. ischiadi- 
cus ; 4 and 5 L. X.). 

3. Movements at the Ankle and of the Toes 

1. Dorsal extension of the inner edge of the foot (M. tibialis anticus. X. 
peroneus ; 2 S. X.). 

2. Dorsal extension of the outer edge of the foot (Mm. peroneus longus et 
brevis, X. peroneus; 2 S. X.). 

3. Plantar flexion of the foot (Mm. gastrocnemius et soleus. X. tibialis ; 
1 S. X.). 

4. Adduction of the inner edge of the foot (M. tibialis posticus. X. tibialis). 

5. Abduction of the foot (M. peroneus brevis. X. peroneus). 

6. Dorsal extension of the toes (Mm. extensor digitorum communis et ex- 
tensor hallucis longus. X. peroneus: 1 and 2 S.X."). 

7. Plantar flexion of the toes (Mm. flexores digitorum et hallucis longi et 
flexor digitorum brevis. X. tibialis: 1 and 2 S.X.). 



CHAPTER II 

THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS 

1. Paralysis of the Ocular Muscles 

etiology. — The largest part of all the ocular paralyses arise from affections 
which involve either the peripheral oculomotor nerves or their nuclei in the 
brain-stem. We accordingly make a distinction between peripheral and nuclear 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS 855 



paralyses of the ocular muscles. As we shall take up the latter more fully in the 
description of chronic bulbar paralysis, we have here to mention only the most 
important and most frequent causes of the peripheral ocular paralyses. These 
are as follows : 

1. Injuries which directly affect the nerve-trunks or their branches : blows on 
the eye, knife-stabs, fractures of the skull involving the orbit or the base of the 
skull, and the like. 

2. Compression of the nerves from morbid processes in their neighborhood. 
Tumors of the base of the skull, especially, very often lead to ocular paralyses. 
Periostitis at the base of the skull or in the orbit may also cause similar symp- 
toms, and so may syphilitic diseases of the nerves and their surroundings, the 
meninges or periosteum, aneurisms of the basilar artery, acute or chronic menin- 
gitis in its different forms, etc. In all these cases we usually have to do with a 
pure mechanical compression of the affected nerves by the morbid new growths in 
their immediate vicinity. More rarely the pathological process directly invades 
the nerves themselves. 

3. The so-called rheumatic ocular paralyses are quite common. These arise 
after some decided exposure to cold, such as a draught from an open window, and 
are in all probability very largely of a peripheral nature. They depend, as is 
supposed, upon an acute neuritis of the affected nerve, and hence correspond 
completely to the other rheumatic paralyses, such as rheumatic facial paralysis. 
Among the " rheumatic paralyses " we usually class the paralyses which appar- 
ently come on spontaneously and completely recover, for which no other special 
cause can be made out. 

-±. The ocular paralyses that sometimes arise after certain acute diseases are 
also of a peripheral nature, and are due to degenerative neuritis of the affected 
nerves. They are most frequent as a result of diphtheria, and are very much 
more rare in typhoid fever, acute rheumatism, etc. Of chronic diseases, diabetes 
mellitus may sometimes give rise to ocular paralyses, especially to paralysis of 
accommodation. The ocular paralyses occurring as a symptom of alcoholic poly- 
neuritis or polioencephalitis may be referred to a toxic influence that is recog- 
nized. 

5. Finally we often see ocular paralyses as a symptom of more extensive nerv- 
ous disease, especially in tabes, multiple sclerosis, etc. The details of these con- 
ditions will be found in the description of the several diseases. 

Symptoms. — Since we must refer to the text-books of ophthalmology in regard 
to the more precise symptomatology, and the more special methods of ophthalmic 
investigation, we will here give only a brief review of the chief symptoms of ocu- 
lar paralyses which are important in nervous pathology. 

The disturbance in the mobility of one eye is usually first noticed by the 
patient himself from the appearance of double images — double vision, or diplopia. 
These arise because, on looking to one side, the eye on the paralyzed side can not 
be brought into the corresponding position (strabismus), and consequently the 
retinal images no longer fall upon the same spots, the two images are no longer 
projected outward in a corresponding fashion, so that two different images are 
therefore produced of the same external object. In pathological convergence of 
the visual axes homologous double images arise, in pathological divergence 
crossed images — that is, in the first case, on closing one eye, the image disap- 
pears on the same side, in the second case it disappears on the opposite side. 
By alternately fixing the gaze on one or the other of two fingers held in line with 
each other, and by regarding* the disappearance, on closing one eye, of the double 
image of the finger not fixed, we can easily demonstrate this on ourselves. If, 
then, crossed double images arise, for example, on looking to the right, we must 
have a divergent strabismus — that is, an imperfect function of the left internus ; 



856 



DISEASES OF THE NERVOUS SYSTEM 



but if there are homonymous double images, there must be a convergent strabis- 
mus, and consequently a weakness of the right abducens. It makes it much easier 
to test the double images if we put a colored glass before one of the patient's eyes. 
Ealse projections of the visual field arise, in connection with the double images 
and with the abnormal strength of innervation which the patient has to use for 
his ocular muscles, so that the patient's judgment of the position of external ob- 
jects is uncertain. In the more extensive ocular paralyses this often leads to a 
pronounced feeling of dizziness. In order to avoid this unpleasantness many pa- 
tients confine themselves to monocular vision, close the affected eye, or put their 
heads in a position to avoid the double images. 

Finally, we must mention a symptom to be observed in almost every ocular 
paralysis — the so-called secondary deviation of the healthy eye. If, after the 
sound eye has been covered, we have the paretic eye fix itself upon a point which 
it can not reach at all, or which it can reach only after the utmost exertion, we 
see, when the covering hand is taken away from the sound eye, that the latter 
has been moved much too far in the corresponding direction. The abnormal 
exertions of innervation with the affected eye, somewhat after the analogy of 
certain associated movements, pass over to the associated muscle of the healthy 
side and cause in it too extensive a contraction. 

Physical examination gives the following results, according to the extent of 
the paralysis: 

In complete paralysis of one oculo-motor nerve (the levator palpebrse supe- 
riors, the superior, inferior, and internal recti, the inferior oblique, the sphincter 
of the iris, and the ciliary muscle) the first thing that is noticed, besides the dis- 
turbance in the movements of the eye, is the more or less complete drooping of 
the upper lid — ptosis. If the patient wishes to lift the upper lid he can not do so 
at all or only to a slight degree. If he tries very hard there is usually an evi- 
dent contraction of the corresponding frontalis muscle. If we ask the patient to 
follow with his eyes the motion of any object, such as the finger, held before him, 
while he keeps his head still, we notice at once that the affected eye does not move 
upward, downward, or inward. The pupil is dilated (mydriasis) and no longer 
contracts to light. Accommodation is lost, and distinct vision for near objects 
is impossible. As a rule, the whole eye seems rather prominent (paralytic exoph- 
thalmus), because the backward traction of the recti is very largely absent. In 
old oculo-motor paralysis there is often a secondary contracture in the unpara- 
lyzed external rectus (and superior oblique), by which the eye is persistently 
drawn outward. Partial oculo-motor paralyses are not infrequent, especially 
isolated ptosis, also paralysis limited to the levator palpebrse and superior rectus, 
paralysis of the internal, inferior, or superior rectus, or finally isolated paralysis 
of accommodation, and they may usually be easily recognized from what has 
been said. 

Paralysis of the abducens is characterized by the inability to move the exter- 
nal rectus. The eye can no longer be moved, or it can be moved only imperfectly, 
outward beyond the median line. In old paralysis the eye is drawn inward from 
a secondary contracture of the internal rectus, and convergent strabismus arises. 
Paralysis of the abducens may often be isolated, but it is sometimes bilateral, or 
combined with other ocular paralyses. 

Paralysis of the trochlear nerve, the superior oblique muscle, is not perfectly 
easy to recognize; but it is rarely of special practical importance. The action 
of the superior oblique coincides mainly with that of the inferior rectus. If the 
trochlear be paralyzed the eye turns somewhat inward on looking downward, be- 
cause the superior oblique acts also to abduct the eyeball, and therefore acts 
chiefly on looking downward and outward. The paralysis of the trochlear nerve is 
sometimes made manifest by the failure of the eye to revolve, which rotation 



THE DIFEEEENT EOEMS OF PEKIPHEEAL PAEALYSIS 857 



normally takes place on looking- downward, and is due to the superior oblique 
muscle. This latter movement takes place in each eye about a sagittal axis, in 
such a way that the left eye is turned from the left and up to the left and down- 
ward, and the right eye from the right and up to the right and downward. In 
regard to diagnosis, it is also characteristic that the double images in trochlear 
paralysis appear only in the lower half of the field of vision, and especially on 
looking downward. Hence it happens that the disturbance of vision is especially 
manifest in going up or down stairs, because in such cases the double images of 
the steps are disturbing. 

The following must be added in regard to the separate clinical forms of ocular 
paralysis : Eheumatic ocular paralysis affects the abducens most frequently, and 
not infrequently the oculo-motor or one of its branches, as in isolated ptosis. We 
have seen a rare case in which exposure to severe cold had been followed by a 
complete paralysis of all the external muscles of the right eye, with complete 
ptosis, and almost absolute immobility of the eye in all directions. The rheu- 
matic ocular paralyses are almost always acute in their onset, and they are often 
during the first period associated with sensations of pain about the eye and in the 
head. Vomiting (of reflex origin?) is also not rare at the beginning of the affec- 
tion. The course of most cases is favorable, since they usually completely re- 
cover in a few weeks, though sometimes not for months. In some cases the 
paralysis may remain stationary. 

The diphtheritic ocular paralyses usually appear, like the other diphtheritic 
paralyses, a week or two after the termination of the disease. They most fre- 
quently affect the muscles of accommodation, so that the patient complains 
chiefly of indistinct vision for near objects ; but we sometimes see paralyses of 
the external ocular muscles also, the abducens or the internal rectus. The prog- 
nosis of diphtheritic paralyses is almost invariably favorable. 

Finally, we must mention here the so-called " recurrent or periodical oculo- 
motor paralysis," to which Mobius and others have lately called attention, and 
whose nature is still almost wholly inexplicable. In the cases of this sort re- 
peated paralyses of one oculo-motor nerve, often associated with headache and 
vomiting, just as in migraine, come on at longer or shorter intervals (in women 
sometimes at the menstrual period) in the same individual, who has often had 
them since childhood. All branches of the oculo-motor are usually affected alike, 
but sometimes the internal ocular muscles are spared. In milder cases there may 
be only ptosis. The individual attack sometimes lasts only a few days, but often 
some weeks. The attacks usually become gradually more severe later on. The 
nature of recurrent oculo-motor paralysis is still quite unknown, but it seems 
to be growing more probable that in a part of the cases at least the disease is 
closely related to migraine (q. v.), and forms in a measure only an unusual devel- 
opment of migraine — migraine ophthalmoplegique. The genuine cases of the 
disease, however, must, of course, be distinguished from the recurrent oculo- 
motor paralysis that sometimes occurs in tabes, cerebral syphilis, tumors of 
the base of the skull, etc. [The relation to migraine seems very doubtful. 
There is rarely complete recovery between the attacks, and there is a tend- 
ency for the attacks to increase in frequency and duration as well as in 
severity. In three cases which have come to autopsy lesions have been found 
affecting the nerve — tumors or inflammatory thickening. Some of the cases 
have also had anaesthesia in one or more branches of the distribution of the 
trigeminus during the attack. Besides the recurrent oculo-motor paralysis and 
recurrent facial paralysis (vide infra), recurrent trochlear, and abducens paraly- 
ses and recurrent paralysis of several cranial nerves at once have been re- 
ported. — K.] 

Nothing generally applicable can be said as to the course and prognosis of the 



858 



DISEASES OE THE NEKVOUS SYSTEM 



other forms of ocular paralyses, since in them everything depends upon the form 
of the underlying disease. 

Treatment. — In regard to the fulfillment of any possible causal indication we 
must remember especially that ocular paralysis is not very infrequently of syphi- 
litic origin. Iodide of potassium and energetic mercurial inunction may some- 
times give very good results in such cases. Hence these remedies must also be 
tried in doubtful cases. 

Of other remedies galvanic treatment gives the speediest relief. We pass 
weak currents transversely through the temples, or, what is usually better, we put 
the anode to the back of the neck and apply the labile cathode to the closed eye, 
especially to the region corresponding to the paralyzed muscles. Great caution, 
weak currents, and the avoidance of any great variations in the currents are of 
course necessary. We may also try preparations of strychnine internally, or, 
better, subcutaneously in the vicinity of the eye. We must refer to special trea- 
tises with regard to a correction of the double images by covering the affected 
eye, spectacles with one dark or ground glass, or prismatic spectacles, or in regard 
to operations, such as tenotomy, that are sometimes performed. 

2. Paralysis of the Motor Branch of the Trigeminus 

{Paralysis of the Muscles of Mastication) 

Paralysis of the muscles of mastication, the masseters and temporals, supplied 
by the third branch of the trigeminus, is a rare affection. It is most frequently 
seen in diseases of the base of the skull which compress the motor branch of the 
fifth. We shall also learn later on to recognize paralysis of the muscles of mas- 
tication as a rare symptom of chronic bulbar affections. 

The chief symptom of motor paralysis of the trigeminus is the difficulty or 
impossibility of chewing. In unilateral paralysis the patient can chew only on 
the healthy side; in bilateral paralysis he can no longer chew at all. Paresis 
of the muscles of mastication can be readily determined by the lack of strength 
in resisting the attempt to draw down the lower jaw or by the patient's inability 
to make a deep imprint in biting a bit of wood (lead-pencil, etc.). In complete 
paralysis of the muscles of mastication the lower jaw hangs loosely down, and it 
can also no longer be moved sideways, from the co-existing paralysis of the ptery- 
goids. We can not usually detect clinically disturbances in the other muscles 
supplied by the trigeminus (mylohyoid, buccinator, tensor palati, and tensor tym- 
pani), but there are often sensory disturbances in the distribution of the tri- 
geminus at the same time. 

The prognosis and treatment depend upon the primary disease. Local faradi- 
zation or galvanization of the paralyzed muscles is to be tried. 

3. Facial Paralysis 

{Mimetic Facial Paralysis. Bell's Palsy) 

iEtiology. — Facial paralysis is one of the commonest peripheral paralyses, as 
we can understand from the superficial position of the nerve, exposing it to exter- 
nal injuries, and from its course through the narrow Fallopian canal. We consider 
it improbable that a special " neuropathic family predisposition " plays a part in 
the occurrence of peripheral facial paralysis, as Charcot's school maintains. The 
most important causes of facial paralysis are : 1. Exposure to cold, draughts, 
sleeping by an open window, riding in the cars with the window open, etc. The 
paralyses arising in this way are termed " rheumatic," and we also include in this 
class those peripheral paralyses which are apparently spontaneous — that is, those 
without any marked exposure to cold that can be discovered. In all these cases 
we probably have to do with a neuritis of the nerve-trunk, which comes on in a way 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS 859 



as yet unknown (infectious? toxic?). [In a recent autopsy of a case of so-called 
u rheumatic " facial paralysis, Minkowski found a simple' degenerative parenchym- 
atous neuritis, without any swelling of the nerve-sheath or increase of connect- 
ive tissue. — K.] 2. Diseases of the middle ear and especially caries of the petrous 
bone. As the facial passes through the Fallopian canal, which is in the immediate 
vicinity of the tympanic cavity, we can easily understand how so often in caries of 
the petrous bone, and often perhaps in purulent affections of the middle ear, in- 
flammation may invade the trunk of the facial, or how the facial may be com- 
pressed by inflammatory exudations, etc. 3. In rare cases a pressure paralysis of 
the facial nerve arises in swelling of the parotid gland or tumors in its vicinity. 4. 
Diseases of the base of the skull or brain, tumors, syphilitic new growths, and 
acute or chronic inflammations, often give rise to the development of a facial 
paralysis by invasion of the trunk of the facial or compression of it. 5. We shall 
have to speak repeatedly in the following sections of the frequent implication of 
the facial nerve in diseases of the 
brain and medulla and of the impli- 
cation of the facial muscles in multiple 
neuritis, in juvenile muscular dys- 
trophy, and other diseases. 

Symptoms and Course. — The mani- 
fold character and different functions 
of the nerves, which unite in the 
trunk of the facial, are the causes of the 
•quite large array of symptoms in facial 
paralysis. Most of these symptoms are 
manifest only in peripheral facial pa- 
ralysis, and the following description, 
therefore, refers chiefly to this. 

The paralysis of the facial muscles 
of expression is the most striking and 
characteristic (see Fig. 105). The 
paralyzed half of the face is lax and 
expressionless, the wrinkles in the 
forehead are obliterated, the eye is 
abnormally wide open, as the weight of 
the lower eyelid draws it down, and the 
eye also waters (epiphora), the naso- 
labial fold is obliterated, the corner 
of the mouth droops, and saliva fre- 
quently flows from it. The paralysis 
becomes still more marked on any movement of the face, on wrinkling the fore- 
liead, turning up the nose, laughing, talking, whistling, or inflating the cheeks. 
The eye can be only partly closed. On attempting it, the upper lid sinks down 
from its weight (a weakening of the levator palpebras superioris), the eye is 
turned upward, so that the pupil is covered, but quite a wide space is left between 
the eyelids (lagophthalmus). This defective closure of the lids facilitates the 
entrance of dust, etc., into the eye, and sometimes gives rise to conjunctivitis, or 
even to severer inflammation of the eye. Speech is rendered difficult and indis- 
tinct from defective movements of the lips, and mastication becomes impaired 
from the imperfect movement of the cheeks. The patient -can no longer whistle 
"because he can no longer pucker the lips sufficiently on the affected side. If he 
tries to puff out the cheeks or keep them inflated we notice plainly the flaccidity 
of the cheek on the paralyzed side. On drawing down the lower lip the paralysis 
of the platysma myoides is sometimes very plainly seen. The tongue is often 




Fig. 105. — Right facial paralysis (after SEELiGMttL- 
ler). The folds are smoothed out and in part 
entirely absent on the paralyzed side, while they 
are strongly marked on the ieft. The mouth and 
nose are drawn to the left. 



860 



DISEASES OE THE NERVOUS SYSTEM 



apparently protruded to one side, but this is due merely to the distorted position 
of the mouth. Very often, however, we see, when the mouth is open and the 
tongue is at rest, that the half of the tongue corresponding to the paralyzed side 
lies deeper than the other half, a condition which is probably connected with a 
paralysis of the stylo-hyoid and digastric muscles. In some cases in which the- 
geniculate ganglion or the facial trunk above it were affected, some writers have 

claimed to find a paresis of the soft 
palate on the affected side; the 
fibers from the facial are said to 
pass through the superficial petro- 
sal nerve to the spheno-palatine 
ganglion, and thence to the soft 
palate. It droops more, and on 
phonation the soft palate is raised 
obliquely to the healthy side. Ac- 
cording to more recent investiga- 
tions, however, the soft palate is 
apparently innervated only by 
fibers from the vaso-accessory and 
not from the facial. 

Disturbances of taste in the 
anterior two thirds of the tongue 
have been repeatedly found on the 
paralyzed side, but they usually 
attain only a slight degree. They 
are explained by an affection of 
the fibers of the chorda tympani, 
which run for some distance in the 
facial, as has been described on 
page 827. At the beginning of the 
paralysis many patients complain 
of subjective sensations of taste_ 
Later on the dullness of taste may 
often be discovered by careful test- 
ing. Tactile sensibility in the 
tongue is only exceptionally di- 
minished (sensory fibers in the 
chorda?). A diminished secre- 
tion of saliva (fibers in the 
chorda), and consequently 
3 mouth on the paralyzed side, 
Disturbances of hearing are 




Fig. 106.— Schematic representation of the trunk of the 
facial from the base of the skull to the pes anseri- 
nus. Different localizations of the lesion in paralysis. 
N.f. Facial nerve. N.p.s. Great superficial petrosal. 
N.c.c.p.t. Nerve communicating: with the tympanic 
plexus. N.st. Stapedius. Ch.t. Chorda tj-mpani. Gf. 
Fibers of taste. Sps. Nerve governing the secretion 
of saliva. N.a. Acoustic nerve. G.g. Geniculate gan- 
glion. F.st. Stylomastoid foramen. N.a.p. Posterior 
auricular nerve. 



an 
are 
fre- 



abnormal feeling of dryness in the patient 
sometimes said to have been observed, 
quent, but they are usually due to some complicating aural trouble (vide 
supra), or to a co-existing affection of the acoustic nerve. Paralysis of the sta- 
pedius muscle, however, sometimes seems to cause symptoms, including a marked 
sensitiveness to all loud sounds, and even an abnormal acuteness of hearing, espe- 
cially for low notes (hyperacusis, oxyokoia). These symptoms are due to the fact 
that in paralysis of the stapedius its antagonist, the tensor tympani, causes a 
greater tension of the membrana tympani. Reflex movements, winking, etc., are. 
of course, lost in complete peripheral facial paralysis. Eor the special reflexes, 
which are often seen in the later stages of facial paralysis, vide infra. 

By testing all the symptoms described, in most cases we can decide with accu- 
racy upon the place where the break in conduction in the facial must occur. If 
we examine the accompanying plan of the facial (Fig. 106), devised by Erb, we 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS 861 



•can easily understand the following chief symptomatic forms of facial paralysis. 
Of course we must not forget that many points (innervation of the soft palate, 
of the secretion of saliva and tears, etc.) are still very much in need of further 
investigation. 

1. Paralysis of the facial muscles; but taste, secretion of saliva, hearing, and 
soft palate normal; seat of the affection in the portion between 1 and 2, usually 
the trunk of the facial below the Fallopian canal. 

2. Paralysis of the facial muscles, disturbance of taste, and eventually dimin- 
ished secretion of saliva; but hearing and soft palate normal; seat of the affec- 
tion within the Fallopian canal between 2 and 3. 

3. Paralysis of the facial muscles, disturbance of taste, diminished secretion of 
saliva, abnormal acutenessof hearing; but soft palate normal; seat between 3 and 4. 

4. Paralysis of the facial muscles, disturbance of taste, diminished secretion 
of saliva, abnormal acuteness of hearing, and paresis of the soft palate ( ? vide 
supra) ; seat in the geniculate ganglion between 4 and 5. 

5. Paralysis of the facial muscles, diminished secretion of saliva, abnormal 
acuteness of hearing, paresis of the soft palate (?), but no disturbance of taste; 
seat above the geniculate ganglion between 5 and 6. 

The changes in electrical excitability, and some other changes, may be best 
described in connection with the course of facial paralysis. Ordinarily rheumatic 
paralysis usually begins quite suddenly; less frequently it is more gradual. 
Sometimes there are, for a short time, subjective prodromata, such as abnormal 
sensations of taste, slight ringing in the ears, and very often painful sensations 
in the ear, behind the ear, and in the face, which symptoms may be referred to 
the beginning of acute inflammatory processes in the nerve. In a few cases the 
occurrence of herpes vesicles has been observed in the distribution of the affected 
facial, a condition which may be most readily explained, in accordance with what 
was said on page 815, by reference to the numerous anastomoses between the 
branches of the facial and those of the trigeminus. Among other rare complica- 
tions of simple peripheral facial paralysis we may mention neuralgic pain in the 
different areas of the trigeminus and slight optic neuritis. 

In regard to the further course we distinguish the three following forms : 

1. The mild form, of facial paralysis, to which especially many rheumatic 
paralyses belong. The affection is usually referred only to the facial muscles, 
disturbances of taste, etc., being wholly absent. Electrical excitability in the 
facial and the paralyzed muscles remains entirely normal. Recovery is rapid, 
usually in two or three weeks. In these cases we may certainly suppose that 
there are no severe and deep-seated anatomical changes in the nervous or mus- 
cular fibers. 

2. The middle form of facial paralysis (Erb). In this there is no complete 
reaction of degeneration, but only a partial one. The excitability of the nerve is 
somewhat diminished, but it is not lost. In the muscles, however, in about two 
or three weeks, there appears a decided increase of galvanic excitability to direct 
excitement. The anodic closure contraction (AnSZ) is also greater than the 
<cathodic closure contraction (KaSZ), and the contractions are slow. In regard 
to prognosis we may decide from this that the recovery will still be quite rapid. 
It usually follows in from four to six weeks. 

3. The severe form of facial paralysis is that in which there is a complete 
reaction of degeneration in the nerve and muscles, the details of which we have 
learned in the previous chapter — loss of faradic and galvanic excitability of the 
nerve, loss of faradic excitability of the muscles, and quantitative and qualitative 
changes in the galvanic excitability of the muscles. In this form there are always 
coarse processes of degeneration in the nerve and atrophy of the muscles, so that 
recovery follows, if at all, only after three to six months, or even later, because 



862 



DISEASES OF THE NERVOUS SYSTEM 



the processes of regeneration require at least as much time for their accomplish- 
ment. We often see in the later stages of these cases special symptoms of motor 
irritation (Hitzig). These consist, first, of a slight or sometimes very pronounced 
tonic contracture of the paralyzed muscles, which is sometimes very striking; if 
such cases are examined carelessly, we may easily mistake the (flaccid) healthy 
side of the face for the paralyzed side; second, of single spasmodic contractions 
of the muscles, a true facial tic (vide infra) following the paralysis of the facial; 
third, of special associated movements — if the patient closes his eyes, winks, etc., 
there always follows a marked distortion of the corner of the mouth, which can 
not be suppressed; we have seen this symptom frequently in students in whom a 
peripheral branch of the facial has been injured in a duel; fourth, of an increased 
reflex irritability — on pricking the skin, or blowing on it, vigorous muscular con- 
tractions follow. We have often ourselves seen contractions in the affected 
facial muscles following a blow on the bridge of the nose, on the nasal bone, or on 
the forehead on the healthy side. These reflexes come from the skin, or perhaps 
in part from the periosteum and the fasciae also. All these symptoms — the con- 
tracture, the abnormal twitchings, and the associated movements — may last for a 
very long time — for years in incurable or in imperfectly cured cases. 

Prognosis. — The prognosis of facial paralysis depends, of course, in the first 
place, upon the primary disease, if any exists. Paralysis in tumors of the base of 
the brain, caries of the petrous bone, etc., is almost always incurable. The course 
of the paralysis in affections of the middle ear depends upon the curability of the 
latter disease. Very important data for the accurate prognosis of rheumatic 
paralysis are given by the electrical examination, as has been carefully described 
above. Of course, we can never form a definite judgment from this at the begin- 
ning of the paralysis, but only at the end of the first week. If, at the end of the 
first week or fortnight, the electrical excitability of the nerve still remains normal, 
we can almost certainly prophesy a rapid and favorable course. If reaction of 
degeneration appears, we can not count upon recovery in the most favorable cases 
before two or three months. Relapses almost never follow directly upon the 
course of a paralysis, but it is by no means rare to see peripheral facial paralysis 
occur several times in the same patient after intervals of some years. We have 
seen a man of about thirty who had a peripheral facial paralysis four times within 
a few years, which disappeared each time after a few weeks — a condition which 
possibly is to be regarded as analogous to the " periodical oculo-motor paraly- 
sis " (see page 857). 

Diagnosis. — The symptoms of facial paralysis are so pronounced that the 
paralysis itself can always be easily recognized. In regard to the precise form of 
the paralysis and its cause, we can often decide only by considering the setiologi- 
cal factors, such as injuries, exposure to cold, or aural affections. In distinguish- 
ing between peripheral and central (bulbar or cerebral) paralyses, the other co- 
existing bulbar or cerebral symptoms must first of all be considered. We shall 
learn to recognize more accurately later the different modes in which, in these 
cases, facial paralysis may be combined with paralysis of the other cerebral nerves, 
or the nerves of the extremities. In doubtful cases electrical examination is 
often of decisive value. Reaction of degeneration can be present only in periph-: 
eral paralysis, or in such bulbar paralyses as affect the fibers of the facial below 
the facial nucleus or affect the nucleus itself. In all cerebral paralyses the elec- 
trical excitability is perfectly retained. It may also be mentioned here briefly 
that in all cerebral facial paralyses the frontal muscles and the orbicularis palpe- 
brarum are usually unaffected, while in peripheral paralyses they also are 
paralyzed. 

Treatment. — The treatment of the underlying disease is of the greatest impor- 
tance in all cases where any aural affection, any removable compressing swelling, 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS 86a 



as of the parotid, or syphilis, lies at the bottom of the trouble. The methods of 
treatment indicated in such cases are self-evident. In fresh rheumatic facial 
paralysis it is advisable at first to give a few doses of ' salicylate of sodium or 
antipyrine. In other cases electricity is the only remedy which can give sure 
results, although we must not overestimate its efficiency. In the earlier stages of 
the paralysis we may recommend the stabile conduction of a weak constant 
current through the auriculo-mastoid fossa?, four to six times a week for two or 
three minutes, at first the anode, then the cathode, to the affected side. Later on 
the chief treatment is peripheral galvanization, or eventually faradization of the 
muscles. We place the anode in the auricular fossa and slowly stroke the dif- 
ferent nerve-branches and the muscles with the cathode. We can often confirm 
the fact, immediately after each sitting, that the eye closes better after galvaniza- 
tion of the orbicularis. Faradization excites a reflex irritation of the nerves from 
irritation of the skin, and hence is perhaps of service. Internal remedies (strych- 
nine, etc.) are probably quite useless. 

In secondary contractures we may obtain some favorable results by methodical 
stretching of the muscles by wooden wedges inserted under the cheeks and by 
massage. 

-i. Paralyses in the Region of the Muscles of the Shoulder 

Isolated paralyses of these muscles are rare, with the exception of the practi- 
cally important paralysis of the serratus. Disturbances in their functions are 
more frequent, as one symptom in complicated paralytic states, especially in pro- 
gressive muscular atrophy, and in diseases in the neighborhood of the foramen 
magnum or of the upper cervical vertebra?. In syringomyelia paralyses in the 
distribution of the accessory nerve are not uncommon. 

Paralysis of the Sterxo-cleido-mastoid (spinal accessory nerve). — The chin 
is somewhat raised and turned toward the affected side in consequence of the 
antagonistic contracture of the other sterno-mastoid. Motion in the opposite 
direction is difficult. In bilateral paralysis of this muscle it is very difficult to 
turn the head with the chin raised, and it can be done only imperfectly. The head 
readily falls backward and, when the patient is lying down, it can be lifted only 
with the greatest difficulty if at all. 

Paralysis of the Trapezius (spinal accessory nerve). — The shoulder sinks 
downward and forward so that the supra-clavicular fossa becomes deeper. The 
median border of the scapula moves outward and is not parallel to the vertebral 
column, as under normal conditions, but it runs obliquely from below and inward, 
upward and outward. Voluntary raising of the shoulder, " shrugging the shoul- 
der," is impaired, and it can be done only by the levator scapula?. The arm sinks 
down from its own weight, and there is often pain in the shoulder from stretch- 
ing the ligaments of the joint. If the clavicular portion is paralyzed, the shoulder 
does not move on deep breathing. Raising the arm above the horizontal is also 
affected, from the impaired fixation of the scapula. 

Paralysis of the Pectoralis Major and Minor (anterior ilioracic nerves). — 
Abduction of the upper arm is difficult, the hand can be placed on the shoulder 
of the healthy side only by the help of the anterior bundle of the deltoid, and 
the palms can not be clapped together hard when the arms are stretched forward. 
The function of the pectoral in forcibly drawing down the arm when raised to 
the perpendicular (as in chopping wood, pulling down a hanging rope, etc.) is 
very important. 

Paralysis of the Rhomboidei (X. dorsalis scapula?) causes the inner edge of 
the scapula to be somewhat raised from the thorax while its lower angle moves 
outward. It becomes difficult to approximate the scapula to the vertebra?, and 
wholly impossible to do so if the trapezius be also paralyzed. The movements of 



864 



DISEASES OE THE NEKVOTJS SYSTEM 



the extended arm inward and backward are also impaired on account of the de- 
fective fixation of the scapula. Isolated paralysis of the levator anguli scapulas 
causes no noticeable symptoms, but if the trapezius be also paralyzed it becomes 
wholly impossible to raise the scapula. Then the approximation of the scapula 
to the vertebral column (rhomboidei) and the raising of the scapula (levator an- 
guli scapulas) are completely abolished. 

Paralysis of the Latissimus Dorsi (subscapular nerves). — There is no de- 
formity when at rest, but the arm can not be strongly adducted inward and 
backward or held firmly to the trunk, and the hand can not be placed on the 
sacrum. The latissimus, like the pectoralis major, acts in drawing down vigor- 
ously the raised arm. Finally, when the latissimus is paralyzed, it affects the 
throwing back of the shoulders, as in the position of the soldier. 

Paralysis of the Eotators of the Humerus Inward and Outward. — Move- 
ments of rotation at the shoulder- joint are best tested when the forearm is flexed 
at a right angle. In paralysis of the inward rotators (especially the subscapular, 

innervated by the sub- 
scapular nerve), the 
arm, when rotated out- 
ward, can not be 
brought back again to 
its normal position. 
All manipulations, too, 
which the paralyzed 
arm tries to make on 
the opposite side of the 
body, are considerably 
impaired. In paralysis 
of the outward rota- 
tors — the infra-spinat- 
us, innervated by the 
supra-scapular nerve, 
and the teres minor, 
innervated by the axil- 
lary — rotation of the 
arm outward is abol- 
ished. In writing and 
sewing (using the nee- 
dle), the paralysis 
causes very marked 
disturbance. Paraly- 
sis of the teres major 
(subscapular nerve) 
causes hardly any no- 
ticeable disturbance, 
since this muscle acts 
merely as an aid to the 
latissimus dorsi and 
pectoralis major. 

Paralysis of the 
Serratus Anticus Ma- 
jor (paralysis of the long thoracic nerve). — This paralysis is quite common, and 
therefore is of practical importance. Its most frequent cause is mechanical injury 
of the long thoracic nerve, such as may occur especially in porters, field-hands who 
carry sacks, soldiers in fighting, etc. We also see at times a neuritic paralysis of 





Fig. 107.— Paralysis of the right serratus (personal observation). Wing- 
like protrusion of the right scapula when the arm is stretched forward. 



THE DIFFEREXT FORMS OF PERIPHERAL PARALYSIS 865 



the serratus, coming on with pain in the shoulder either without any discoverable 
cause, or as the result of taking cold (" rheumatic serratus paralysis ")• Finally, 
serratus paralysis may follow acute infectious diseases, especially typhoid fever, 
where it is probably also of neuritic origin. We have seen serratus paralysis 
after acute articular rheumatism and once after gonorrhoea. Bilateral paraly- 
sis of the serratus is seen as one symptom of extensive muscular atrophy, espe- 
cially in juvenile muscular dystrophy. A congenital absence of both serrati also 
occurs with the corresponding disturbances of function. 

As the arm hangs down quietly, the scapula on the paralyzed side is some- 
what raised and stands out a little from the chest-wall, from the action of the 
antagonists (the traction of the levator anguli scapulas, the trapezius, and the pec- 
toralis), its lower angle is a little approximated to the vertebral column, and 
therefore its median edge runs obliquely upward and outward (traction of the 
rhomboidei). This faulty position of the scapula, however, is in many cases only 
of slight degree. 

If the patient wishes to raise his arm, he can raise it only to the horizontal 
position, and we fail to see the projection of the tense indentations of the serratus 
on the lateral wall of the chest; but as soon as we seize the scapula firmly 
and push it forward — that is, supply the missing action of the serratus — the pa- 
tient can at once raise the arm. If the arm is raised outward to the horizontal 
line, the scapula approaches the vertebral column. The somewhat projecting 
lower angle then comes almost behind the spinous process. The muscular masses 
of the trapezius and rhomboidei are crowded together and form a swelling which 
is absent on the healthy side when the arms are in the same position. If the 
patient moves his arm forward, which has been raised outward, the scapula turns 
about its vertical axis and makes a wing-like projection almost perpendicular to 
the surface of the back (vide Fig. 107). We can now take the scapula between 
two fingers and grasp its whole inner surface. The latter forms a deep hollow 
with the middle part of the back. Serratus paralysis can almost always be recog- 
nized at the first glance from this extremely characteristic and peculiar position 
of the scapula. In some cases the patient can still raise the arm almost com- 
pletely to the perpendicular in spite of paralysis of the serratus. This is prob- 
ably done by the help of the middle portion of the trapezius. Disturbances of 
sensation are often entirely absent, but, on careful testing, we can often find a 
slight disturbance in the region of the scapula and shoulder in traumatic and 
neuritic paralysis. 

The course of serratus paralysis is usually quite tedious, but, as a rule, in ordi- 
nary peripheral paralyses, recovery takes place after several months. Many cases 
are incurable. Treatment consists chiefly in the application of electricity to the 
paralyzed nerve and muscles. 

5. Paralyses of the Muscles of the Back and Abdomen. 
The muscles of the back and abdomen are rarely paralyzed except as a com- 
plication of more extensive disease. Paralysis of these muscles is seen most 
frequently in the different forms of juvenile muscular dystrophy (q. v.). If the 
erector spina? on both sides is atrophied and paralyzed, the vertebral column 
when the patient is sitting forms a curve with the convexity backward. The 
patient supports himself by putting the hands on the thighs, lest the trunk fall 
forward. When the trunk is bent forward it is difficult or impossible to regain 
the upright position. On standing, the trunk sinks backward, so that a plummet 
dropped from the upper thoracic vertebra? would fall behind the sacrum. The an- 
terior portion of the pelvis is raised by the contraction of the abdominal muscles 
necessary to maintain the equilibrium. If the abdominal muscles are paralyzed, 
the patient can no longer raise the trunk to an erect position, when lying on 
55 



866 



DISEASES OF THE XEKVOUS SYSTEM 



his back, without the aid of the arms. On standing erect, the belly is very promi- 
nent, the anterior portion of the pelvis is sunk, and the spinal column is bent in 
marked lordosis. A plummet dropped from the upper thoracic vertebrae would 
strike about in the middle of the sacrum. The implication of the smaller spinal 
muscles, not mentioned here, is difficult to determine positively. If the extensor 
of the back as well as the abdominal muscles are paralyzed, it is no longer pos- 
sible to keep the trunk erect. 

6. Paralyses ix the Region of the Upper Extremity 
Paralysis of the Deltoid Muscle (axillary [circumflex] nerve). — Deltoid 
paralysis occurs either as one symptom of complicated paralyses involving the 
brachial plexus, or as an isolated traumatic and rheumatic paralysis ; that is, neu- 
ritic, beginning with pains in the region of the shoulder. After acute articular 
rheumatism (q. v.), when the shoulder has been involved, we have also repeatedly 
seen deltoid paralysis (" arthritic or arthropathic paralysis ") with atrophy vof the 
muscles. Einally deltoid paralysis is a common symptom in the most varied 
spinal and cerebral diseases. The characteristic symptom of deltoid paralysis is 
the impossibility of raising the upper arm when it is hanging down vertically, 
but we must remember that the different parts of the deltoid need not always 
be equally affected. The anterior bundle of the muscle raises the arm obliquely 
forward and inward, the middle bundle outward, and the posterior bundle back- 
ward; the latter also serves chiefly to draw the arm outward and backward when 
it has been raised forward. The arm is raised forward and outward by the 
action of the deltoid only up to the horizontal, and it is raised backward only to 
an angle of about forty-five degrees. To raise the arm completely to the per- 
pendicular the serratus anticus must act (vide supra). If the anterior bundle 
of the deltoid be chiefly paralyzed, the patient can no longer put his hand to his 
head, raise the arm to the opposite shoulder, etc. If the posterior bundle be 
paralyzed he can no longer put his hand in his trousers' pocket. In complete 
paralysis the arm usually hangs down loosely. If the patient, nevertheless, makes 
a vigorous effort to raise his arm, the shoulder is usually raised and the scapula 
turned from the contraction of the trapezius and serratus. In a few cases only 
has it been observed that, where the deltoid is wholly^ paralyzed, the patient can 
still raise his arm by the aid of the upper portion of the pectoralis major or of 
the supra-spinatus and trapezius. It is easy to avoid mistaking anchylosis of the 
shoulder-joint for deltoid paralysis by making a few passive movements of 
the arm. 

Paralysis of the Biceps axd Brachialis Anticus (musculo-cutaneous nerve) 
is only exceptionally an isolated paralysis, but it is quite often seen combined with 
other paralyses. The forearm, when in supination, can not be flexed, but in pro- 
nation the supinator longus can still display its action of flexion. The action of 
supination by the biceps, which it exerts when the forearm is flexed, is also absent. 
\Ye can readily recognize this action on ourselves by making a rapid and forcible 
movement of supination when the forearm is flexed and then feeling the contrac- 
tion of the biceps with the fingers. We sometimes see at the same time a disturb- 
ance of sensibility on the radial side of the forearm from an affection of a 
cutaneous branch of the musculo-cutaneous nerve. 

Radial [Musculo-spiral] Paralysis. — The anatomical course of the radial 
nerve causes pressure paralysis of this nerve to be among the commonest 
peripheral paralyses. It is seen especially when the nerve is pressed against the 
humerus during sleep by the body or head lying on it, in drunkenness, sleeping 
on a wooden bench, on the hard ground, etc. The paralysis is usually noticed 
immediately on waking. Other traumatic influences, direct injuries of the nerve, 
compression in dislocation of the shoulder, in fractures of the humerus, in pres- 



THE DIEEEEEXT FORMS OE PEEIPHEEAL PAEAETSIS S6T 



sure from crutches, in bandaging or fettering the arm. etc., are also frequent 
causes of radial paralysis. It is worthy of note that paralysis of the extensor digi- 
torum has been repeatedly seen to follow subcutaneous injections of ether on the 
extensor side of the forearm. Exposure to cold (rheumatic radial paralysis) plays 
no very great part in the aetiology of paralysis. Eadial paralysis is also rare after 
acute infectious diseases. Eor lead paralysis, which is localized chiefly in the dis- 
tribution of the radial, vide infra. 

The radial innervates the triceps and the muscles on the extensor side of the 
forearm. Paralysis of the triceps is present only in the cases where the point of 
lesion is situated quite high, up. as in crutch paralyses, dislocation paralyses, 
plexus paralyses, etc., but it is absent, or at least it is only faintly manifest, in 
most of the ordinary pressure paralyses, in which the place where the radial turns 
about the humerus is the point of compression. Triceps paralysis is readily recog- 
nized by the impossibility of extending the forearm, but we must always make the 
experiment with the upper arm raised, so as to exclude the action of gravity in 
extending the forearm. 

Paralysis of the muscles on the extensor side of the forearm may at once be 
recognized, since the hand hangs down relaxed in a flexed position (see Eig. 108). 
Any dorsal extension by 
the extensor carpi ulnaris 
and the extensores carpi 
radialis longus et brevis 
is impossible, and the 
lateral movements of the 
hand in abduction and ad- 
duction are rendered dif- 
ficult. The fingers are 
flexed, the first phalanx 
can not be extended by 
the extensor communis 
digitorum, extensor indi- 
cis, and extensor minimi 
digiti; but if the first phalanges be extended passively and supported, the ex- 
tension of the terminal phalanges is perfectly normal, from the action of the 
interossei which are supplied by the ulnar nerve. The thumb is flexed and 
adducted, and can neither be abducted nor extended actively (extensores 
ossis metacarpi et primi et secundi internodii pollicis). If the forearm 
be extended and pronated it can not be supinated (supinator brevis), but the 
flexed forearm can be supinated by the biceps. Elexion of the forearm in supina- 
tion, which is done by the biceps and brachialis anticus, is retained, but flexion 
when half pronated (" middle position ") is weakened, from the paralysis of the 
supinator longus. If we have the patient make short and rapid movements of 
flexion of the forearm in this position we do not see the characteristic normal 
prominence of the tense supinator longus. The very characteristic prominence 
of this muscle is also wanting if the patient tries to hold his pronated and semi- 
flexed forearm firm against forcible attempts at extension. The supinator longus 
is only exceptionally spared in radial paralysis. 

The functional disturbance of the hand in radial paralysis is very consider- 
able. The action of the flexors is also weakened, since their points of insertion 
are approximated, on account of the constant drooping of the hand. We often 
see, too, sensory disturbances, as well as motor, in the distribution of the radial, 
but these are usually slight. The chief seat is on the radial half of the back of the 
hand and the dorsal surface of the thumb, and index and middle fingers (compare 
Eig. 87, page 801). The electrical excitability of the paralyzed parts corresponds 




Fig. 108.— Position of the hand in paralysis of the radial nerve. 
(From Seeligmtller. ) 



868 



DISEASES OF THE NERVOUS SYSTEM 



to the laws that generally obtain. At the onset, and in mild cases, it is normal; at 
a later period, in severe cases, there are pronounced atrophy and reaction of de- 
generation. It is worthy of note that in all forms of radial paralysis, especially in 
lead paralysis, we very often find a peculiar chronic thickening and swelling of 
the tendons on the back of the hand, the chief cause of which is probably the 
mechanical tension of the tendons. 

Ulnar Paralysis. — Except from the frequent implication of the muscles sup- 
plied by the ulnar nerve in extensive paralyses and atrophies, especially in pro- 
gressive muscular atrophy, ulnar paralysis arises chiefly from traumatic influ- 
ences, pressure, wounds, fractures of the humerus, especially fractures of the in- 
ternal condyle, dislocations of the shoulder- joint, etc. Primary neuritic paralyses 
or paralyses following acute diseases, such as typhoid fever, are\much more rare. 

Flexion of the hand, and especially its lateral movement to the ulnar side, is 
disturbed (flexor carpi ulnaris). Flexion of the last three fingers is imperfect 
from partial paresis of the flexor profundus digitorum, and the little finger can 
not be moved at all (hypothenar muscles). Paralysis of the interossei and the 
last two lumbricales is most striking, by which flexion of the proximal phalanges 
and extension of the terminal phalanges of the fingers becomes impossible. The 
defective extension of the terminal phalanges is most plainly seen when we hold 
the proximal phalanges firmly and ask the patient to extend the fingers fully. 
The last two fingers remain less extended than the index and middle fingers, 
whose lumbricales are innervated by the median nerve. Spreading the fingers, 
and still more bringing them together again, is also much impaired (interossei, 
lumbricales). The thumb can not be adducted against the metacarpal bone of 
the index-finger (adductor pollicis) or held firmly in this position. 

In almost all old cases of ulnar paralysis a very characteristic position of the 
hand is developed, besides the muscular atrophy which is especially noticeable in 

the interosseal furrows of 
the back of the hand. By 
the contraction of the mus- 
cles antagonistic to the 
paralyzed interossei (ex- 
tensor and flexor communis 
digitorum), the first pha- 
langes are put in marked 
dorsal extension, but the 
terminal phalanges are 
flexed, so that the hand as- 
sumes an actual clawing 
position — " claw-like hand,'" 

Fig. 109.— Paralysis of the ulnar nerve. Atrophy of the inter- main en qriffe (see Fi°\ 
ossei. The terminal phalanges can not be extended. (From . " . . ft . 

the Erlangen Medical Clinique.) 109). A Similar position 01 

the fingers occurs as a con- 
genital anomaly (in small children), and is probably due to defective develop- 
ment or complete absence of the interossei. 

The disturbance of sensibility, if it be present at all. aftects the volar surface 
of the last two fingers, the dorsal surface of the last three fingers, and a portion 
of the back of the hand (see Figs. 87, 88, and 89). Trophic disturbances of the 
skin of the fingers are not infrequently seen. 

Median Paralysis. — Isolated peripheral median paralysis is seen chiefly as a 
traumatic paralysis, much more rarely as neuritic paralysis. Disturbances in the 
muscles innervated by the median are comparatively common as a complication 
of more extensive paralyses, in cerebral and spinal diseases (progressive mus- 
cular atrophy). 




THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS 869 



The disturbances of motion are very striking. Pronation of the forearm is 
almost wholly abolished (pronator radii teres and quadratus). The hand can be 
flexed only toward the ulnar side by the flexor carpi ulnaris (paralysis of the 
flexor carpi radialis). The terminal phalanges of the fingers can no longer be 
flexed (flexor sublimis digitorum and a part of the profundus), but flexion of the 
primary phalanges is normal by means of the interossei. The patient can grasp 
an object only by the last three fingers, which can still be partly flexed by the 
flexor profundus digitorum (ulnar nerve). The terminal phalanx of the thumb 
can no longer be flexed (flexor longus pollicis), and the first phalanx can be flexed 
only when the thumb is also adducted by the adductor and the inner head of the 
flexor brevis (ulnar nerve). The thumb can not be opposed at all (touching the 
terminal phalanx of the little finger with the thumb), since the muscles that act 
for opposition (opponens, abductor brevis, and outer head of the flexor brevis) 
are all innervated by the median nerve. The thumb therefore lies with the meta- 
carpus turned backward in extension as a result of the unopposed action of the 
extensor longus ("ape position"). 

If there is any disturbance of sensibility, it is found on the volar surface of 
the thumb and the two adjacent fingers, and also on the dorsal surface of the 
terminal and middle phalanges of the index and middle fingers, and the radial 
side of the ring-finger (see Figs. 88 and 89). In severe cases trophic disturb- 
ances, vesicles on the fingers, a shining atrophic skin, and changes in the nails are 
often present. 

Combined Paralyses of the Arm Muscles. — Combined paralyses, in which the 
affected muscles belong to the distribution of several nerves, occur in various 
forms, especially as a result of injuries which affect the brachial plexus in the 
neck or shoulder — plexus paralyses. There is either direct injury of the nerves 
by a blow or wound, or indirect injury from luxation of the humerus, fracture of 
the head of the humerus and the clavicle, tumors in the supra-clavicular fossa, etc. 
Plexus paralyses from primary neuritis also occur. 

Among the many possible combinations of plexus paralyses, one form, first 
described by Erb, and since then repeatedly observed, deserves special mention. 
In this the deltoid, biceps, brachialis anticus, and supinator longus (muscles 
whose nerves all rise from the roots of the fifth and sixth cervical nerves) are 
paralyzed at the same time. The same combination of paralysis therefore occurs 
as if the motor roots of the fifth and sixth cervical nerves were themselves af- 
fected. The arm hangs down relaxed, and can not be raised at all; the forearm 
can not be flexed at all, but the hand and fingers have their normal mobility. 
The cause of the paralysis must have its seat at the point where the nerve-fibers 
for the muscles mentioned lie near one another (see Fig. 99). The supinator 
brevis and infra-spinatus are also not very infrequently paralyzed at the same 
time, so that the forearm, when pronated and hanging down, can not be supinated, 
and the humerus, when rotated inward, can not be turned outward. The supra- 
spinatus and subscapularis may also be involved in the paralysis. Sensory dis- 
turbances are usually slight, but they may sometimes be found on the outer side 
of the upper arm and forearm. 

This same combination of paralyzed muscles is found in a part of the delivery 
paralyses first described by Duchenne. These are sometimes seen in infants after 
hard labor, and are the result of injuries of the brachial plexus in turning, in 
bringing down the raised arm, in the Prague method, in extracting the child by 
the shoulders, in forceps delivery, etc. Such obstetrical paralyses may get entirely 
well in a few weeks or months, but not infrequently permanent atrophic paralyses 
remain. 

Another rare form of plexus paralysis occurs from injury of the fibers coming 
from the eighth cervical and first dorsal nerves. This leads to paralysis of the 



870 



DISEASES OF THE NERVOUS SYSTEM 



smaller muscles of the hand (thenar, interossei) and the flexor muscles on the 
palmar side of the forearm. Slight disturbances of sensibility are usually 
present at the same time in the ulnar and median region. 

In some cases of complicated paralyses of the brachial plexus, which are usu- 
ally traumatic (Seeligmiiller and others), co-existing symptoms on the part of the 
sympathetic have been observed, consisting of contraction of the pupil, narrowing 
of the opening of the lids, and a retraction of the eyeball on the paralyzed side. 
These symptoms, pointing to a paralysis of sympathetic nerves (vide infra, page 
905), are probably always due to a lesion of the ramus communicans of the first 
dorsal nerve, as follows from clinical and experimental investigations (Klumpke). 
Vaso-motor symptoms in the face are usually absent, but we sometimes find a 
peculiar flattening of the cheeks, which has not yet been correctly explained. 

Occupation Paralyses. — In certain occupations in which certain muscles or 
groups of muscles or nerves are over-excited or exposed to persistent pressure, 
paralyses may occur which merit a brief mention. Thus we see not infrequently 
atrophic paralysis of the muscles of the ball of the thumb in file-cutters, linen- 
ironers, basket-weavers, locksmiths, joiners, etc., and atrophy of the interossei in 
cigar-rollers. Bruns has described an isolated paralysis of the flexor pollicis 
longus as sometimes occurring in drummers as a result of over-exertion. The 
prognosis of these paralyses, which are often associated with paresthesias and 
slight sensory disturbances, is not unfavorable, provided the patient can give up 
his harmful calling. 

General Prognosis and Treatment of the Peripheral Paralyses of the Upper 
Extremity. — In the prognosis of the peripheral paralyses of the arm the same 
points hold good that have been spoken of in the prognosis of facial paralysis. 
In these, too, there are mild and severe cases, the latter having complete reaction 
of degeneration, and a course that lasts at least several months before recovery. 
A number of traumatic and neuritic paralyses can be cured only up to a certain 
point, or they may be even entirely incurable. \ 

The treatment can fulfill a causal indication only in comparatively rare cases, 
when we can succeed in removing by operation any compressing tumors, cica- 
trices, splinters of bone, formations of callus, etc. When nerves have been cut, 
suture of the nerve is an extremely important measure, which promotes recovery 
and which may be the only possible means to secure recovery. In fresh neuritic 
paralyses the well-known anti-rheumatics (antipyrine, salicylate of soda) are 
sometimes used, especially if there is also pain. 

In other cases the electrical treatment of paralyses promises the best success. 
We use the galvanic current chiefly, although we generally employ the faradic 
current at the same time. In regard to the method of application, we may employ 
the stabile action of the constant current on the very point of the lesion, espe- 
cially in fresh cases, but the chief method is the electrical irritation of the para- 
lyzed nerves and muscles. We treat the nerve above the point of the lesion in 
order to act in some degree against the hindrance to conduction from above and 
to overcome it. The muscles are irritated by galvanism by stroking the cathode 
over the individual paralyzed muscles. If there is reaction of degeneration, with 
anodic contractions predominating or exclusively present, we use the anode for 
the exciting pole. The other pole is placed on the back of the neck or on the seat 
of the lesion. Faradization of the muscles may also be of service, especially if 
the muscles react to faradism; but, even if this is not the case, the sensory far- 
adic irritation has perhaps a favorable influence, since it produces a reflex irrita- 
tion of the motor nerves. The single sittings should last five or ten minutes, and 
should take place daily or three or four times a week. The fresher the paralysis, 
the more favorable in general is the prognosis. Of course in such cases it is 
usually impossible to decide how much of the improvement is to be referred to 



THE DIEFEREXT FORMS OF PERIPHERAL PARALYSIS 871 



the treatment and how much to spontaneous recovery, but we can not deny that 
we sometimes obtain noteworthy success even in old and severe cases by great 
patience and perseverance. The treatment must in such cases be kept up for 
months, or years, with occasional interruptions. 

Embrocations with spirits and with similar substances must often be pre- 
scribed in practice, but they act favorably only when associated with methodical 
massage of the paralyzed muscles. We sometimes see a certain advantage, too, 
from local warm bathing, or from the use of the baths in Teplitz, Wiesbaden, 
Wildbad, etc. 

7. Paralysis of the Diaphragm 
Isolated paralysis of the diaphragm occurs but rarely, from wounds of the 
phrenic nerve in the neck, also as primary or secondary neuritic (post-diphtheritic) 
paralysis, and finally in hysteria. Muscular paresis of the diaphragm seems to de- 
velop sometimes as a result of inflammation of the serous layer of the diaphragm. 
The paralysis of the diaphragm which comes on as one symptom in more extensive 
paralyses, is more frequent and practically more important. In diseases of the 
upper cervical cord, in ascending myelitis, or in compression of the cervical cord 
by vertebral caries or meningeal tumors, in progressive muscular atrophy, in mul- 
tiple neuritis, etc., the development of paralysis of the diaphragm is the cause of 
the rapidly fatal termination which follows the appearance of disturbance of 
respiration. The roots of origin of the phrenic nerve are the third and fourth 
cervical. 

The symptoms of paralysis of the diaphragm are readily recognized, especially 
in the ordinary bilateral affection. We detect the modification of the respiratory 
movements at the first glance. While we are struck by the marked upper- thoracic 
respiration, which becomes very labored on the slightest cause, while the visible 
and palpable protrusion of the epigastrium on inspiration is entirely absent. In- 
stead of this there is usually an inspiratory retraction in the epigastric region. 
The respiration is but little accelerated in simple paralysis of the diaphragm as 
long as the patient is perfectly quiet ; but in other cases the development of a 
severe bronchitis, from the defective respiration in the lower lobes of the lungs, 
causes constant dyspnoea. The explanation of the bronchitis may be found in the 
fact that the action of abdominal pressure is very much diminished by the con- 
stant high position of the diaphragm, which may be made out by percussion, and 
consequently the cough and the expectoration of secretion are very imperfect. 

The prognosis is favorable only in hysterical and rheumatic paralyses ; other- 
wise it is usually very unfavorable. In regard to treatment, the only thing that 
can be tried is to stimulate the diaphragm from the phrenic in the neck by fara- 
dism or galvanism, while the other pole is placed on the region of the insertion of 
the diaphragm in the thorax. A transverse conduction of the constant current 
through the diaphragm, associated with changes of the current, may also have a 
favorable influence. 

8. Paralyses in the Regiox of the Lower Extremity 
Paralysis of the Crural Xerve. — Crural paralysis is but rarely isolated. 
It is seen after injuries, after compression of the nerve by tumors of the pelvis or 
thigh, in disease of the vertebrae, psoas abscess, etc. There is also a primary 
neuritis of the crural nerve, and finally paralysis of the quadriceps sometimes 
follows acute articular rheumatism and other affections involving the knee-joint. 

The most important muscles innervated by the crural nerve are the ilio- 
psoas and the extensor cruris quadriceps. The paralysis of these muscles is read- 
ily recognized. The thigh can not be flexed on the trunk, and the trunk can be 
raised from, the recumbent position (ilio-psoas muscle) only with difficulty (by 



872 



DISEASES OE THE NERVOUS SYSTEM 



the help of the abdominal muscles, vide supra). If the thigh be flexed passively 
in bed the dependent lower leg can not be extended or raised in the air (extensor 
cruris quadriceps). In peripheral paralysis of the quadriceps the patellar reflex 
of course is absent. Walking and standing are very difficult or almost impossible, 
since the ilio-psoas is necessary for the stride forward and the quadriceps for 
fixation of the knee-joint. Paralysis of the sartorius and pectineus causes no 
special symptoms, but it can be recognized by the failure of these muscles to 
contract when their movements are opposed. If there is amy disturbance of sen- 
sibility it is found in the lower half of the anterior surface of the thigh and 
on the inner side of the leg down to the great toe (saphenous nerve, see Figs. 
90 and 91). 

Paralysis of the Obturator Nerve is very rarely seen as an isolated phe- 
nomenon. The chief symptoms are the defective adduction of the thigh (the ad- 
ductor magnus, longus, and brevis, and the gracilis), and the impossibility of 
crossing one leg over the other. Rotation of the thigh outward is also disturbed 
(obturator externus). Some disturbance of sensibility may be found on the inner 
side of the thigh. 

Isolated Paralyses in the Distribution of the Gluteal Nerves are not common, 
but the muscles supplied by these nerves are often very markedly implicated in 
more extensive paralytic conditions, especially in muscular dystrophy and mul- 
tiple neuritis. Paralysis of the glutaeus maximus is rendered noticeable by the 
fact that this muscle extends the thigh on the pelvis. It is therefore especially 
called into play in going up-stairs, climbing mountains, and rising from a sitting 
or recumbent position. All these movements are rendered nearly impossible when 
the muscles are paralyzed. While walking on level ground is only slightly af- 
fected, the patient can not step up upon any step, he can get up from a chair only 
with effort, etc. On rising from a sitting position from the floor the trunk is 
raised by supporting the arms on the thighs (seethe illustration in the chapter on 
juvenile muscular atrophy). When the patient is in bed we may test the func- 
tion of the glutaeus maximus by holding the flexed thigh tightly with the hand 
and making the patient extend it. The glutaeus medius and glutaeus minimus are 
abductors of the thigh, and also fix the thigh on the pelvis. If they are paralyzed 
the patient has a very characteristic waddling gait. On account of the predomi- 
nance of the adductors the feet are then advanced near each other or even one 
over the other. The glutaeus medius is also a rotator of the thigh inward, so 
that when it is paralyzed the outward rotators (pyriformis, obturator internus 
and externus, gemelli, and quadratus femoris) exert a predominant action. 

Paralyses in the Region of the Sciatic come from traumatic lesions, from 
continuous pressure on the nerve from working in a squatting position (field 
work, etc.), from pelvic tumors, and in hard labors (pressure of the forceps, or, 
with a narrow pelvis, pressure of the presenting head on the nerves). Isolated 
primary neuritic paralysis in the sciatic region is rare, but we quite frequently see 
peroneus paralysis as a symptom of more extensive multiple neuritis (alco- 
holic polyneuritis, neurotic muscular atrophy, etc.). Diabetic neuritis may also be 
localized in the peroneal nerve. Very marked paralytic symptoms in the region 
of the sciatic are seen in diseases of the conus terminalis and the cauda equina 
(lesions of the lumbar vertebrae and sacrum). 

Peroneus Paralysis. — Of the two main branches of the sciatic, the peroneus 
and the tibial, the former is far more frequently affected than the latter. Even 
in injuries of the sciatic trunk, the peroneus paralysis is usually much more evi- 
dent than the injury of the tibialis fibers. We can readily understand that the 
peroneal nerve itself is quite often subject to external injury from its superficial 
position. The symptoms of peroneus paralysis are very readily recognized. The 
flaccid drooping of the toe strikes the observer at once. On walking, this becomes 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS 873 



very marked, and the tip of the foot often sticks to the floor. The patient, there- 
fore, has to raise the thigh higher, and to put the foot down awkwardly, toe first 
(" high action," " steppage "). Dorsal extension of the foot (tibialis anticus) and 
of the proximal phalanges of the toes (extensor communis digitorum longus and 
brevis and extensor hallucis longus), and also abduction of the foot and raising its 
outer border (the peronei), are almost impossible. In old cases a permanent toe- 
drop (talipes equinus or varo-equinus) develops, usually as a result of secondary 
contracture of the muscles of the calf, and this is often associated with a perma- 
nent flexed position of the toes from secondary contracture of the interossei. 

Paralysis of the Tibial Nerve makes plantar flexion of the foot impossible 
(gastrocnemius and soleus). The patient can no longer rise on his toes. Adduc- 
tion of the foot (tibialis posticus) and plantar flexion of the toes (flexor com- 
munis digitorum and flexor hallucis longus) are also abolished. As a result of 
secondary contractures, talipes calcaneus sometimes develops, and also a claw- 
like position of the toes, with dorsal extension of the first and plantar flexion of 
the last phalanges from paralysis of the interossei. If the popliteus be also 
paralyzed, the flexed lower leg can no longer be rotated inward. 

In Paralysis of the Trunk of the Sciatic there is sometimes added to the 
symptoms mentioned the inability to flex the leg backward on the thigh (to be 
tested when the patient is lying on his side or standing), which is due to a paraly- 
sis of the biceps, semi-membranosus, and semi-tendinosus. In unilateral paraly- 
sis of the sciatic, walking is still possible, since the leg is fixed at the knee by the 
quadriceps extensor and is rigid like a wooden leg. 

The distribution of the disturbance of sensibility on the posterior surface of 
the whole leg is given in Fig. 91. Vaso-motor and trophic disturbances, cyanosis, 
coldness and atrophy of the skin, and changes in the nails are often present. 
Atrophy and the electrical reactions of the paralyzed muscles occur under the 
same conditions as in all other peripheral paralyses. 

Paralyses from diseases of the cauda equina will be described later in the 
chapters on the pathology of the spinal cord. 

Treatment of all the paralyses last described follows the same rules as are 
given for the management of peripheral paralyses in the upper extremity. 

9. Toxic Paralyses 

Lead Paralysis. — Of all the toxic paralyses, that from lead poisoning is prac- 
tically the most important. It is a common symptom of chronic lead poisoning, 
and is seen chiefly in those persons whose occupation gives rise to a long-con- 
tinued absorption of small amounts of lead, especially, therefore, in type-setters, 
type-cutters, and type-founders; in artists and house-painters, from lead colors; 
in potters, from lead glaze ; in tinkers, file-cutters, etc. Lead paralysis may occur 
as the only symptom of chronic lead poisoning, or it may be associated in various 
ways with other symptoms (lead colic, lead encephalopathy, etc.). 

The investigations of Leyden, Zunker, Schultze, and others agree in their 
main conclusions that the anatomical cause of lead paralysis is certainly a degen- 
erative disease and ultimate atrophy of the peripheral motor nerve-fibers belong- 
ing to the paralyzed muscles caused by the toxic influence of lead. The degen- 
erative atrophy of the muscles is therefore to be regarded in part as a purely sec- 
ondary disease, although it is possible that the muscles may also be injured by 
the lead at the same time with the nerves. The spinal cord, and especially the 
motor ganglion-cells in the anterior horns of trie gray matter, remain, as a rule, 
unaltered, but undoubtedly, in severe, incurable cases, there may also finally de- 
velop a toxic atrophy of these ganglion-cells. 

Lead paralysis shows an extremely typical localization in the great majority 
of cases, and it affects by far the most frequently a part of the radial distribution. 



DISEASES OE THE NERVOUS SYSTEM 



A paralysis of the extensor communis digitoruin comes on rapidly or slowly. 
Extension of the proximal phalanx of the middle and ring, and later of the index 
and little ringers, becomes impossible, but the extension of the terminal phalanges 
by the interossei remains normal. There often follows later a paralysis of the 
extensor and abductor longus pollicis and the extensors of the wrist, and in severe 
cases a paralysis of the interossei and thenar muscles, while the supinator longus 
and the triceps almost always remain free in a remarkable way. In much rarer 
cases lead paralysis affects the deltoid, biceps, brachialis anticus, and supinators. 
Paralysis of the lower extremities is also very rare. We have seen a very char- 
acteristic case in which, besides extensive paralysis of both arms, walking was for 
some time almost impossible on account of bilateral paralysis of the ilio-psoas 
and extensor cruris (crural nerve). The patient recovered completely. Other 
observers have seen peroneus paralysis from lead poisoning [sometimes without 
noticeable involvement of the arm muscles. — K.]. Paralysis of the laryngeal 
muscles has also been described. 

Eead paralysis is usually bilateral. Ordinarily the right forearm is first 
affected and the left arrn some days or weeks later. In all severe cases a pro- 
nounced atrophy and electrical reaction of degeneration develop in the paralyzed 
muscles. It is an interesting point that changes in the electrical excitability 
(slow galvanic contractions, etc.) may sometimes be made out in muscles which 
can be perfectly well moved by the will (see page 850). The sensibility is almost 
invariably normal, or at most only very slightly altered, so that the sensory nerves 
are manifestly unaffected by the lead. 

Lead paralysis permits a favorable prognosis in the cases where the patient 
can be removed from the injurious influence of the poison. Recovery takes place 
after several weeks, or in severe cases after some months. Relapses of paralysis 
and complications with other morbid results of chronic lead poisoning, however, 
are, of course, frequent. v 

The treatment is the same as in all other peripheral paralyses. Electricity is 
first to be considered. Local sulphur baths and the internal use of iodide of potas- 
sium are also recommended. 

[In the severer forms of chronic lead poisoning the central nervous system 
may be affected as well as the peripheral nerves. In the chapter on poisons {q. v.) 
brief reference has been made to some of the other conditions due to lead poison- 
ing. Besides lead colic and lead arthralgia various forms of anaesthesia and 
pallesthesia may occur. In the forms of lead encephalopathy, besides the general 
symptoms of headache, mental unrest, and convulsions referred to above, we some- 
times meet with symptoms suggestive of a localized lesion, monoplegia or hemi- 
plegia, hemianopsia, amaurosis, etc. In other cases the existence of progressive 
dementia with tremors, convulsions, etc., may lead to a mistaken diagnosis of gen- 
eral paralysis. In other cases the symptoms are suggestive of combined sclerosis 
of the spinal cord — ataxic paraplegia (q. v.). In cases of doubtful diagnosis it 
may be of assistance to examine the urine for lead, after iodide of potassium has 
been given in five- to ten-grain doses thrice daily for a week. The method of mak- 
ing such an examination will be found in the treatises on urinary analysis. If 
large doses of iodide be given there is some danger that the lead will be liberated 
too rapidly and that more acute symptoms may ensue. J. J. Putnam has shown 
that lead is sometimes found in the urine of healthy persons. The pathology of 
chronic lead poisoning is still undetermined. The cerebral symptoms have been 
attributed to disseminated foci of encephalitis or to more chronic degenerative 
processes. Since lead poisoning may cause contracted kidney the possibility of 
uraemia is also to be considered. Lead has been found in the urine in various 
cases of chronic degeneration of the spinal cord, and it may act as a cause of such 
affections, especially of combined scleroses. It is still uncertain whether such 



THE DIFFEEEXT FOEALS OF LOCALIZED SPASM 875 



degeneration is due directly to the toxic influence of the lead, or to the severe 
ana?mia produced by lead (compare the chapter on pernicious anaemia). In all 
severe cases of chronic lead poisoning iodide of potassium should be given for a 
long time to insure the elimination of the lead. — K.] 

Arsenical Paralysis. — Arsenical paralysis is rare in chronic arsenical poison- 
ing (colors containing arsenic, hangings, etc.), but it is much commoner after 
acute poisoning. After the first violent gastro-intestinal symptoms are over, a 
severe form of nervous disease manifests itself either immediately or two or 
three weeks later. The chief symptom of this affection is an extensive atrophic 
paralysis of the arms and legs. The legs are often affected alone, or at least the 
trouble is much more pronounced in them. The muscles of the trunk may also 
be involved in the paralysis. In general the rule holds in arsenical paralysis also 
that the extensor muscles are more affected than the flexors. Electrical reaction 
of degeneration is found in the atrophied muscles. The accompanying disturb- 
ances of sensibility are also very characteristic, either anaesthesia, or especially 
paresthesia and severe pains in the sacrum, arms, and leg's. The nerve-trunks are 
sometimes very sensitive to direct pressure. Ataxic disturbances, similar to those 
in alcoholic neuritis, also occur as well as paralysis. Trophic disturbances in 
the nails, hair, etc.. have been repeatedly observed. 

There are only a few investigations in man as to the anatomical cause of 
arsenical paralysis, but there can hardly be a doubt that the chief disturbance is a 
severe neuritic change. All the morbid symptoms are in harmony with this (see 
the chapter on multiple neuritis) as well as the general course of the disease, 
which in most cases ends favorably. Of course we must not exclude the fact that 
both in lead and in arsenical paralysis the cells in the anterior horns may also be 
affected in some severe cases. 

Of the other less frequent toxic paralyses we may mention here phosphorus 
paralysis, copper and zinc paralysis, and mercurial paralysis, which in a few cases 
has been seen after the therapeutic use of mercury. Polyneuritis must also be 
considered to be the chief cause of all these paralyses. Of organic compounds, 
carbonic oxide and bisulphide of carbon may lead to toxic paralyses. Details as to 
the important alcoholic paralysis will be found in the chapter on multiple neuritis. 



CHAPTEE III 
THE DIFFERENT FORMS OF LOCALIZED SFASM 

1. Spasm m the Motor Distribution of the Trigeminus 

Tonic spasm of the muscles of mastication is called trismus. As an independ- 
ent disease it is very rare, but it often occurs as one symptom in complicated 
forms of spasm and other nervous affections, as in tetanus, in the epileptic attack, 
in hysteria, meningitis, etc. Both jaws are pressed firmly together, and we can 
feel through the cheeks the hard and tense masseters. In unilateral spasm of the 
pterygoids the lower jaw is pushed laterally in the opposite direction. 

Clonic spasm of the muscles of mastication — masticatory facial spasm — con- 
sists of a paroxysmal and constant movement of the lower jaw. almost always in 
a vertical, but rarely in a horizontal direction. The single movements follow one 
another usually in a regular, rapid rhythm, and produce an audible chattering 
of the teeth. The mucous membrane of the mouth and the tongue is often in- 
jured. 



S76 



DISEASES OF THE NERVOUS SYSTEM 



The cause of these spasms can not always be established. Sometimes they 
seem to be of reflex origin, as in affections of the lower jaw, the teeth, or even of 
distant parts. We once saw a case which lasted for a year which was said 
to have arisen from a severe fright, and which therefore must be regarded as 
" hysterical,"' and also a case of clonic spasm in a ten-year-old boy in the mas- 
seters and mylo-hyoids of hysterical origin. 

The treatment, apart from the treatment of the primary affection, must 
aim at removing the cause of the disease, if there be one. such as decayed teeth. 
In other respects electricity is of value in many cases, applied either by passing 
the constant current through the muscles, by faradizing them, or by using the 
wire brush. Of internal remedies we may try narcotics, bromide of potassium, 
atropine, etc. 

Artificial feeding is of great importance, if the patient can not take food vol- 
untarily from a persistent trismus. It is best to introduce a small oesophageal 
tube through the nose into the oesophagus. Rectal feeding is insufficient for a 
permanent method, but still it is sometimes of service. In some cases a suc- 
cessful attempt has been made to overcome the closure of the jaws gradually by 
pushing wooden wedges between the teeth. 

2. Clonic Eacial Spasm 

{Mimetic Facial Sj^asm. Facial Tic. Convulsive Tic) 

We know little that is definite as to the aetiology of facial spasm, the most fre- 
quent and practically the most important form of isolated spasm. In some 
cases, perhaps, the disease is to be referred to a lesion of the trunk of the facial, 
from exposure to cold, aural affections, or disturbances at the base of the skull, 
vsuch as aneurism of the vertebral artery pressing on the trunk of the facial, as 
was seen in one case), or else to a reflex irritation of the nerve as in trigeminal 
neuralgia, etc. It may be that many cases are not of peripheral but of central 
origin, from the facial center in the cerebral cortex. The disease may also appear 
after violent mental excitement. Einally, imitation and the habit of grimacing 
play a part in many cases, especially in children, that is not to be underestimated 
(hysterical facial spasm). At any rate we may see from what has been said that 
we should not judge all cases of mimetic facial spasm in the same way, but it is 
the most characteristic cases, due apparently to organic causes, which usually 
we are wholly unable to explain. Repeated obseiwations have established the 
fact that the disposition to the disease is heightened by a general hereditary 
neuropathic taint. The tendency to twitch the facial muscles is very often noticed 
in nervous and irritable persons, but there is an essential difference between this 
grimacing and the true facial spasm with its lightning-like muscular contractions. 

The symptoms of true convulsive tic consist of alternating, short, lightning- 
like contractions in almost all the muscles supplied by the facial. The disease is 
usually unilateral, often extending over the whole distribution of the facial, but 
sometimes confined only to individual parts — partial facial spasm. Sometimes 
the contractions are almost constant, though varying in intensity, so that the 
patient involuntarily makes the strangest faces; but they often appear in sepa- 
rate attacks, which last but a short time, and are interrupted by completely free 
intervals. The attacks arise without any special cause, or they may be excited by 
talking, voluntary movements, sensory and mental impressions, etc. In some 
very severe cases the contractions also invade the neighboring territory — the mus- 
cles of mastication, the tongue, the muscles of the neck, and even the upper arm. 
Voluntary motion in the muscles is perfectly normal, except for the disturbing 
influence of the spasmodic movements. All sensory disturbances are also lack- 
ing; there is neither anaesthesia nor pain. 



THE DIFFERENT FORMS OF LOCALIZED SPASM 877 



A common partial form of facial spasm, which is entirely or almost entirely 
isolated, deserves special mention — blepharospasm, or spasm of the eyelids — that 
is, a tonic or clonic spasm in the orbicularis palpebrarum. The tonic form 
may be of reflex origin in affections of the eye, but sometimes it is excited from 
other regions of the trigeminus. It is, as a rule, bilateral, and it may last for 
days or weeks, sometimes with occasional interruptions. Graefe first noticed that 
the spasm could sometimes be instantly checked by pressure on the points of 
exit of the branches of the trigeminus, and often by pressure upon certain parts 
of the vertebral column or other parts of the body, so that the eyelids " fly up 
as if by a spring." The author has no doubt that in such cases we usually have to 
do with conditions of hysterical spasm. Clonic spasm of the lids, nictitating 
spasm, consists of a spasmodic winking and contraction of the eyes, which is some- 
times almost constant. Here, too, we can often make out a reflex origin for the 
spasm, but frequently we can not find any cause. 

Facial spasm, in its severe forms, and especially blepharospasm, is always a 
troublesome disease for the patient, and causes very much disturbance. The 
course is often very tedious. Sometimes there are long intervals, as we have 
seen during pregnancy, and then the spasm begins anew. In not very rare cases 
the affection becomes habitual and lasts for life. 

Treatment is, therefore, usually a difficult and thankless task. The best results 
may be obtained where we can succeed in removing any reflex cause of the spasm, 
as in extracting decayed teeth, treating affections of the eye, or, in some cases, 
resecting the supra-orbital nerve. In applying electricity, our chief attention 
must be directed to any pressure points, to which we make a stabile application of 
the anode of the constant current. If there are no pressure points, we put the 
anode on the trunk of the facial and the different branches of the pes anserinus. 
In cases of reflex origin Berger obtained good results by applying the anode to the 
occiput, just under the protuberance, while the cathode was held in the hand — 
galvanization of the medulla. The single sitting should last five or ten minutes. 
The f aradic current — a slowly " swelling current " * — has also been recommended. 
Of internal remedies we should first try bromide of potassium, and then arsenic, 
atropine, curare, or oxide of zinc. The action of these drugs is always very uncer- 
tain. A favorable result, however, has been obtained by nerve-stretching, in a part 
of the cases operated on, at least so far that the ensuing paralysis troubles the 
patient less than the constant twitching. When the paralysis ceases the twitch- 
ings usually begin again, but in some cases the benefit has been permanent. Fi- 
nally, we must mention that the use of the red-hot iron has sometimes been fol- 
lowed by a decided improvement of the spasm in old cases. We employ cauteriza- 
tion along the cervical vertebrae, on the trunk of the nerve, or on any existing 
pressure points, by means of Paquelin's thermo-cautery. 

In the cases which are not to be regarded as a form of organic spasm, but are 
to be classed as hysterical, due to bad habits, etc., a methodical training of the 
will by gymnastic exercises may be attended with the best results. 

3. Spasm in the Region of the Hypoglossal !Nerye. Lingual Spasm 
Although the tongue is often implicated in complicated forms of spasm, such 
as hysterical or epileptic spasms, isolated spasms in it are very rarely seen. 
They are relatively most common in hysteria. They occur, however, either in a 
clonic or a tonic form, and then they cause a marked disturbance of speech, or 
even of respiration, if the spasm draw the tongue backward. In the latter case 
it may be necessary to use inhalations of chloroform, and to draw the tongue 
forward by force. 



[* A current that begins weak, and is gradually made stronger and then weaker. — K.] 



878 



DISEASES OF THE NEKVOUS SYSTEM 



4. Spasms in the Muscles of the Neck 

Tonic and clonic spasms in the region of the muscles of the neck are not very 
frequent, but they appear in very various forms, and are at times a very severe 
and persistent affection. We can usually discover nothing definite as to the aeti- 
ology of this condition. Only in a few cases can we make out coarse anatomical 




Fig. 110.— Severe case of spasm of the accessory nerve (trapezius and sterno-mastoid muscles). 
(From the Ex-langen Medical Clinique.) 

disease of the nervous system or of the cervical vertebras rheumatic or other evil 
factors, reflex influences, etc.; but a general neuropathic constitution certainly 
plays a great part in the development of these forms of spasm. Although the 
spasms in the different muscular regions are often combined with one another, 
we can still distinguish the chief separate forms. 

Spasms in the Distribution of the Accessory Nerve. — In clonic spasm of 
the accessory there are brief or more persistent twitchings of the head, which 
may attain great severity. Where there is a predominating unilateral spasm 



) 



THE DIFFERENT FORMS OF LOCALIZED SPASM 879 



of the sterno-mastoid, the head is turned to the opposite side at every contrac- 
tion of this muscle, and the chin is also somewhat raised. In unilateral spasm 
of the trapezius, when only the upper portion of the muscle is usually affected, 
the head is drawn backward toward the affected side against the shoulder. 
In bilateral and combined spasm of these muscles we see severe shaking and 
nodding movements of the head — the so-called nodding spasms, " salaam convul- 
sions " — which have been observed chiefly in children. They may also be excited 
in like manner by contractions of other muscles of the neck (rectus capitis, longus 
colli). In tonic spasm of the accessory the head is constantly fixed in the ab- 
normal position described above, and it can not be brought back passively to its 
normal position at all, or only incompletely. The oblique position of the head in 
unilateral tonic spasm of the sterno-mastoid is called spastic torticollis (caput 
obstipum spasticum). The affection called rheumatic torticollis hardly belongs 
here, since it is probably due to a rheu- 
matic myositis of the sterno-mastoid. 

Tonic and clonic spasm of the spleni- 
us (Fig. Ill) is also isolated, or com- 
bined with spasm of the accessory. In 
this the head is drawn backward and 
toward the affected side, and thus we 
can feel the muscular swelling pro- 
truding to the outside of the cervi- 
cal portion of the trapezius. Spasm of 
the obliquus capitis is probably the 
cause of the so-called rotatory tic, in 
which there are genuine spasmodic rota- 
tory movements of the head. 

The course of the forms of spasm 
described is usually very tedious. There 
are mild cases which recover in a short 
time, but, on the other hand, many of 
these forms of spasm develop into a very 
distressing, habitual, chronic affection. 
In these cases any steady occupation, 
such as reading or writing, is rendered 
almost impossible by the constantly re- 
curring spasmodic lateral and rotatory 
movements of the head. Any mental excitement, a feeling that he is noticed, etc., 
increase the patient's spasms, while they become milder when he is completely at 
ease. In some cases the twitching ceases entirely when the body is wholly at rest, 
but it returns at once on any voluntary movement. Combinations of the different 
forms of spasm occur in the most varied ways. Facial tic may be associated with 
spasm of the muscles of the neck. In the severest cases the spasm may extend 
even to the muscles of the upper arm. The occurrence of mental disturbances 
(melancholia, confusional insanity) has been repeatedly seen. All this favors the 
theory of the central nature of the disease. The patient's general condition may 
finally become very poor. Many fall into the morphine habit. 

Treatment. — In some cases electricity has brought about recovery, or at least 
improvement. The method of treatment consists of the application of the anode 
to the affected nerves and muscles, or of the use of a swelling f aradic current, or 
of the f aradic brush to the skin over the affected muscles. V ery often we have to 
change the method, and we must try to find out, by testing, the most efficient way 
to employ electricity. We may try cautious massage of the affected muscles. We 
have greater confidence in methodical gymnastic exercises carried out persistently 




Fig. 111.— Spasm of the right splenius capitis. 
(From Duchenne.) 



880 



DISEASES OF THE NERVOUS SYSTEM 



for a long time. Of other remedies, narcotics, such as subcutaneous injections 
of morphine, are indispensable in severe cases, but we must be very careful in 
their use. We may also try bromide of potassium, antipyrine, arsenic [bella- 
donna], and other nervines. In severe cases we resort to the use of the red-hot 
iron to the back of the neck. Other observers, and we ourselves, have seen good 
results from it, but of course benefit does not always follow. We may also advise 
nerve-stretching, but it is of doubtful advantage. [Resection of the affected 
nerves has also been performed in many cases with some alleged benefit. Brissaud 
and other French observers claim that many of the cases of torticollis are of psy- 
chical origin (hysterical?), and that they are cured by appropriate mental treat- 
ment. — Kj Finally, it must be mentioned, that we may give great relief to many 
patients by suitably applied mechanical supports. 

5. Spasms in the Muscles of the Shoulder and Arm 
Clonic spasms in the upper extremity are probably usually of central origin. 
They are rarely isolated, as in the pectoralis major, but are more frequently com- 
bined with other forms of spasm and other nervous symptoms. They sometimes 
seem to be of reflex origin, as in the clonic spasms associated with brachial neu- 
ralgia, and also the spasms sometimes seen in amputation-stumps. For many of 
these forms of spasm the cause is still wholly unknown. 

Isolated tonic spasms, in single muscles, or groups of muscles, in the upper 
extremity, have been repeatedly observed. Tonic spasm of the rhomboidei causes 
an oblique position of the scapula, so that its inner border runs obliquely upward 
and outward from below and inward. This makes it hard to raise the arm above 
the horizontal line, as in serratus paralysis, but the separation of the scapula from 
the chest-wall, which is so very characteristic of the latter, is wanting. Tonic 
spasm in the levator anguli scapulae is rare, except in connection with spasm of 
the rhomboidei or trapezius. In it the shoulder is raised and the head is bent 
a little to the affected side. Isolated tonic spasms in the pectoralis major, latis- 
simus dorsi, deltoid, etc., are, on the whole, easy to recognize, but they are 
of very rare occurrence. Tonic flexor spasms of the hand and fingers are more 
common. We have ourselves seen several such cases, which lasted for months. In 
one case the spasm could at once be relieved by placing the anode of a moderately 
strong galvanic current on the median nerve. In another case the flexor spasm of 
the fingers had followed a mild acute inflammation of the wrist-joint. Brief 
tonic spasms of the flexors of the fingers and of the thumb muscles are of quite 
common occurrence. They are seen especially in persons who have to do some 
severe and persistent bodily work, also in alcoholic subjects, patients with gastric 
disease or chronic nephritis, in hysteria, etc. Some of these forms of spasm 
should perhaps be classed as tetany, a special form of spasm which will be fully 
described later. 

We can scarcely give any general rules for prognosis or treatment. It is always 
important to remove any trouble which may cause the spasm. We may also try, 
first of all, electricity (a stabile galvanic current, applying the anode to the 
affected muscles and their nerves) and methodical gymnastics, the latter espe- 
cially in all cases having any relation to hysteria (q. v.). i 

6. Spasms in the Muscles of the Lower Extremity 
Clonic spasms in the muscles of the lower extremity are always, with rare 
exceptions, a symptom of spinal or cerebral disease. Of the tonic spasms the 
most frequent and the best known are the painful spasms in the calves, or cramps, 
which are apt to come on after great muscular exertion, mountain-climbing, or 
dancing. Many persons have an especially marked predisposition to such cramps, 
which readily come on, especially after making certain movements or holding the 



THE DIFFERENT FORMS OF LOCALIZED SPASM 881 



foot in a certain position. Similar painful cramps sometimes come in other 
muscles besides the calves, as in the abductor hallucis, etc.' Constantly recurring, 
extensive, and painful spasms in the leg- muscles may, as we have seen, form a 
very distressing affection which is hard to remove. In most of these cases there 
are probably conditions of irritation occurring in the muscles themselves. Other 
tonic spasms in the muscles of the lower extremity are rare, but individual cases 
of isolated tonic spasm in the abductors, in the ilio-psoas, in the muscles of the 
calves, etc., have been observed. More extensive tonic contractures of the muscles 
of the leg are not very rare in hysteria, especially in the hysteria of children. 

Saltatory Reflex Spasm. — In this place we may mention a peculiar form of 
spasm, to which Bamberger has given the name of " saltatory reflex spasm." 
This shows itself in the muscles of the lower extremities, never when the patient 
is quiet in bed, but only when he tries to stand or to walk. As soon as the soles 
of the feet touch the floor, such vigorous contractions are set up in the muscles of 
the legs as to force the patient to keep up a constant hopping, jumping, or trip- 
ping. The heels are also usually raised spasmodically, and in many cases the 
patient would certainly fall if he were not supported. In the pure forms of 
saltatory spasm, on physical examination we can usually make out nothing but 
an extraordinary increase of the reflexes, especially of the tendon reflexes, but in 
some cases there may also be other nervous symptoms. According to our present 
theories there can scarcely be a doubt that the cases described as " saltatory re- 
ilex spasm " are without exception hysterical. 

[Certain similar affections exist as endemic neuroses. In the " jumpers " of 
Maine the spasms may be produced by any excitement. In other forms the 
victims are compelled to imitate everything they see or hear. The curious 
affection observed in Siberia, Java, and elsewhere, known as latah or myriachit, 
is allied to this trouble. Alcoholism, cold, and privation seem to be important 
^etiological factors, and these affections probably have some relation to hys- 
teria. — K.] 

Arthrogryposis. — As an appendix we would here consider briefly a remark- 
able disease, the so-called arthrogryposis, which occurs chiefly in children in the 
first years of life, and consists of persistent tonic spasms and contractures of one 
or often of all four extremities. The disease usually develops quite acutely, and 
may run its course with fever and rather severe general symptoms. The legs are 
found either in a position of rigid extension, or they are drawn up spasmodically 
to the body, and can not be extended passively even with violence. The arms 
are flexed, and the hands and fingers are also fixed in some position of contracture. 
The milder cases may recover after a few weeks, but we have seen two cases which 
ended fatally, in which the autopsy gave an absolutely negative result. The 
nature of this quite rare affection is still wholly unknown to us. Several authors 
have of late tried to identify arthrogryposis with tetany (q. v.), which we can not 
admit, at least not in all cases. In contrast to tetany we have in arthrogryposis 
an unbroken tonic rigidity of the extremities lasting for days or even weeks. In 
regard to treatment, prolonged warm baths are especially to be recommended. 
The cautious use of galvanism, massage, the bromide salts internally, etc., may 
also be tried. 

7. Spasms in the Respiratory Muscles 

Tonic spasm of the diaphragm has been seen in a few rare cases. The lower 
part of the thorax is much expanded, the epigastrium is protruded, and the 
respiration, which shows intense dyspnoea, can be performed only by the upper 
part of the thorax. The depression and immobility of the diaphragm can be made 
out on percussion. Many patients have a severe pain in the region of the dia- 
phragm. The condition is not without danger and demands instant interference : 
56 



882 



DISEASES OE THE NERVOUS SYSTEM 



inhalations of chloroform, subcutaneous injections of morphine, a warm bath 
with a cool shower-bath after it, faradization of the skin in the region of the 
diaphragm, galvanization of the phrenics, etc. 

Clonic Spasm of the Diaphragm. — Singultus. — The well-known " hiccough " 
or " sob," due to a sudden spasmodic contraction oi the diaphragm, associated 
with a brief inspiratory sound, is in its mild forms a very frequent condition, 
which soon passes off; but it sometimes increases to a persistent, obstinate, and 
very troublesome affection, which may last for weeks or months. Hysterical hic- 
cough is the most frequent. This comes on especially after mental excitement, 
and it may sometimes last, with short interruptions, for weeks or even months. 
Persistent hiccough may also be excited reflexly in affections of the stomach, in- 
testines, peritoneum, etc. In some cases the hiccough depends upon a direct 
lesion of the phrenic nerve, as we have seen in one case of tubercular mediastino- 
pericarditis. We have also seen hiccough lasting for hours in cerebral apoplexy, 
and in chronic myelitis extending to the cervical cord. 

In the milder cases hiccough soon passes off without special treatment. Hold- 
ing the breath, pressure on the closed glottis, blows on the back, etc., are proce- 
dures generally known by the laity, and they are often used to suppress hiccough. 
In hysterical hiccough intelligent and at the same time energetic mental treat- 
ment will often rapidly lead to the voluntary suppression of the spasmodic move- 
ments and thus to complete recovery. Such treatment is often aided by the in- 
fluence (in part merely suggestive) of some internal remedy, such as bromide of 
potassium, or the use of electricity. In severe hiccough due to organic disease we 
must sometimes resort to narcotics (large doses of bromide of potassium, opium, 
morphine, inhalations of chloroform). The constant current to the phrenic 
nerve or faradization of the region of the diaphragm sometimes acts beneficially. 

Complicated respiratory spasms, either in the form of spasmodically acceler- 
ated and forced breathing, or spasms combined with all sorts of other symptoms, 
with many gurgling noises, eructations, etc., are almost exclusively confined to 
hysteria. We have ourselves counted in one such case over two hundred respira- 
tions a minute ! The best remedy for most of these forms of spasm, and one 
which often acts instantly, is a cool bath with energetic cold shower-baths. The 
yawning spasm (chasmus, oscedo), sneezing spasm (sternutatio convulsiva, 
ptarmus), laughing and weeping spasms, coughing spasm, etc., also belong to the 
respiratory spasms. We once saw an instructive example of the latter in a boy 
ten years old, undoubtedly due to hysteria. A peculiar, hollow, barking cough 
came on as a " reflex " (that is, due to association of ideas) either spontaneously 
or on pinching any part of the skin. The affection lasted for some weeks, and 
then disappeared quite suddenly. 



CHAPTER IV 

WRITER'S CRAMP AND ALLIED PROFESSIONAL NEUROSES 

Writer's cramp (graphospasm, mogigraphia) is the commonest form of a 
whole class of peculiar disturbances of motion, to which Benedikt gave the appro- 
priate name of " professional neuroses of co-ordination." Their characteristic 
feature is that the disturbance in a certain group of muscles appears only when 
these muscles come into harmonious action, in some definite and usually some 
delicate and complicated occupation. Although the persons who suffer from 
writer's cramp can move and use the muscles of their right arm and hand for 



THE DIFFEKENT FOKMS OF LOCALIZED SPASM 



883 



ordinary purposes in a perfectly normal manner, these same muscles at once 
refuse their service when the patient begins to write. In this case the disturbance 
can not lie in the innervation of the individual muscles themselves, but it must 
be referred to the form of their associated action — that is, it must be a disturb- 
ance of co-ordination. It therefore becomes very probable that the cause of the 
spasm is to be sought, not in the peripheral parts, but in the centers. We are 
convinced that writer's cramp and the allied occupation neuroses are due to dis- 
turbances of the central (cortical) innervation. Writer's cramp is a morbid con- 
dition in writing similar to stuttering in speaking. Over-exertion in writing 
plays the most important part as an serological factor. Writer's cramp is there- 
fore seen chiefly, but of course not exclusively, in those persons whose occupation 
entails continuous writing, especially in secretaries, merchants, bureau officials, 
etc. A general nervous predisposition seems also very notably to increase the 
tendency to writer's cramp. Most cases are associated with pronounced neuras- 
thenic symptoms. Mental factors (fright, anxiety) sometimes play an unmistak- 
able part. Attention has also been called to the fact that bad pens, such as hard 
steel pens, improper methods of holding the pen in writing, etc., may favor the 
development of writer's cramp. 

Symptoms. — The essential symptom of writer's cramp is the appearance of 
certain disturbances at every attempt to write, which render writing very difficult 
or entirely impossible. The affection usually begins gradually, but increases quite 
rapidly. For the precise characterization of the disturbance Benedikt has dis- 
tinguished three forms of writer's cramp, but they run into one another in various 
ways. The spastic form is the most frequent. The patient scarcely begins to 
write when contractions or tonic spasms come on in the different fingers. The pen 
is either pressed spasmodically deep into the paper, or, when it is moved, it makes 
very faulty irregular movements. We very often see a tonic spasm of the pro- 
nators of the forearm set in on each attempt to write. Writing is under such cir- 
cumstances wholly impossible, or it is done only with the greatest exertion, and 
the characters are also utterly distorted, unequal, and mingled with false strokes 
and blots. Finally, in the tremulous form of writer's cramp there is such a 
marked tremor in the right hand at every attempt to write that the letters are 
completely illegible. We have seen several such cases in children, which we have 
regarded as distinctly hysterical. 

In the paralytic form the disturbance is chiefly a tired feeling in the right 
arm of rapid onset, like paralysis, and it is often associated with pain. This form 
of disturbance in writing ought not properly to be classed with writer's cramp, 
since it is absurd to speak of a " paralytic " form of " cramp." 

As has already been said, the motility of the right arm in every other respect is 
usually perfectly normal, but sometimes analogous symptoms also appear in the 
same patient in many other fine employments, such as sewing, piano-playing, etc. 
The sensibility is usually unaffected, except for the muscular pains already men- 
tioned, and a frequent feeling of numbness in the forearm and fingers. A few 
painful pressure-points have sometimes been found on the cervical and dorsal 
vertebras. We should also examine the peripheral nerves, since painful thick- 
enings are sometimes said to be found in them, which possibly stand in a causal 
relation to the disease. If we are dealing with people who are generally neurotic, 
as is almost always the case, they often complain at the same time of headaches, 
mental uneasiness, general weakness, etc. In such cases the degree of the dis- 
turbance, as we have said, is always very much influenced by mental conditions 
(excitement, anxiety), just as is the case in stuttering. We knew a patient who 
could not write a word, in spite of the greatest effort, if any one were looking 
at him, but otherwise he wrote a beautiful flowing hand. 

The diagnosis of writer's cramp is almost always easy. We must guard 



884 



DISEASES OF THE NERVOUS SYSTEM 



against confusing it with other nervous diseases, such as chorea, paralysis agi- 
tans, multiple sclerosis, beginning muscular atrophy, or agraphia, which, of 
course, under some circumstances may lead to disturbances in writing. 

The prognosis is always to be given with reserve. Complete recoveries with- 
out doubt do occur, but many cases are extremely obstinate and others are 
incurable. Relapses are also very common even after improvement has set in. 
Many patients are obliged to choose another calling in consequence of their 
trouble. 

The treatment begins first with the command to give up writing entirely for 
several weeks. If this command can be obeyed, the mere rest may be of service 
in mild incipient cases. Certain contrivances for writing, which the patient can 
best test himself, are often of advantage, such as sticking the pen-holder through 
a cork, using a large pen-holder, a change in the way of holding the pen and in the 
position of the arm, etc. Nussbaum has invented a kind of bracelet to which the 
pen-holder is fastened, and which is held firmly by the outspread fingers. Learn- 
ing to write with the left hand, which is often tried by patients, usually leads to 
no good result, since the cramp very soon appears in the left hand also. 

Of the special methods of treating writer's cramp the application of galvanism 
deserves the first mention. Avoiding all strong currents and variations of the 
current, we apply the stabile anode to the brachial plexus, and also to the different 
nerves (especially if they be sensitive to pressure) and the affected muscles, for 
five or ten minutes. The cathode is placed in the vicinity of the cervical vertebrae. 
If painful points are found, they receive special treatment. We may also use 
galvanism, as an experiment, through the head. Of late, massage and especially 
methodical gymnastics have shown still more favorable results than electrical 
treatment, but the use of them demands special technical skill, and therefore 
they have so far obtained excellent results chiefly in the hands of certain special- 
ists; but such a methodical re-education in the movements employed in writing 
should always be tried. We can very rarely promise success from internal reme- 
dies such as subcutaneous injections of strychnine, atropine, etc., but those meth- 
ods of treatment often act favorably which aid the general strength of the nervous 
system, such as cold-water cures, sea-bathing, and residence at a mountain resort. 
In writer's cramp, just as in stuttering, we see very plainly the influence of 
mental factors (rest, increasing or diminishing self-confidence, excitement, etc.) 
upon the trouble. 

As an appendix we will mention here some other professional neuroses that 
are occasionally seen. They are the piano-player's cramp, which is seen espe- 
cially in young conservatory pupils, violin- and 'cello-player's cramp, telegrapher's 
cramp, tailor's cramp, milker's cramp, the peculiar disturbances of innervation in 
the hands which often occur in cigar-rollers, etc. In the lower extremities there 
seems to be an analogous affection in ballet-dancers, and also in sewing-machine 
girls, turners, etc. We have seen professional cramp in the tongue in a clario- 
net-player. The special points in the symptomatology and treatment of all these 
forms of cramp are in large part analogous to the conditions described in writer's 
cramp. In piano-players the neurosis appears chiefly in the paretic form — mild 
fatigue — and is usually associated with quite severe pains, that come on during 
playing, in certain parts of the arm. In regard to treatment, the best results are 
obtained by energetic massage, but general treatment (iron, cold baths, a country 
residence) is never to be neglected. Finally, it may here be noted that in certain 
laborious occupations that are persistently practiced, a severe group of nervous 
symptoms may also arise. For example, Hirt has lately described an affection 
which occurs in sewing-machine girls, and is characterized by disturbances of sen- 
sibility, pain, paresthesia, and in some cases anaesthesia, ataxia, absence of the 
tendon reflexes, and swaying with the eyes shut. The disease thus recalls very 



SIMPLE AOT) MULTIPLE DEGENERATIVE NEURITIS 885 



closely the picture of locomotor ataxia, but it is curable with proper treatment. 
Therefore Hirt suspected an affection of the peripheral nerves. Similar symptoms 
are also seen in other classes of laborers, as in farm-hands after laborious toil in 
the fields. 



CHAPTER V 

SIMPLE AND MULTIPLE DEGENERATIVE NEURITIS 

1. Simple Neuritis 

1. Primary Simple Neuritis. — In the previous chapters we have become ac- 
quainted with a series of morbid conditions which most probably are to be referred 
to primary inflammatory changes of a particular peripheral nerve. We have seen 
that many cases of sciatica and of neuralgia in other nerve regions, and probably, 
too, all the so-called rheumatic peripheral paralyses (rheumatic facial paralysis, 
deltoid paralysis, etc.), are due to such a neuritis. We have very little infor- 
mation as to the special causes of such forms of neuritis ; we may only suspect 
that in such cases there are definite infectious or toxic substances which act on 
the affected peripheral nerves. In many cases, especially in most neuralgic affec- 
tions, it seems rather to be slight inflammatory changes in the nerve sheath and 
the interstitial connective tissue of the nerve, but in all forms of neuritis leading 
to motor paralysis it is chiefly a destruction of the nerve-fiber itself caused by the 
action of the injurious substance (" parenchymatous inflammation," or, better, 
"degenerative neuritis"). In severe, and especially in acute, cases the paren- 
chymatous and the interstitial changes may develop simultaneously. We will go 
more fully into the description of the anatomical details in the section on " mul- 
tiple neuritis " below. 

We may merely mention here, as of practical importance, those cases of pri- 
mary simple neuritis which, after the analogy of facial paralysis which has been 
fully described, lead to acute peripheral paralysis in other nerve regions. To this 
class belong, first of all, neuritic axillary paralysis (deltoid), neuritic paralysis 
in the ulnar, long thoracic (serratus anticus major), crural, peroneus, etc.; 
neuritic plexus paralyses also occur, especially in the brachial plexus. In many, 
although of course not in all of these cases, a marked exposure to cold is to be 
looked upon as the cause of the neuritis ("rheumatic neuritis"). The disease 
itself usually begins with more or less severe pain and paresthesia in the neigh- 
borhood of the affected nerve, a symptom which is often of decided significance in 
diagnosis and is usually referred to the involvement of the nerve sheath and in- 
terstitial tissue (nervi nervorum!), especially when motor nerves are attacked. 
At the same time with the pain, or soon after it, appear signs of motor weakness 
in the muscles supplied by the affected nerve. The paralysis may vary extreme- 
ly in intensity. In mild cases the symptoms soon disappear and recovery en- 
sues. In severer forms electrical reaction of degeneration and atrophy of the 
paralyzed muscles develop; but even here, as has already been said, we may usu- 
ally expect a favorable issue. The affected nerves are often very sensitive to 
pressure. Slight disturbances of cutaneous sensibility are often to be made out 
on careful examination when there is neuritis of a mixed nerve trunk; but, as a 
rule, the motor disturbance is almost always much more apparent than the sen- 
sory. The treatment follows the methods in vogue in all peripheral paralyses. 

2. Secondary Simple Neuritis. — There can scarcely be a doubt that secondary 
neuritis may occur in consequence of disease of neighboring organs. Neuritis 



886 



DISEASES OF THE NERVOUS SYSTEM 



sometimes develops in open wounds which permit the direct entrance of inflam- 
matory agents to the nerve ; the inflammation is distributed chiefly in the sheath 
and the connective tissue of the nerve. It is, however, of rare occurrence — much 
rarer than we were formerly disposed to assume. Simple mechanical injuries 
and lacerations of peripheral nerves are much commoner, occurring in all sorts 
of affections in their neighborhood — fractures, luxations, caries of the bone, 
tumors, etc. In such cases we should not speak, without qualification, of " in- 
flammation," since we usually have to do, as has been said, with purely mechan- 
ical consequences. Apart from the ordinary secondary descending degeneration 
(vide supra, page 849), such mechanical lesions of the nerves have in themselves 
not the slightest tendency to extend upward in the form of a " neuritis ascendens" 
or " migrans" as was formerly believed, and the assumption of an " ascending 
neuritis," following diseases of internal organs (sexual organs, kidneys, intes- 
tines, etc.), and finally leading not infrequently to secondary myelitis, so- 
called " reflex paralysis," etc., is warranted only in the rarest cases. It is certain, 
however, that inflammatory processes may sometimes attack neighboring nerve 
trunks and that an acute inflammation may sometimes extend immediately up 
the neurilemma of the outgoing nerve to the cerebral and spinal meninges. So 
far as these processes deserve clinical significance they will receive special men- 
tion in the appropriate places. 

[It has long been known that, when a nerve has been cut, the portion below 
the injury rapidly degenerates — Waller's law of degeneration. The portions that 
degenerate are the axis-cylinder processes that have been separated from the 
cell-body of the neurone. As a result of more delicate methods of research, it has 
been found that the rest of the neurone — the cell-body and the axis-cylinder 
stump — also undergoes slighter changes. There may be, therefore, really an 
ascending degeneration in the nerve, but it is very slight and has little or no 
clinical significance.— K.] 

Those cases of secondary neuritis which follow other and quite different dis- 
eases (usually acute infectious diseases) have quite a different origin. Since in 
such cases the degeneration often develops in several nerve regions at once, we 
will return more in detail to this form of secondary neuritis in the next section 
(see the following pages). 

2. Multiple Degenerative Neuritis 

^Etiology. — Although the occurrence of extensive primary disease in the 
peripheral nerves was practically unknown not very long ago, many investiga- 
tions in the last few decades (Dumenil, Joffroy, Leyden, and many others) have 
taught us that no part of the entire nervous system is so much exposed to all 
possible harmful influences as the peripheral nerve-fiber. We are at present 
acquainted with a long list of types of nervous disease which are due exclu- 
sively, or at least chiefly, to more or less extensive degeneration of the peripheral 
nerves. The more we investigate the causes of these diseases, the more we be- 
come convinced that it is almost always, in the last instance, chemical poisons 
which enter the body or are formed in the body itself and exert a destructive 
influence on the peripheral nerve-fiber. It is indeed possible that all such poisons 
act from the outset upon the whole peripheral neurone — that is, the ganglion-cell - 
and peripheral nerve-fiber — but the visible injury (degeneration) is often mani- 
fested exclusively in the peripheral nerve-fiber, and probably first in the branches 
most remote from the trophic center, the nerve-cell. Only when the action of 
the poison is severe and long-continued can the whole neurone — that is, the 
motor ganglion-cell in the anterior horn of the cord — be visibly injured or even 
completely degenerated. [Changes may also occur in the peripheral sensory neu- 



SI1LPLE AXD MULTIPLE DEGEKEKATIVE KEUEITIS 887 



roues, not only in the peripheral portions of their nerve-fibers, but also in their 
ganglion-cells in the spinal ganglia and in their axis-cylinder processes in the 
spinal cord. — K.] The toxic origin of peripheral nerve degeneration is most 
clearly seen in those morbid conditions which we can refer with certainty to a 
definite, well-recognized poison. These are the special " toxic neuritia.es," in 
the strict sense of the word, with which we have already become acquainted 
in the description of lead and arsenical paralyses. We have seen that, by the 
action of these poisons, extensive destruction of the peripheral nerves may ensue, 
which, of course, is followed by serious clinical symptoms. Disregarding several 
other rare forms of poisoning (copper, zinc, silver, phosphorus, mercury, etc.), 
there still remains one extremely important and comparatively common form of 
poisoning which leads to multiple neuritis, and that is chronic alcoholism. Al- 
coholic neuritis is by far the commonest form of multiple neuritis, and it will 
therefore require a special description later. 

Besides these neuritides, directly of toxic origin in the strict sense of the 
word, we find a second large group of cases which come on secondarily in the 
course of or as a sequel to other diseases. To this class belong, in the first place, 
most of the cases already mentioned (page 832) of "paralysis after acute dis- 
ease." Since it is usually an acute infectious disease (diphtheria, typhoid 
fever, scarlet fever, septic infection, puerperal disease [pneumonia], etc.). we 
may reasonably assume that it is the toxines formed under the influence of the 
corresponding agents of infection which lead to the death of the peripheral nerve- 
fiber; but similar conditions also occur in chronic infectious diseases. Tubercu- 
losis in particular seems to stand in close relation to multiple neuritis, although, 
of course, it is often hard to exclude complication with some septic infection or 
the simultaneous action of other intoxications (especially alcohol, vide infra). 
[A more or less extensive neuritis is not uncommon in leprosy. The distribution 
of the neuritis is less symmetrical than in other forms of neuritis, and the morbid 
changes in the peripheral nerves, which involve the perineurium and interstitial 
tissue more than the nerve-fiber itself, are thought to be due to the direct inva- 
sion of the nerves by the bacteria rather than to the general toxic effect of the 
disease. The chief symptoms are marked anaesthesia and muscular wasting. The 
anaesthesia in the anaesthetic form of leprosy is due to these lesions of the periph- 
eral nerves. — K.] It is certain that post-syphilitic nervous diseases (tabes, 
q. v.) are due, at least in part, to degenerations of the peripheral nerves ; but in 
these cases there is usually extensive disease at the same time in the central 
uervous system, so that we do not class these conditions as true neuritis. [Syphi- 
litic processes may, of course, involve individual nerves, somewhat in analogy 
with leprous neuritis, but it is doubtful whether true multiple neuritis is ever 
of syphilitic origin. Malaria is also said to cause multiple neuritis. Xeuritis is 
more apt to follow the pernicious forms of malaria occurring in the tropics — 
Jamaica, India. Madagascar, etc. It may come on suddenly during the comatose 
period of a pernicious attack. In some of the acute cases there have been well- 
marked changes in the nerve-sheaths, in other cases there have been ordinary 
degenerative changes. The neuritis has been referred to the toxines produced by 
the Plasmodium. Trophic and vaso-motor symptoms (cyanosis) seem more 
marked than in other forms of neuritis. There is a possible relation between 
malarial neuritis and beri-beri (q. v.). — K.] Of non-infectious diseases, diabetes 
mellitus, first of all, is sometimes most closely related to the onset of multiple 
neuritis. Here, again, we can scarcely help thinking that there is again some ab- 
normal chemical substance which has caused the neuritis, but the question of dia- 
betic neuritis is still in great need of further investigation. It is a fact that 
neuritic affections of various sorts occur in severe and also in mild forms of dia- 
oetes, but of course we may often think, on the other hand, that the glycosuria 



888 



DISEASES OF THE XERVOUS SYSTEM 



is only a sequel of the neuritis, or that it has come on at the same time with it 
(from the same cause, especially previous alcoholism). In a few cases polyneu- 
ritis has been seen in severe (usually ulcerative) carcinpmata, but in these cases 
secondary septic processes may play the chief part, as in tuberculosis (vide supra). 

The third group, finally, is composed of those cases of multiple neuritis which 
must be termed primary multiple degenerative neuritis. Of course, alcoholic 
or diabetic neuritis, for example, may come on apparently as a primary disease, 
but the true primary form of the disease includes only those cases where no other 
special preceding cause can be discovered, and where the neuritis apparently 
comes on as an independent disease, due to a special specific cause. The whole 
course of the disease, which often has an acute febrile character (vide infra),. 
shows that we must in such cases also consider toxic-infectious influences, but we 
know nothing as yet as to the precise form of this infection. We can sometimes 
find no special cause. There has often been previous exposure to severe cold. 
Such cases are called " rheumatic multiple neuritis," without, of course, implying- 
that they have any definite connection with articular rheumatism. It is worthy of 
mention that primary polyneuritis has sometimes been observed to occur in epi- 
demic form. [The peculiar form of epidemic neuritis known as beri-beri will be 
spoken of later. — K.] 

We must add in conclusion that we have very often seen cases of multiple 
neuritis where we could discover several of the above-mentioned causes at the 
same time, especially when alcoholism and tuberculosis or alcoholism and dia- 
betes mellitus could unite their noxious effects. We have also seen alcoholic poly- 
neuritis come on directly after some acute febrile disease (pneumonia, etc.),. 
which distinctly reminds us of the appearance of delirium tremens in acute 
diseases. 

Pathological Anatomy. — The anatomical changes of neuritis consist, as has 
been said, mainly in a degenerative destruction of the nerve-fibers. We do not 
know whether the toxic agents act directly on the peripheral nerve-fibers or on the 
peripheral motor neurones in their entirety. The visible coarse anatomical de- 
struction is usually found, at all events, only in the peripheral offshoots of the 
neurone — that is, in the " peripheral nerves," and apparently it is most marked in 
the most distant terminal arborizations of the nerves. In the larger nerve-trunks 
and plexuses the changes are usually much less pronounced than in the smaller 
nerve-branches. 

Only in a few acute cases do the interstitial connective tissue and the nerve- 
sheath show the changes of true acute inflammation. In such cases we find the 
affected nerves swollen and decidedly reddened from the great vascular injection; 
with the naked eye we can sometimes see several or many small hemorrhages. 
The microscope shows the nerve-sheath and the interstitial tissue infiltrated with 
many round cells, but as a rule the interstitial tissue is little or not at all in- 
volved in the disease. The pathological anatomical process consists exclusively 
in a destruction of the axis cylinder and medullary sheath (see Fig. 112). If 
we stain the diseased nerve-fibers with osmic acid we see the sheath of Schwann 
filled with many large and small flakes and globules of the 'medullary substance 
of the nerve which are stained black. The fatty globules formed bv this degenera- 
tion are taken up by individual leucocytes (perhaps also by the endothelial cells?), 
and thus the so-called " fatty granular cells " are formed. If the process has 
lasted some time and the acute symptoms have ceased, either the regeneration of 
the nerve-fiber begins, or, when the special nerve-tissue is permanently destroyed, 
there is a new formation of an abundant interstitial connective tissue. If we 
now examine a transverse section of a diseased nerve we find the individual nerve- 
fibers no longer close together, as under normal conditions, but separated from 
one another in many places, where some fibers have wholly disappeared, by a 



SIMPLE AND MULTIPLE DEGENERATIVE NEURITIS 889 



large amount of interstitial connective tissue. If the new formation of con- 
nective tissue attains a higher degree, the nerve then becomes firmer and denser 
than normal, and, when there is a very large amount of connective tissue (after 
the analogy of callus formation) it also becomes thicker, so that in some places 
may sometimes speak of a neuritis nodosa. If, however, the polyneuritis 



-that is, to a complete new growth of the 



we 

recovers, it is due to regeneration- 
destroyed nerve- 
fiber. The remark- 
ably great power 
of regeneration of * 
the peripheral nerves y 
is one of the most /p- " ..- * 

important facts in 
the pathology of the 
nervous system. It 
is explained in a 
simple manner by 
the persistence of 
the cell of origin 
(the motor ganglion- 
cell in the anterior 
horn) from which 
the destroyed termi- 
nal branches grow 
out again like the 
severed branches of a 
tree. Therefore the 
severest peripheral 
paralyses and atax- 
ias may sometimes 
completely recover. 

In the cases of 
" chronic multiple 
neuritis " the dis- 
ease succeeds an acute neuritis or develops in an insidious fashion from the start. 
In the latter case the first acute stage of hyperemia and cell infiltration is wholly 
wanting and the disappearance of nerve-fibers and the secondary new growth of 
connective tissue is a chronic process from the first. Such conditions perhaps 
should not properly be called " neuritis," but " primary chronic degenerative 
atrophy of the nerves " ; but the name is of less consequence than a clear idea of 
the nature and development of the morbid process. There is also nothing strange 
in finding in some cases slight changes in the motor ganglion-cells themselves. 
When the action of the toxic substance is severe or long continued the whole 
motor neurone, including its cell of origin, suffers. The paralyzed muscles in 
every peripheral neuritis soon become very much atrophied. Microscopic exami- 
nation shows all stages of atrophy of the fibers up to complete disappearance. 
The transverse striation is for the most part preserved, and the number of the 
muscular nuclei is much increased. In individual cases we also find degenera- 
tive destruction of the muscular fibers, hypertrophy, swelling, waxy degeneration, 
etc. A genuine myositis — that is, the formation of small inflammatory foci in 
the interstitial tissue — is sometimes joined to the neuritis. In such cases of 
" neuro-myositis " the poison seems to act from the start simultaneously on the 
nerves and muscles. 

Besides its action on the peripheral motor neurones and the muscles, the 




Fig. 112, 



-Radial nerve in alcoholic polyneuritis. Osmic-acid preparation. 
(Personal observation.) 



890 



DISEASES OF THE NERVOUS SYSTEM 



action of the morbific influence may extend still farther. Thus we find co-exist- 
ing* changes in the columns of Goll, and even in the brain, which under some cir- 
cumstances may excite special clinical symptoms. 

Symptoms and Course of the Different Forms of Multiple Neuritis. — In 
order to attain a correct understanding of the symptomatology of multiple neu- 
ritis, we must first remember that the disease is not astiologically one absolutely 
single affection, and that therefore we must expect a priori certain differences in 
the clinical picture. These differences are due not only to the degeneration of 
different nerve-trunks, but also, in part, to the fact that the same specific variety 
of nerve-fiber is not always the one most affected. In general, of course, the 
rule undoubtedly holds good that the motor nerve-fibers afford the least resistance 
to all the injurious influences previously mentioned. Therefore peripheral paraly- 
ses are the chief and the most common symptom of polyneuritis. The sensory 
nerves are usually less affected; at least pronounced anaesthesia is exceptional. 
The involvement of the sensory nerves is shown rather by symptoms of irritation 
(pain, paresthesia), which probably are to be referred less to a direct invasion 
of the sensory fibers than to an irritation of them as a result of the interstitial 
changes. There is, however, one frequent, important, and very interesting symp- 
tom in multiple neuritis, occurring alone or with the paralysis : a genuine motor 
ataxia. Its origin is not positively explained, but we regard it as most probable 
that the ataxia is due to disease of the centripetal fibers which also exist in the 
peripheral nerves, whose function is to regulate (in a certain sense reflexly) and 
to co-ordinate complicated voluntary movements. It is itself an extremely inter- 
esting fact that ataxia of movement without co-existing paralysis may occur in 
apparently purely peripheral diseases without any discoverable changes in the 
spinal cord; but ataxia may also be due to disease of the spinal processes of the 
spinal ganglion-cells — that is, to degeneration in the columns of Goll. From a 
symptomatological standpoint we must therefore distinguish two forms of neuritis 
— a paralytic form (the usual form) and an ataxic form (so-called acute curable 
ataxia, and also, especially, the pseudo-tabes of alcoholic subjects) ; but combina- 
tions of the two forms occur, since paralytic conditions and disturbances of co- 
ordination may be united. 

Passing now to the description of the general aspect and course of polyneu- 
ritis, it seems best to keep separate the different forms which may be distin- 
guished either clinically or aetiologically. 

1. Primary Acute and Chronic Multiple Neuritis 
The disease usually begins acutely, sometimes almost in an apoplectiform 
manner, and without any definite occasion, precisely like an acute infectious 
disease. Febrile symptoms, with temperatures from 102°-104° (39°-40° C), 
come on in persons previously in good health, usually in adults before or during 
middle life, with severe general disturbance, loss of appetite, dullness, head- 
ache, and sometimes even mild delirium. In these acute cases albuminuria 
and a slight enlargement of the spleen have sometimes been observed, which 
symptoms also point toward the infectious nature of the disease. In other 
cases the initial general symptoms are much less severe, or they may be en- 
tirely wanting. The pains, which are hardly ever absent, are very characteris- 
tic. They are described as pulling and tearing, are felt chiefly in the loins 
and the extremities, and sometimes follow approximately the course of the large 
nerve-trunks. Since in some cases a number of the joints are swollen, the disease 
at first may be mistaken for acute articular rheumatism. The first symptoms of 
paralysis, usually in the lower extremities, appear very soon after these initial 
symptoms, or at the same time with them. The patient notices that he can not 
readily move one leg, and soon after he notices the same of the other. The paraly- 



SIMPLE AND MULTIPLE DEGENERATIVE XEURITIS 89 1 



sis may remain confined to the legs, but more frequently it extends to one or 
both arms. In regard to its distribution, the forearms and lower legs are gener- 
ally more affected than the upper arms and thighs, and the extensors (radial and 
peroneal region) are also more affected than the flexors; but other varieties of 
distribution may occur, for instance, affection of the glutei and thigh muscles, 
etc. If we examine the paralyzed parts more carefully we find a perfectly atonic 
and more or less extensive paralysis. The reflexes are almost always diminished, 
the tendon reflexes are usually entirely absent, and the cutaneous reflexes are 
weak, or they also have almost wholly disappeared. In only a few cases are the 
reflexes increased — a symptom which is to be regarded as analogous to cutaneous 
hyperesthesia. We can usually make out, after a few days, a decided diminu- 
tion of electrical excitability in the affected nerves and muscles, which soon 
becomes a pronounced reaction of degeneration. If the paralysis is of longer 
duration, there is a decided atrophy of the muscles. In these cases the severe 
initial symptoms of sensory irritation, as a rule, rapidly disappear, although 
slight pains, paresthesia, and especially a considerable sensitiveness of the para- 
lyzed parts to pressure and to passive motion, often last for a long time. In 
many acute cases the hyperesthesia of the skin and of the deeper parts reaches 
a very high degree, but it is remarkable that the objective disturbances of sensi- 
bility are very slight in the great majority of cases ; although on careful testing 
we can often find slight diminution of sensibility for touch or temperature. Other 
observers and we ourselves have also repeatedly seen the symptom of so-called 
delayed conduction— that is, delayed sensation of pain (vide supra, page 793). 
We usually find no disturbances in the distribution of the cerebral and bulbar 
nerves. An affection of the optic nerve has been mentioned in only a few cases. 
Eacial paralysis and, much less frequently, paralysis of the tongue or of the ocular 
muscles may also occur. We have ourselves repeatedly seen total bilateral facial 
paralysis. We may mention as a rare complication acute mental disturbances 
(confusion, anxiety, weakness of memory, vide infra). Details of this very 
peculiar " polyneuritic psychosis " will be given below in the description of 
alcoholic polyneuritis. The marked increase in the frequency of the pulse, which 
is usually present, is important, and probably depends upon a disturbance of 
the vagus. Trophic disturbances in the skin, hair, and nails are not very rare. 
Profuse sweating sometimes occurs. (Edematous swelling of the affected ex- 
tremities has also been repeatedly observed. The functions of the bladder and 
rectum, however, almost always remain unaltered, but in some cases slight dis- 
turbances of the bladder may of course be discovered. 

In regard to the course of the disease, in the severest cases it may soon termi- 
nate fatally, almost always because the paralysis extends to the muscles of respira- 
tion. The inspirations are labored, and are performed with the upper part of the 
thorax only, while the epigastrium is motionless, or sinks in on inspiration from 
the paralysis of the diaphragm. There is also paralysis of the other muscles of 
respiration, the abdominal muscles, etc., so that, after the disease has lasted a 
week or ten days, death ensues with all the signs of respiratory insufficiency. 
Such cases have been repeatedly described in the past under the title of acute 
ascending paralysis (Landry's paralysis, q. v.). A second class of cases also 
begins quite acutely, but then takes a chronic course. The initial acute febrile 
symptoms cease after a few days, although the paralysis continues to develop 
to some extent. Then the affection seems to come to a stand-still, and the first 
signs of improvement gradually begin to appear. Since there is a more or 
less pronounced atrophy of the muscles in these cases, it always takes consid- 
erable time — usually several months — for recovery ; but it is often astonishing 
to see how the most extensive paralysis may finally get entirely well. A third 
class of cases follows a chronic course from the outset, although even in these 



S92 



DISEASES OE THE NERVOUS SYSTEM 



cases there may be more acute exacerbations of the disease. In these cases quite 
extensive atrophic paralysis gradually develops in the lower extremities, and 
usually in the upper extremities also. The reflexes disappear; the sensibility is 
as a rule somewhat, but very rarely much diminished. Pains are always present 
at first, but later on in the disease they often become subordinate. The blad- 
der and rectum usually remain normal in their functions or show only slight 
disturbances. If the disease advance gradually it may terminate fatally even 
at a late period, after a course of months, usually from a final paralysis of respi- 
ration ; but, on the other hand, even after a protracted course, the disease may 
come to a stand-still, and even progress to a complete or at least to a partial 
recovery. 

The diagnosis of multiple neuritis is, as a rule, easy for one who is acquainted 
with the disease and notes the different symptoms carefully. In regard to diag- 
nosis, the chief importance should be placed on the generally acute beginning, 
with pronounced symptoms of sensory irritation, with frequently a very consid- 
erable sensitiveness of the .nerves and muscles to pressure and general cutaneous 
hyperesthesia ; and also on the appearance of a rapidly extending paralysis, whose 
peripheral nature may be attested by the presence of reaction of degeneration, 
muscular atrophy, and the absence of the cutaneous and tendon reflexes. Such a 
paralysis can be produced by nothing but an affection of the peripheral nerves or 
poliomyelitis (vide infra). This latter disease was, in fact, formerly confused 
with multiple neuritis, but a careful attention to the initial symptoms, especially 
to the pain and disturbances of sensation, usually makes the differential diag- 
nosis possible. 

The prognosis of multiple neuritis is doubtful, as is shown by the description 
of the course of the disease, but it is by no means very unfavorable. If the pa- 
tients gets through the first acute stage of the disease without accident, we may 
hope for recovery, or at least actual improvement, even with extensive paralysis. 
Such striking results in the way of recovery, after paralysis that has lasted for 
months, are also important in regard to diagnosis, since such extensive processes 
of regeneration are possible in affections of the peripheral nerves, "but scarcely in 
spinal diseases; and hence they are sometimes an additional confirmation of the 
diagnosis of a neuritis. 

Treatment. — In the first stage of the disease, especially if severe pains, swell- 
ing of the joints, or high fever be present, it is advisable to try the exhibition of 
salicylic acid, from which several observers have seen a favorable effect. We give 
ten grains (gramme 0.5) of the acid every hour, or a few larger doses of salicylate 
of sodium, a drachm to a drachm and a half (gramme 4-6). Instead of salicylic 
acid we have used antipyrine and phenacetine with good results. When the pain 
is very severe we must use narcotics, such as injections of morphine. Embroca- 
tions of chloroform, and sometimes protracted warm baths, have also a palliative 
effect. In the further course of the disease proper care, a suitable position for 
the limbs, and diet — nourishing food — are the main things for the patient. The 
regenerative processes of recovery begin spontaneously, if they begin at all, but we 
may hasten recovery and make it complete by a subsequent electrical treatment, 
especially galvanism. For the completion of the recovery, bathing (simple warm 
baths, salt baths, etc.) is serviceable, and also the baths at Teplitz, Wiesbaden, 
JSTauheim, and Oeynhausen, and the cautious use of massage. 

2. The Ataxic Form of Multiple Neuritis 

("Acute Curable Ataxia''' 1 ) 

We can not make a sharp division between the ataxic and the paralytic forms 
of multiple neuritis. Both conditions, paralysis and ataxia, may occur in the 
same patient. It is important, however, to know that almost pure ataxia (without 



SIMPLE "AND MULTIPLE DEGENERATIVE NEURITIS 893 



paralysis) may develop acutely, and that it is undoubtedly to be referred to de- 
generation of the peripheral nerves. 

Under the ataxic form of polyneuritis must be classed, first, the cases of ataxia 
repeatedly observed after various acute infectious diseases, especially ataxia after 
diphtheria (q. v.), and also after typhoid fever, small-pox, septic affections, dysen- 
tery, etc. ; but there is also a primary acute ataxia which comes on without any 
discoverable cause or after exposure to severe cold in previously healthy persons. 
Severe general initial symptoms are, as a rule, not present, and the pain is not 
very great. The ataxia usually develops in the legs, more rarely in the arms. 
There may be slight disturbances of sensibility at the same time, but not neces- 
sarily. The patellar reflex is usually but not always absent. As a rule, with 
proper care and nursing the patient recovers completely in a few weeks. The 
diagnosis of this primary acute ataxic form of polyneuritis is usually not difficult. 
The disturbance of the patient's g*ait may at first arouse the suspicion of tabes, 
but the rapid onset, the perfectly normal pupillary reflexes, and usually also 
the normal micturition, oppose it. We often find in some muscular regions a true 
paresis besides the ataxia, which is not like the conditions in tabes. We once saw, 
for instance, a severe ataxia of the legs associated with double facial paralysis. 
In any doubtful case a favorable termination in recovery forms the final criterion 
in favor of polyneuritis. 

3. The Acute and Chronic Neuritis of Alcoholic Subjects — Alcoholic 

Paralysis 

(Pseudo-tabes [Ataxia] of Alcoholic Subjects) 

It has long been known that peculiar nervous affections often occur in alco- 
holic subjects (M. Huss, Leudet, and others) ; but formerly a disease of the 
spinal cord was assumed to be the cause of the symptoms, and only of late have 
we obtained the knowledge that the greatest part of the cases of this class are to 
be classed as acute and chronic multiple neuritis (Lancereaux, Moeli, and others). 
The practical importance of this alcoholic neuritis is not slight; first, because it 
may easily be confused with other nervous diseases, especially with myelitis and 
tabes, and, second, because its proper and timely diagnosis is of great significance 
in regard to treatment. Alcoholic neuritis, furthermore, is by no means rare, 
being certainly by far the commonest of all forms of polyneuritis. The more we 
consider the significance of this factor the more all other causes are thrown into 
the background. Not infrequently, of course, other causes must be considered at 
the same time with alcoholism; we see, for example, polyneuritis very often in 
alcoholic subjects who are also tuberculous, and sometimes in the combination 
of alcoholism and diabetes, etc.; but in all such cases chronic alcohol poisoning 
probably plays the chief part. Alcoholic neuritis occurs in drinkers of spirits, 
and also, as we have often noticed, in habitually excessive beer drinkers. It is 
alleged to be less frequent in drinkers of wine. 

Alcoholic polyneuritis, like the other varieties of multiple neuritis, occurs in 
different forms. According to its course we may distinguish acute and chronic 
cases, and according to its symptoms a paralytic and an ataxic form, but there 
are no strict boundaries between these forms. 

Alcoholic paralysis begins quite suddenly or more gradually. Motor weakness 
develops, having its chief seat usually in the legs, and thus rendering walking 
almost wholly impossible. This weakness generally begins with quite severe tear- 
ing and drawing pains and considerable tenderness on pressure over the affected 
muscles. Most writers agree that the muscles on the anterior side of the lower 
leg (peronei, tibialis anticus) are very often affected. We can agree with this for 
many cases, but by no means for all. We have often seen at the onset the great- 
est trouble in the muscles of the thigh (crural region), and especially in the glu- 



894 



DISEASES OF THE NEKVOTJS SYSTEM 



taei. Such patients can still walk with effort on level ground, but they can not go 
up a step or rise from a chair. With greater paralysis the patient is absolutely 
bedridden. The muscles of the legs are flabby, they become more or less atrophied, 
their electrical excitability diminishes, there is sometimes pronounced reaction of 
degeneration (especially the middle form), and the patellar reflex and other 
tendon reflexes are usually absent, although there are some remarkable exceptions 
to this rule. The bladder and rectum are entirely normal or show only slight dis- 
turbances. The sensibility of the legs is rarely perfectly normal on careful test- 
ing, but the sensory disturbances, except for pain and parsesthesia, are overshad- 
owed by the paralysis. We often find a slight blunting of sensibility for touch 
and pain, and very often the so-called delayed sensation of pain (vide supra, 
page 793). The skin reflexes are diminished. 

In many cases the paralysis extends to the arms also, and chiefly in the radial 
distribution, so that both hands hang lax in volar flexion, and they and the 
fingers can be extended but little. The combination of double radial and peroneal 
paralysis has been often mentioned as characteristic of alcoholic paralysis. Even 
in patients who can still extend their hands and fingers well we often find that 
the strength of the movement is diminished. In severe polyneuritis the other arm 
muscles may also be affected. Muscular atrophy, electrical reactions, sensibility, 
and the reflexes are the same as in the legs. 

The facial muscles are rarely affected, but they have been in a few cases. In 
some very acute and severe cases of polyneuritis there is also paralysis of the 
ocular muscles, so that the eye may become completely immovable ; but in the few 
cases that have come to autopsy there seems usually to have been no neuritis of 
the oculo-motor nerves themselves, but many small haemorrhages in the neighbor- 
hood of the third ventricle — that is, in the region of the oculo-motor nuclei (so- 
called polio-encephalitis hemorrhagica superior, q. v.). 

Mental disturbances (" polyneuritic psychoses ") have been frequently ob- 
served in alcoholic polyneuritis. They often differ little from delirium tremens, 
but in other cases a very peculiar type of disease develops. The patient is con- 
fused, mixes up persons and places, is very restless, especially at night, apparently 
has hallucinations, and is consequently excited and anxious, but in the intervals 
is happy and contented. The most striking disturbance is an extraordinary weak- 
ness of memory for all recent events. Half an hour after eating the patient no 
longer knows that he has eaten. If we show him an object or utter a word or a 
short sentence to him, he forgets it completely in a few minutes. The more care- 
fully we test the patient in regard to this, the more frequently shall we discover 
this remarkable disturbance of memory; but the recollection of the distant past 
and of things learned before the trouble is not at all or very slightly affected. 
The patient's initial confusion is chiefly the direct result of this actual failure of 
memory. The severe mental disturbances sometimes last only a few days, but 
the disturbances of memory may often be noticed for weeks, when they gradually 
disappear. 

The ataxic form of alcoholic polyneuritis may also come on acutely, so that 
the patient's sudden inability to walk is due to a genuine ataxia of the legs. The 
ataxia, of course, is generally associated with manifest paralysis, at least in 
some muscular territories (glutsei, peronei, radials). The ataxia may often be 
masked by a greater paralysis, so that we can discover it only by careful exami- 
nation. The patellar reflex is usually, but not invariably, lost; the sensibility is 
only slightly affected, apart from the pain and parsesthesia. The functions of 
the bladder remain wholly, or almost wholly, normal. 

The chronic form of alcoholic ataxia, the special pseudo-tabes of alcoholic 
subjects, is more important because it is often harder to diagnosticate. In this 
form a type of disease develops comparatively slowly, which may closely resemble 



SIMPLE AND MULTIPLE DEGENERATIVE NEURITIS 895 



genuine tabes : ataxic gait, lancinating pains, sometimes even a sort of girdle sen- 
sation, absence of patellar reflex, slight disturbance of the bladder, definite dis- 
turbances of sensibility, etc. The disease resembles true tabes still more closely if 
temporary double vision occurs. In such cases we can avoid mistaking it for true 
tabes only by careful examination. The most important mark of distinction is 
afforded by the pupils, which almost always preserve their normal reaction in 
pseudo-tabes. We may also note that in pseudo-tabes the disturbances of the 
bladder are usually slight, and they may be entirely absent ; that the muscles and 
nerves are tender on direct pressure, and that from the first we can usually find 
besides the ataxia a slight genuine paresis, which in some muscles (vide supra) 
may be marked. [We rarely if ever find in pseudo-tabes the anaesthesia or anal- 
gesia over the lower part of the chest, on one or both sides, in the area of the 
third to the seventh dorsal roots, so characteristic of true tabes. — K.] Finally, of 
course, the causal factor, pronounced chronic alcoholism, is an essential considera- 
tion. It is worthy of note that in alcoholic pseudo-tabes the anatomical lesion is 
probably not often limited to the peripheral nerves, but also involves the spinal 
processes of the spinal ganglion cells — that is, the region of the columns of Goll. 

The course of this pseudo-tabes may extend over several years, but the progno- 
sis is far more favorable than that of true tabes ; decided improvement and even, 
in mild cases, complete recovery may occur; but there are also severe incurable 
forms, since dangerous complications (tuberculosis, etc.) often set in. 

All the more acute forms of alcoholic neuritis afford quite a good prognosis, 
provided the abuse of alcohol can be permanently checked. We may then often 
see complete recovery in a few weeks or months. On the other hand, relapses are 
common, and these usually have a tedious course. 

The first task in the treatment of alcoholic neuritis is to insist upon the 
absolute abandonment of the use of alcohol. If this be done, the milder cases 
usually get well of themselves. The favorable course is aided by electrical (gal- 
vanic) treatment and tepid salt baths. Internally we prefer strychnine prepara- 
tions (pills of nitrate of strychnine or extract of nux vomica). 

[4. Beri-beri — Endemic Multiple Neuritis 
The peculiar disease of endemic origin, long known in India and Japan as 
" beri-beri " or " kak-ke," has been found by Scheube to be in its clinical and ana- 
tomical relations a well-characterized multiple neuritis. Cases are occasionally 
seen in seaport towns in sailors arriving from. Asiatic ports, and Putnam has de- 
scribed cases occurring in fishermen returning from the Newfoundland banks. 
Independent outbreaks of the disease have also occurred among the insane in asy- 
lums in Alabama, Arkansas, Dublin, and elsewhere. Men are more frequently 
affected than women, and colored races more than the white. The cause of the 
disease is still obscure. Pekelharing and Winkler attributed it to a specific staphy- 
lococcus, but their observations have not been confirmed by later observers. 
Insufficient or improper diet probably increases the susceptibility to the disease, 
but it is doubtful if an exclusive diet of rice or fish, as was once believed, can ac- 
tually cause beri-beri. Bondurant in Alabama found a close connection between 
the outbreak of the disease and the use of a polluted water-supply. In other cases 
there seems some association with malarial poisoning. Overcrowding and foul 
air favor its development. The disease may begin suddenly or insidiously, and it 
is often ushered in by moderate fever and gastro-intestinal symptoms : anorexia, 
vomiting, abdominal pain, and diarrhoea. Two forms of the disease — a " wet " 
and a " dry " — are usually recognized. The symptoms in the " dry " form are sim- 
ilar to those of ordinary multiple neuritis : pain, paresthesia, tenderness, loss of 
power with degenerative muscular atrophy, especially in the extensors of the foot, 
slight disturbances of sensation, and diminution or loss of patellar reflex. The 



896 



DISEASES OF THE NERVOUS SYSTEM 



" wet " form, which is commoner, often begins with dyspnoea and a rapid pulse, 
and oedema may soon follow. The oedema is most marked in the regions supplied 
by the affected nerves, but there is also effusion into the serous cavities. The 
heart's action is weak, and the heart may soon become greatly dilated, and adven- 
titious murmurs may be heard. In severer cases the urine contains a small 
amount of albumen, the dyspnoea and rapid pulse persist, and the patient suc- 
cumbs to cardiac exhaustion. A certain amount of serous effusion is usually 
present at the autopsy, together with the changes in the heart. There is also a 
degenerative neuritis of the peripheral nerves, often including the vagus, and a 
corresponding degeneration of the muscles supplied by them, and often degenera- 
tion of the ganglion-cells in the anterior cornua. In some cases of the "wet" 
form the disease progresses rapidly, with increasing oedema and cardiac weakness, 
leading to death in a week or two. Other cases may run a more chronic course, 
with atrophic paralysis, and eventually recover. The prognosis is grave. Twenty 
per cent, of the cases among the chronic insane died in Alabama, and the mortal- 
ity has been even greater in other epidemics, although Scheube estimates the aver- 
age mortality at five per cent. In the way of prophylaxis good hygiene, a good 
soil and sanitary dwellings, pure water and plenty of nutritious food, seem essen- 
tial. Cathartics, especially hydragogues, seem of some benefit in the early stages. 
The condition of the heart demands especial attention, but caution is necessary 
in administering digitalis or strophanthus (the chief drugs to employ) lest the 
weak heart be urged to undue effort. Hence we should begin with small doses 
(gramme 0.2-0.3, minims iij-v, of the tincture), increasing gradually. In the 
later stages the treatment is the same as for other forms of multiple neuritis 
(strychnine, electricity, massage). — K.] 



CHAPTER VI 
NEW GROWTHS IN THE PERIPHERAL NERVES 

The new growths in the peripheral nerves are usually divided into false and 
true neuromata. True neuromata consist of newly formed, usually medullated, 
nerve-fibers {neuroma myelinicum of Virchow), which are imbedded in a con- 
nective-tissue stroma, which is frequently very abundant. These neuromata de- 
velop most frequently in the cut ends of nerves in amputation-stumps (amputation 
neuromata), but they may form after other injuries of the nerves, and perhaps 
many neuralgias and persistent pains after injuries are due to the formation of 
such little neuromata. 

The so-called multiple neuromata or neuro-fibromata are of special pathologi- 
cal interest. They may be found in enormous numbers (many hundreds) on 
almost all the peripheral nerves, on the sympathetic plexuses in the abdominal 
cavity, and on the cranial nerves (vagus, etc.). The smallest of these tumors 
may be as large as a millet-seed, the largest may grow to the size of a pigeon's 
egg or the thumb. The nerves are changed by them into thick cords covered 
with irregular enlargements which can be felt everywhere under the skin during 
life (on the nerves of the arm, the crural, the intercostal nerves, etc.). This 
remarkable condition can naturally be explained only by a congenital abnormal 
predisposition of the nervous system to tumor formation, a theory which is sup- 
ported by a few observed cases of the hereditary occurrence of such multiple 
neuromata. The name " neuroma," however, is not correctly chosen. It is rather 
a fibroma (a tumor of connective tissue), through which the nerve-fibers usually 



NEW GEOWTHS IN THE PEEIPHEEAL NERVES 897 



pass in good condition (" neuro-fibroma "). Hence it happens, as we have seen 
ourselves in one case, that, in spite of an extensive formation of neuro-fibromata, 
there are no nervous symptoms at all, no pain, no anaesthesia, no paralysis; but 
other cases have also been reported in which the tumors caused manifest and even 
.severe symptoms. 

Of other new growths on the nerves we may mention sarcoma. This also is 
often multiple, and then it may lead to very complicated types of disease. The 
.so-called tubercula dolorosa deserve special mention. By this term we mean 
little nodules which may be felt beneath the skin, usually readily movable and 
very sensitive to pressure. They are not very rare, and are usually associated 
with drawing pains, which are rarely decidedly neuralgic and are not very strictly 
localized. They are situated in the extremities, especially in the arms, and in 
the back, the neck, etc. It is worthy of note that the symptoms are only at times 
wery prominent, and then they disappear again, and that with this disappearance 
is certainly sometimes associated a spontaneous disappearance of the nodule. 
The anatomical nature of the tubercula dolorosa is not always to be established 
with certainty.. Many of them are true neuromata, but others belong to other 
kinds of new growths. 

The only successful treatment of neuromata is extirpation, which is to be 
undertaken only when the symptoms are very severe. If extirpation be not 
practicable, or if we have to do with multiple neuromata, the patient's trouble 
can be alleviated by symptomatic means, narcotics, and electricity. If we can 
compress the nerve above the neuroma, we can often cause by this means a tem- 
porary cessation of the pain. 
57 



898 



DISEASES OE THE NERVOUS SYSTEM 



II.— VASO-MOTOR AND TROPHIC NEUROSES 



CHAPTER I 

GENERAL PRELIMINARY REMARKS 

{Erythromelalgia. Acute Angioneurotic (Edema. Myxo&dema. Acromegaly. Hydrops Articulorum. 
Intermittens. Injuries of the Cervical Sympathetic) 

General Consideration of Vaso-motor Disturbances. — Physiology, as is well 
known, distinguishes two varieties of vaso-motor nerves — the vaso-constrictors 
and the vaso-dilators ; but since experiments have detected the latter variety in 
only a few places — for example, in the chorda tympani, the nervi erigentes, and 
the sciatic — they have not acquired a very great significance in human pathology. 
We are at present much more disposed to refer every abnormal constriction of 
the vessels to an excitation, and every abnormal dilatation of the vessels to 
a paralysis of the vaso-constrictor nerves, although perhaps pathological con- 
ditions of excitation of the vaso-dilators may not be at all rare. In regard to 
the precise anatomical course of the vaso-motor nerves, we must first state 
that vaso-motor excitations may certainly proceed from the cerebrum, as is shown 
by the well-known symptoms of blushing and pallor from mental emotions. In 
experiments on dogs, Eulenburg and Landois have succeeded in producing a 
fall of temperature on the opposite side by irritating certain portions of the 
cortex in the immediate vicinity of the motor centers, and by extirpation of the 
same parts they have produced a rise in temperature. Furthermore, we know 
with certainty that there is an important vaso-motor center in the medulla oblon- 
gata (in the region of the upper olivary body in rabbits), the excitation of which, 
directly or reflexly, is followed by an almost universal vascular constriction, and 
its destruction by an almost universal vascular dilatation. We must probably 
seek the further course of the vaso-motor nerves very largely (or exclusively?) in. 
the lateral columns, from which they pass out chiefly by the anterior roots. It 
is not known with certainty whether there is any decussation of the vaso-motor 
fibers, or, if there is, where it occurs. The larger part of the vaso-motor nerves 
collect, at any rate, in the principal trunks of the sympathetic, from which, as is 
well known, the separate plexuses that surround the vessels arise. It is not im- 
probable, however, that there is also in part a direct passage of vaso-motor fibers 
from the cord into the peripheral nerves. In conclusion, we must mention that, 
according to Goltz's experiments, there are reflex vaso-motor centers in the cord 
for the different parts of the body. 

The clinical vaso-motor symptoms are chiefly to be observed in the external 
skin. We distinguish them as follows : 

1. Symptoms of Vaso-motor Paralysis. — We conclude that there is a paraly- 
sis of the vaso-motors if there is an abnormal redness of the skin. Such a red- 
ness is almost always associated with an objective and often a subjective feeling 
of an increase of temperature. Such conditions are observed either in connection 
with other nervous symptoms — as in fresh spinal or cerebral paralyses, and also 
very often in certain functional neuroses, such as hysteria and neurasthenia — or 
in the form of independent affections — the pure vaso-motor neuroses, injuries of" 
the cervical sympathetic, etc. Of course in these cases it is usually hard to de- 



GENERAL PRELIMINARY REMARKS 



899 



cide whether there is really a vaso-motor paralysis or irritation of the vaso-dila- 
tors. There are cases in which the only symptoms are a persistent or paroysmal 
diffuse redness of the skin, especially of the head, associated with a great feeling 
of heat, with palpitation of the heart, strong pulsation of the arteries, anxiety, 
ringing in the ears, and sweating. 

2. Symptoms of Vaso-motor Spasm. — Spasm of the small vessels becomes 
apparent by a striking pallor and coolness of the skin. There is often, with this, 
a decided feeling of formication and stiffness in the affected parts, which may 
even increase to an actual feeling of pain. Such vaso-motor spasms affect the 
hands especially, and form a chronic trouble that is not very rare. They are 
usually seen in people who are generally nervous and irritable, and sometimes 
also in washerwomen. A vascular spasm is sometimes seen in the extremities as 
one symptom of complicated paroxysms, such as nervous angina pectoris (q. v.), 
especially at the beginning of the paroxysm. A persistent spasm of the small 
arteries may give rise to considerable subsequent trophic disturbance. At least, 
the rare cases of so-called " spontaneous symmetrical gangrene " (q. v.), and also 
certain forms of scleroderma and some similar affections, are referred by many 
observers to a primary spasm of the vessels. 

General Consideration of Trophic Disturbances. — We have much less infor- 
mation concerning the trophic nerves than we have concerning the vaso-motor. 
As is well known, the controversy is still going on as to whether we have any 
right to assume the existence of special trophic nerves. The facts of clinical neu- 
rological observation frequently seem to compel the hypothesis of special trophic 
functions, although, of course, it is usually very hard to determine this point, 
because we can seldom wholly exclude the indirect influence of sensory and cir- 
culatory influences (vide supra, anaesthesia of the trigeminus). 

Among those symptoms which chiefly support the theory of the existence of 
specific trophic nervous influences, we have already learned to recognize the de- 
generative atrophy of the muscles and nerves. Various other sorts of trophic 
disturbances in the skin and the deeper parts (bones, joints) are seen in nervous 
diseases. Especially after wounds of the peripheral nerves we often notice a 
peculiar shining, smooth, atrophic condition of the skin — the " glossy skin " 
or " glossy fingers " of English authors. In other cases anomalies in the pig- 
mentation of the skin seem to be connected with the nervous disturbances ; thus 
spots deprived of pigment (vitiligo) often develop as a result of severe neural- 
gias. We must also bring to mind here the appearance of changes in pigmenta- 
tion from nervous causes, especially the aetiology of Addison's disease (q. v.) 
and the occurrence of the so-called nervous nsevi. Among the severe neuro- 
trophic disturbances of the skin many observers, especially Charcot, class the 
appearance of acute bed-sores in many spinal and cerebral paralyses, but we have 
never been able to convince ourselves of the occurrence of a " neurotrophic decubi- 
tus," and we believe that every bed-sore is due in the first instance to external 
injuries (pressure on the soft parts, uncleanliness, and the entrance of the bac- 
teria of inflammation). 

Besides the trophic disturbances in the skin, we often see analogous changes 
in the nails and hair in nervous patients. The nails become brittle and cracked, 
assume a darker color, and often show abnormal conditions of growth, abnormal 
curving, striation, thickening (onychogryphosis), etc. We also see at times a loss 
of the nails. A loss of hair is seen in frontal neuralgia, in certain forms of head- 
ache, and not infrequently as an apparently independent nervous disease (alo- 
pecia). A very rapid whitening of the hair after mental excitement is well known 
to have occurred in some cases. 

Various disturbances of growth and nutrition also occur in the bones and 
joints, and are to be regarded as trophic disturbances. 



900 



DISEASES OE THE NERVOUS SYSTEM 



The implication of the bones in atrophic processes is seen chiefly in pro- 
gressive unilateral facial atrophy (vide infra). A retarded growth of bone in the 
affected extremities is also a symptom frequently seen in the spinal and even in 
the cerebral paralyses that develop in childhood. It is uncertain, however, how 
far this is due to the loss of direct trophic influences or to the indirect influence 
of the loss of motor functions. In conclusion, we not infrequently see very strik- 
ing and apparently trophic disturbances in the bones and joints in tabes and 
syringomyelia (q. v.). 

Erythromelalgia. — We should apparently class here this peculiar disease, 
which is seen most frequently in the feet, although it also occurs in the hands. 
Men seem to suffer from it more frequently than women. The symptoms are 
severe pain, especially in the toes and fingers, but sometimes in the ball of the 
foot, the heel, etc., and also swelling, redness, and marked pulsation of the ves- 
sels. In some cases the affected parts assume a very dark-red or bluish-red 
color. We not infrequently see excessive sweating. [In some cases the condi- 
tion seems due to neuritis ; in others Weir Mitchell, who first described the dis- 
ease, has found arterio-sclerosis in the smaller vessels with no neuritis. — K.] 

The condition described either comes on in paroxysms or is persistent, al- 
though varying in severity. On standing or walking, or when warm, the pain 
usually increases. Other nervous symptoms, such as headache, vertigo, weakness, 
etc., are sometimes associated with erythromelalgia. The course is almost always 
very tedious, and the prognosis therefore doubtful. The treatment consists in 
the use of electricity, cool baths, iodide of potassium, antipyrine, and similar 
remedies. [Mitchell suggests stretching of resection of the nerves. — K.] Com- 
pare the section on acroparesthesia (page 822), which name has sometimes been 
given to apparently allied conditions. 

Symmetrical Spontaneous Gangrene. Raynaud's Disease. — This disease, 
whose nature is still quite obscure, begins with pallor and coldness of the fingers 
("regional ischemia"), associated at first with sensations of crawling and 
numbness, and later with severe pain. After a short time the pallor changes 
to a bluish-red color (" regional cyanosis "), especially in the terminal phalanges, 
which sometimes progresses to the formation of gangrenous spots and vesicles. In 
severe cases a portion of the terminal phalanges is completely destroyed and 
thrown off by dry gangrene. The whole process may last for months. It runs its 
course without fever, but it is sometimes associated with quite severe general 
nervous disturbances. In rare cases spontaneous symmetrical gangrene has been 
observed in other parts of the body, for example, in the thighs, the buttocks, the 
ears, the nose, etc. Several attacks of the disease may sometimes follow one 
another, so that the whole duration of the trouble may be for years. 

In regard to diagnosis, we must first be convinced that the disease comes 
on spontaneously. Extensive areas of gangrene of the skin have repeatedly been 
observed in hysteria, produced artificially by the patient by means of caustics 
(caustic potash, etc.). We must also think of diabetic gangrene, severe arterio- 
sclerosis, syringomyelia, exophthalmic goitre, etc. 

The treatment can be merely symptomatic. Wet applications, baths, cautious 
galvanization, and narcotics (morphine, chloral) when the pain is severe, are 
most employed. 

Acute Angioneurotic (Edema (CEdema* cutis circumscriptum). — This name 
has been given by Quincke, Striibing, and others to a disease characterized by 
the sudden onset of ©edematous swellings in various parts of the body. These 
swellings usually disappear in a few hours, but they are very often repeated. 
Dangerous symptoms may arise if the oedema affect the pharynx or the entrance 
to the larynx. The patient's health otherwise is sometimes perfectly good, but in 
other cases it is more or less affected. Gastric disturbances especially (attacks of 



GENERAL PRELIMINARY REMARKS 



901 



vomiting and gastralgia) have been observed at the same time in such patients. 
Acute angioneurotic oedema is manifestly closely allied to urticaria and ery- 
thema exudativum. 

Myxoedema. — We may here mention myxcedema (cachexie pachydermique of 
Charcot), which was first described in England by William Gull and Ord. The 
disease has taken its name from a peculiar thickening and swelling of the skin, 
which is most marked in the face, but which is sometimes seen in the extrem- 
ities, the trunk, the tongue, and even in the internal organs. This swelling is not 
oedema, but it is due to the development of a sort of myxomatous new growth, 
rich in mucine, in the connective tissue. Other trophic disturbances usually coex- 
ist : atrophy of the teeth and nails, [spade-like hands, coarseness and] loss of hair, 
failure in the sweat secretion and consequent dryness of the skin, etc. Besides 
these there gradually develops a general physical and mental weakness, which may 
increase to great hebetude or even to complete dementia". Disturbances of the 
sensory functions may also occur. It is a fact of especial interest that we find 
quite commonly a diminution and even a complete atrophy of the thyroid gland. 
It is not improbable that all the symptoms of the disease may arise from the fail- 
ure of function of the thyroid gland. This hypothesis is confirmed by the re- 
peated experiments of Kocher and others, that after complete extirpation of the 
thyroid in man almost the same symptoms ensue as in myxoedema (cachexia 
strumipriva). Erom this we must suppose that certain injurious substances accu- 
mulate in the body which are ordinarily rendered innocuous by the thyroid gland. 

This theory has been materially supported by recent extremely interesting 
experience in the treatment of myxoedema. The physiologist Schiff made the 
remarkable observation that the symptoms of cachexia strumipriva did not appear 
in animals if the thyroid gland of another animal were transplanted into the 
abdominal cavity. Horsley, Bircher, and others hereupon made the first experi- 
ments in the treatment of myxoedema in man with extract of the thyroid gland 
(from sheep, calves, etc.). At first subcutaneous injections of thyroid extract 
were usually employed, but it was found that the internal administration of the 
substance of the gland or an extract thereof had a far more favorable influence. 
There are already very many positive observations which show that all the 
symptoms of myxoedema in man may be made to disappear completely in the 
course of a few months by the continued internal administration of the thyroid 
gland. The most convenient and certain form of administration is in tablets. 
Of course we must always be prepared for relapses. [Myxoedema is sometimes 
associated with exophthalmic goitre and rarely with acromegaly. — K.] 

[The condition known as cretinism is also dependent upon loss of function of 
the thyroid gland. Endemic cretinism is common in countries where endemic 
goitre prevails, especially in the central Alps, and also, but less frequently, in the 
Carpathians, the Pyrenees, the mountain districts of Central and South America, 
and the Himalayas. Sporadic cretinism may occur in all parts of the world, and 
Osier has collected sixty cases in America. The affection comes on in infancy, 
and in its severer forms the condition is unmistakable. The victims are short and 
squat of figure, with prominent belly, " blubber lips, retrousse nose, sunken at the 
root, wide-open mouth, lolling tongue, small eyes, half-closed, with swollen lids, 
stolid, expressionless face, and muddy, dry skin." They are idiotic and often una- 
ble to talk, walk, or stand alone. In the milder cases the lax, waxy skin, the prom- 
inent abdomen, and the failure of development may suggest the diagnosis. Mar- 
velous results have been attained in some of these apparently hopeless cases by the 
early and persistent use of the thyroid gland. The striking cretinous aspect has 
disappeared and physical growth and mental development have followed. 

Closely allied to these conditions is the myxedematous infantilism described 
by French authors. The subject preserves the physical and mental characteris- 



902 



DISEASES OF THE KERVOUS SYSTEM 



tics of a child of ten up to the age of thirty or over. The sexual organs are unde- 
veloped, and the secondary sexual characteristics fail to appear. A careful exami- 
nation will often reveal slight indications of myxoedenia — the diminution in size 
or absence of the thyroid, the thick lips, thick dry skin, coarse hair, etc. — thus 
distinguishing it from the anangioplasic form of infantilism due to defective 
development of the arterial system. In this condition the administration of 
thyroid gland produces equally striking results. 

Adiposis Dolorosa. — Under this name Dereum has described a peculiar con- 
dition, occurring in women between forty and sixty years of age with a neuro- 
pathic predisposition. Most of the victims were addicted to alcohol. The trouble 
begins with a gradual enlargement of various portions of the body, associated 
with pain, parsesthesia, and some tenderness. These enlargements may increase 
so as to form huge pendulous masses. Muscular weakness is also present, and 
locomotion finally becomes very difficult if not impossible. Mental weakness 
sometimes supervenes. The masses have been found to consist of fat and con- 
nective tissue. Disease of the thyroid has been found on autopsy, but the true 
nature of the trouble is still obscure. The course is slow, but progressive. Treat- 
ment has thus far been of little avail. Every effort should be made to improve 
the nutrition, and thyroid gland should also be given. 

Scleroderma. — Although ordinarily classed among the skin diseases, sclero- 
derma merits a brief mention here, as it is generally considered to be a vaso-motor 
or trophic neurosis. It occurs chiefly in neuropathic women, and it may follow 
some infectious disease. It sometimes occurs with syringomyelia, Raynaud's 
disease, or other forms of nervous disease. It may be diffuse and symmetrical or 
circumscribed (morphoea). It begins gradually, often after exposure to cold, 
with a feeling of stiffness, most marked in the neck, shoulders, arms, face, or 
scalp. The skin gradually becomes thickened and hard, very white or mottled, 
and movements of the affected parts become slow and stiff, and finally are com- 
pletely lost on account of the rigidity of the skin. Vaso-motor symptoms are 
rare, but pigmentation is occasionally seen. When the face is involved a charac- 
teristic, expressionless " mask " is produced. If the chest be affected, respiration 
may be considerably impaired on account of the immobility. Later on the skin 
and deeper parts may atrophy, although the hardness and stiffness may remain. 
Recovery may occur, but the disease is apt to be permanent, the patient succumb- 
ing to some intercurrent disease. The circumscribed form may occur in patches, 
bands, or streaks, and may be confined to the distribution of one or more nerves. 
The white spots are bordered by a pinkish zone of dilated vessels. Anatomically 
the disease is characterized by changes in the blood-vessels and proliferation of 
connective tissue in the skin. The general condition should be strengthened by 
nutritious diet, good hygiene, salt baths, arsenic, and cod-liver oil. Galvanism is 
of some benefit. Thyroid extract may also be tried. — K.] 

Acromegaly. — A " trophic disturbance " chiefly of the bones, but also involv- 
ing the soft parts, forms the basis of that peculiar and rare disease recently 
termed acromegaly (P. Marie, Erb, etc.). The affection develops slowly in 
women and men, usually in youth or middle age. In worrien cessation of men- 
struation almost invariably precedes the onset of the disease. Besides the gen- 
eral symptoms of dullness, fatigue, and quite severe neuralgic or drawing, deep- 
seated pains in the head and the extremities, there gradually develops a striking 
increase in the size of the hands and feet, and thickness and plumpness of the 
face, due chiefly to enlargement of the nose, chin, and lips, which become puffed 
out to a considerable size. The increase in the lower part of the face (especially 
the lower jaw) in contrast to the normal cranium gives a very characteristic 
aspect to acromegaly. The hyperplasia of the lower jaw may reach so high a 
degree that the individual teeth are separated. In the hands and feet the 



GEKEKAL PKELIMINAKY EEMAEKS 



903 



fingers and toes, and especially their terminal phalanges, become thicker and 
wider, so that we may speak of actual " paws." The hyperplasia not only affects 
the bones, but it makes the skin thick and wrinkled. A manifest kyphosis of the 
spine usually develops. Other 
noteworthy symptoms some- 
times occur. Thus we some- 
times see marked glycosuria, 
an increased secretion of 
sweat, and particularly dis- 
turbances of vision, either 
hemianopsia or amblyopia 
from atrophy of the optic 
nerves. These disturbances 
of vision are connected with 
the noteworthy fact that in 
most cases of acromegaly a 
tumor of the hypophysis cere- 
bri develops, which presses di- 
rectly on the nerves or the 
optic tract. A patient under 
our observation (Fig. 113) died 
with symptoms of a tumor at 
the base of the brain, and the 
autopsy showed a sarcoma- 
tous tumor of the hypophysis 
which had grown through the 
adjacent bony parts. 

The diagnosis of acromeg- 
aly is not difficult. We must 
merely guard against confus- 
ing it with other conditions 
also leading to thickening 
of the bones (partial giant 
growth, arthritis and osteitis 
deformans, diffuse and local- 
ized hyperostoses, etc.). The 
so-called hypertrophic osteo- 
arthropathy is also to be dis- 
tinguished from acromegaly. 
This affection is seen especial- 
ly in patients with chronic 
bronchitis, bronchiectasis, 
chronic tuberculosis, etc., 
and it also leads to a paw- 
like thickening of the fingers, 
but the changes in the lower 

jaw so very characteristic of acromegaly are absent, and also the other nervous 
symptoms, especially those of tumor of the hypophysis. 

The treatment of acromegaly is, unfortunately, almost wholly unpromising. 
The administration of thyroid tablets and also of tablets of the hypophysis has 
been tried without much benefit. 

[Gigantism. — The " giants " who exhibit themselves in circuses and museums 
are victims of a disease closely akin to acromegaly if not identical with it. A 
study of giant skeletons has shown a marked enlargement of the sella turcica, 




Fig. 113.— Acromegaly in a patient thirty years old. 
(Personal observation.) 



904 



DISEASES OF THE NERVOUS SYSTEM 



the site of the hypophysis, and an enlargement of the hypophysis has been 
found at autopsies. The giants themselves often have enormous hands and feet, 
they are feeble and short-lived. In some instances kyphosis has developed later 
in life, with more pronounced symptoms of acromegaly. 

Hyperostosis Cranii. — This is an enlargement of the cranium, beginning in 
early life, involving the anterior part of the skull rather more than the posterior, 
and leading to enormous thickening of the bones, from one to three or more centi- 
metres (one half to one and a half inch). Other bones are sometimes affected. 
The symptoms sometimes resemble those of cerebral tumor, the cranial nerves 
being affected by the bony growth. Headache is common and optic neuritis occa- 
sionally occurs. Marked exophthalmus is sometimes produced by the growth of 
the orbital bones which fills up the orbital cavities. The trouble is supposed to be 
of trophic origin, although the changes in the bones resemble those of inflamma- 
tion. The involvement of the cranial vault and the absence of kyphosis and 
changes in the extremities render it easily distinguishable from acromegaly. 
Treatment has thus far proved unavailing. — K.] 

Hydrops Articulorum Intermittens. — This is the name of a very rare disease, 
in which large swellings, usually of the knee-joint, but sometimes of the other 
large joints, develop at perfectly regular intervals of one to four weeks. These 
swellings of the joints run their course without fever, and usually without any 
great pain, and disappear again in a few days. Such attacks may be repeated at 
intervals of different lengths, during many years. Their nervous character is 
attested especially by the rapid onset and disappearance of the affection, and also 
by the combination of it with other nervous disturbances, such as angina pec- 
toris, exophthalmic goitre, vaso-motor symptoms, hysterical symptoms, etc., 
which combination has often been observed. In regard to treatment, salicylic 
acid, quinine, Fowler's solution, and subcutaneous injections of ergotine have 
been tried, but the trouble is usually very obstinate. 

Disturbances of Secretion. — In addition to the vaso-motor and trophic dis- 
turbances we must consider the disturbances of secretion. These are not infre- 
quent. We have already learned to recognize anomalies in the secretion of saliva 
in facial paralysis, and of the lachrymal secretion in trigeminal neuralgia. 
Analogous symptoms are occasionally noticed in other nervous diseases. Dis- 
turbances of the sweat secretion are the easiest to confirm. Our understanding of 
them comes substantially from the discovery of the " sweat nerves," arising 
mainly from the sympathetic, which was made by Luchsinger. In nervous 
patients we have seen quite frequently, on the one hand, an abnormal increase of 
the sweat secretion (hy paridrosis, ephidrosis), and, on the other, a diminution 
or a complete disappearance of it. The former is seen on the paralyzed side in 
many hemiplegias and in spinal paralyses, the latter in tabes dorsalis. Anomalies 
of the sweat secretion are quite frequent, and are usually combined with vaso- 
motor disturbances in certain general neuroses, such as hysteria and neuras- 
thenia. In a few rare cases a genuine hcematidrosis (bloody sweat) has been 
confirmed. [Colored sweating (chromatidrosis) has been reported in some very 
rare cases of hysteria. — K.] The condition known as unilateral hyperidrosis 
(unilateral sweating) is also especially interesting. In this there is an abnormal 
secretion of sweat, chiefly in one half of the face, more rarely in one arm or over 
the whole of one side. The affection has usually been observed in connection with 
tabes, syringomyelia, hemicrania, exophthalmic goitre, hysteria, etc., and, in at 
least a number of cases, it seems to be due to direct lesions of the sympathetic. 
On the other hand, we have repeatedly seen persons, who were otherwise perfectly 
healthy, in whom the secretion of sweat, coming on under normal conditions from 
heat or physical exertion, remained limited to one half of the body, especially 
the face. 



MIGRAINE 



905 



Injuries and Diseases of the Cervical Sympathetic. — In conclusion, we would 
briefly mention here the symptoms which have been observed in direct injuries 
of the cervical sympathetic, trauma, pressure of neighboring tumors, etc. If we 
have to do with a paralysis of the sympathetic, we see almost constantly on the 
affected side a contraction of the pupil from paralysis of the dilator pupillse sup- 
plied from the sympathetic, in many cases associated with a slow reaction to 
light. We also frequently see a narrowing of the opening of the lids from paraly- 
sis of Miiller's muscle, and in old cases a retraction of the bulbus oculi, flatten- 
ing of the affected half of the face, and occasionally increased redness and 
warmth in the ear and cheeks from vaso-motor disturbance. In a few cases 
we see an increased sweat secretion. We may add that, according to Mobius, the 
normal reflex dilatation of the pupil, from a painful irritation of the skin of 
the face, is absent in paralysis of the sympathetic. The opposite symptoms are 
found in conditions of irritation of the sympathetic. The occurrence of sympa- 
thetic symptoms in certain injuries of the brachial plexus has already been men- 
tioned above (page 870). 



CHAPTER II 

MIGRAINE 

{Hemicrania. Megrim. Sick Headache) 

.ZEtiology. — By migraine or hemicrania we mean a peculiar form of headache,, 
coming on in separate attacks, usually unilateral, and associated with consider- 
able disturbance of the general condition and with pronounced nervous gastric 
symptoms (complete loss of appetite, nausea, vomiting). The affection occurs in 
women and men, somewhat more rarely in the latter, and almost always begins in 
youth, generally at the period of puberty, although typical cases of migraine have 
been repeatedly observed in school-children. Quite frequently, but not always by 
any means, the disease affects persons who must be regarded as " generally nerv- 
ous," who are ansemic, or who suffer from disturbances of menstruation. Heredity 
often plays a part, since hemicrania is both hereditary as such, and often appears 
in families which have suffered from other nervous diseases, such as epilepsy, 
hysteria, or the psychoses. We may mention as exciting causes, which may 
be made answerable both for the onset of the disease and especially for the 
individual attacks, physical and mental over-exertion, great mental excitement, 
disturbances of digestion, indulgence in alcohol, etc. [Eye-strain (vide supra) 
may rarely have some influence in causing migraine as well as other forms of 
headache, and a careful search for any errors of refraction should therefore be 
made. — K.] The special cause of the disease, however, is probably, as a rule, a 
congenital predisposition. 

Many writers lay great stress upon certain vaso-motor symptoms which some- 
times accompany migraine, and therefore believe that the disease is to be consid- 
ered in the main an affection of the sympathetic ; but we must agree with Mobius 
that this assumption is very improbable, and that the accompanying sympathetic 
symptoms are probably only secondary and of reflex origin, in consequence of the 
pain, or are merely a part of the whole attack of migraine. We are still utterly 
ignorant of the special nature of migraine — that is, of the kind or the place of the 
change which forms the basis of the clinical symptoms. The conjecture is inter- 
esting, but of course wholly unconfirmed, that there is in the attacks an " auto- 
intoxication " of the body — that is, the action of some poison developing from 
time to time in the body itself; but we do not know upon what part of the 



906 



DISEASES OF THE NERVOUS SYSTEM 



nervous system this poison may act; we can merely conjecture that the place of 
irritation, upon which the pain and other migrainous symptoms depend, is in the 
brain itself (in the cortex or deeper parts). This conjecture is supported espe- 
cially by the nature of many of the symptoms which accompany the pain of 
migraine — the sensitiveness of the sensory organs, the slight mental change, the 
scintillating scotoma, etc. 

Symptomatology. — Migraine always comes on, as has been said, in separate 
attacks, which are repeated at intervals of varying lengths, although some cases 
often show a remarkably great regularity. The onset of the attack in women 
often has some relation to the menses; in other cases it is due to one of the ex- 
citing causes mentioned above. 

The attack of migraine usually begins with certain prodromal symptoms, 
which the patient soon recognizes as sure signs of his approaching suffering. 
These prodromal symptoms consist of general uneasiness, discomfort, pressure in 
the head, vertigo, at times tinnitus, spots before the eyes, darkening of the visual 
field, chills, malaise, abnormal yawning, etc. In a short time the pain begins. It 
is felt most either in the anterior frontal region or in the temporal or parietal re- 
gion; it generally shows a continuous character, not intermittent as in neuralgia, 
and it may increase to a very great intensity. Usually one side of the head (the 
left most commonly) is the chief seat of the pain, particularly the forehead and the 
neighborhood of the eyes ; but it may also happen that the pain affects the right and 
left sides alternately, and it is sometimes not limited to one side, but embraces 
nearly the whole head. The scalp is usually hyperassthetic on the affected side, and 
the points of exit of the nerves may be sensitive to pressure, but firm pressure on 
the head (with the hands or by tying a towel tight around it) sometimes gives relief. 

The second chief symptom in migraine, besides the headache, is the com- 
plete loss of appetite and great nausea. Sometimes vomiting comes on only at 
the end of an attack, but often there is almost uncontrollable vomiting through- 
out the whole attack. The patient not infrequently notices that the vomitus has 
a very sour taste, and we have ourselves found a decided hypersecretion of gastric 
juice in several cases of migraine. The patients' general condition is almost 
always very much disturbed. They feel very wretched and dull, and are very 
sensitive to external impressions, any bright light, any noise, etc. They are in- 
capable of any mental exertion. In many cases remarkable ocular symptoms oc- 
cur (ophthalmic migraine) : slight or marked ptosis of one eyelid, bright flashes 
before the eyes, scintillating scotoma, and not infrequently pronounced hemi- 
anopsia. These symptoms very often forebode the special attack of pain. Other 
severe nervous symptoms, such as paresthesia in the hands and fingers, tinnitus, 
disturbances of speech, etc., have occasionally been observed. 

The vaso-motor symptoms accompanying the headache may occur in two 
different forms. From them migraine was formerly divided into two sub- 
divisions — hemicrania sympathico-tonica or spastica, and hemicrania sympathi- 
co-paralytica or angio-paralytica. In hemicrania spastica, first described by Du 
Bois-Reymond from observations on himself, the forehead and ear on the affected 
side are pale, the skin is cool, the temporal arteries contracted, the pupil is often 
decidedly dilated, the secretion of saliva increased — in short, there are a whole 
series of symptoms present which all agree in pointing to a condition of irritation 
of the sympathetic (vide supra). In hemicrania paralytica, however, which was 
first described by MollendorfT, also from observations on himself, the face is red- 
dened on the affected side, it feels hot, the temporal arteries are dilated and 
pulsate strongly, there is sometimes unilateral sweating of the face, the pupil is 
contracted — all symptoms, therefore, which can depend only on a paralysis of 
the sympathetic. 

As has already been said, the significance of all these symptoms is not abso- 



MIGRAINE 



90Y 



lutely certain. We must also add that this division is more theoretical than real, 
and that the cases which occur in practice can not by any means always be 
inserted into one or the other typical scheme without further ceremony. The 
vascular symptoms are often only slight, conditions of paralysis and of irritation 
of the sympathetic sometimes seem to alternate with each other in the same 
attack, and we may even frequently meet with apparently contradictory symp- 
toms at the same time, such as pallor joined with contraction of the pupil. The 
vascular changes, when present, are almost never unilateral, but they are approx- 
imately alike in the two halves of the face. In severe attacks the whole face 
usually looks pale and sunken, but the initial pallor may give place to redness. 

The duration of the attacks of migraine differs very much. It usually lasts 
several hours, or a whole day; then the pain gradually disappears, and there is 
often considerable vomiting and sometimes a profuse discharge of urine toward 
the end of the attack. In the intervals between the different attacks most pa- 
tients are perfectly well and free from pain. There are also severe forms of mi- 
graine where the individual attacks may last for several days or more (" etat de 
mar 7 ). Without an accurate history these severe conditions of intense head- 
ache and persistent vomiting may readily be falsely interpreted. 

The whole course of migraine is very chronic, and it may last for years and 
years. It is usually a trouble to which the patient finally becomes accustomed. 
We must generally be quite guarded in our prognosis, for many cases resist very 
obstinately all attempts at cure. We can give the patient only the consolation 
that the trouble generally disappears of itself in advanced life. It is not usually 
attended with any special danger. In only a few cases has it been noticed that 
attacks of hemicrania of years' duration have preceded a severe cerebral disease 
that developed later. * 

Diagnosis. — The diagnosis of migraine is not difficult, if we hold strictly to 
the definition of the disease. The laity, especially women, of course, delight in 
calling every headache and all sorts of other nervous and hysterical conditions 
" migraine." Especially characteristic of true migraine are the heredity, the 
beginning in youth, the occurrence in attacks, the accompanying vomiting, and 
the other attendant nervous symptoms. Errors in diagnosis may arise from the 
fact that attacks of symptomatic migraine may also occur in severe organic dis- 
eases (tabes, brain tumor, etc.). We have seen a patient who suffered for 
years with severe " migraine." He finally died, and the autopsy revealed a 
cysticercus in the fourth ventricle with secondary hydrocephalus. 

Treatment. — Very many patients who suffer from migraine finally renounce 
any special treatment, after they have exhausted all possible remedies. They with- 
draw to their rooms when the attack comes on, darken the windows, take noth- 
ing but some tea, Seltzer-water, or cracked ice, put a cold compress about the 
head, perhaps try a foot-bath, and for the rest wait quietly until the attack is 
over. In fact, our remedies for cutting the attack short are quite uncertain. 
They sometimes aid, but they often leave us in the lurch, especially if used re- 
peatedly. We must note especially that narcotics, such as morphine, are almost 
always ill borne in migraine, and do no good; but antipyrine, sodic salicylate 
(20-30 grains [grammes 1.5-2.0], in strong black coffee), antifebrine, phenace- 
tine, salipyrine, etc., in many cases undoubtedly have a favorable action. Which 
remedy acts the best must usually be tested in the individual case. We have 
ourselves seen excellent results formerly from sodic salicylate, and lately from 
antipyrine, pure or mixed with the other remedies mentioned; the attacks of 
migraine, when the remedy was taken immediately upon the onset of the first 
symptoms, have become distinctly milder and have run their course more rapidly. 
Of course the action often ceases with time, and we must then try another of the 
remedies mentioned. Of the other remedies used we may mention guarana 



908 



DISEASES OE THE NERVOUS SYSTEM 



(Paullinia sorbilis), half a drachm to a drachm (grammes 2-4) of the powder, and 
caffeine, or sodio-salicylate of caffeine, in three- to five-grain doses (gramme 
0.2-0.3), which is sometimes very serviceable. Caffeine is also the chief constitu- 
ent of " migrainine," which has lately been much praised. On theoretical grounds, 
inhalations of nitrite of amyl, three to five drops on a napkin, have been used iu 
spastic hemicrania, and subcutaneous injections of ergotine in the paralytic form 
(aqueous extract of ergot, 2.5; dilute alcohol and glycerine, each 5; or one part 
of dialyzed ergotine in four parts of distilled water : injections of either, three to 
fifteen minims). The practical benefit, however, is very doubtful. Many other 
nervines, such as bromide of potassium and Eowler's solution, have been recom- 
mended for continued use, and also extract of cannabis indica ; and, lately, nitrite 
of sodium, two parts in 120 of water, a teaspoonful one to three times a day, and 
nitro-glycerine, in troches containing T |o to grain (gramme 0.0005-0.001). 
Their action is similar to that of nitrite of amyl. In ophthalmic migraine the 
treatment by large doses of bromide of potassium is praised, especially in France, 
as being very successful. 

In many cases the general treatment is very important. Preparations of iron,, , 
sea-bathing, a mountain residence, and cold-water cures are often of decided serv- 
ice. We have seen remarkably good permanent results in several cases of severe 
migraine from the moderate use of Carlsbad water, either at Carlsbad itself or 
taken at home. We always strongly recommend a trial of this, especially when 
there are also symptoms of hypersecretion of the gastric juice (vide supra).. 
With the moderate use of Carlsbad water we usually combine methodical hydro- 
therapy (cold sponging, half baths with douches, etc.) and an appropriate diet. 
The persistent application of electricity has also shown some good results, but we 
must not build very great hopes upon it. In the spastic form the action of the 
anode on the sympathetic is especially recommended, and in the paralytic form 
the action of the cathode, while the other electrode is to be placed on the cervical 
cord, or as high as possible on the occiput in the region of the medulla. Cautious 
galvanization of the head, and weak primary f aradic currents, may also be used. 
Specialists in massage praise their mode of treatment in migraine ; they massage 
either certain painful spots in the head, or the gastric region. Finally, we must 
mention that migraine often seems to be connected with diseases of the nose, espe- 
cially with hyperplasia of the erectile tissue in the nose, and that in such cases 
treatment of the primary disease with the galvano-cautery may result in the 
cessation of the migraine. 



CHAPTER III 

PROGRESSIVE FACIAL HEMIATROPHY 

( Unilateral Progressive Facial AtropJiy) 

Unilateral facial atrophy is an extremely rare disease^ which consists of a 
very slow and gradual but usually constantly progressive atrophy of one half of 
the face, and affects the skin, and also the fatty tissue, the muscles, and the 
bones, either in a uniform or a very diverse manner. The affection usually be- 
gins in youth. The female sex seems to be more disposed to the disease than the 
male. 

The atrophy, which has its seat much more frequently on the left side than 
on the right, begins usually in a circumscribed spot either on the cheeks or on the 
chin. The skin, as a rule, gradually assumes a whitish or brownish color. The 
affected part, and finally the whole half of the face, gradually sink in more and 



EXOPHTHALMIC GOITEE 



909 



more, so that the disease can be recognized at the first glance. The atrophy 
shows a sharp limitation at the median line. In many cases the mnscles appar- 
ently remain almost wholly intact, but in some cases they show a marked atrophy, 
especially the muscles of mastication. The corresponding half of the tongue and 
the soft palate has sometimes been found implicated. Exceptionally, the atrophy 
involves the neighboring region of 



the shoulder and the upper extremity. 
The bones also atrophy, especially in 
the cases which arise in early youth. 
The hair on the affected half of the 
head often falls out in great amount, 
and it becomes thin and atrophic. 
The sensibility remains perfectly in- 
tact. Marked vaso-motor and secre- 
tory disturbances have only rarely 
been observed. The accompany- 
ing illustration (Fig. 114) shows a 
patient who was described by Rom- 
berg many years ago, and who for 
a long time frequented the German 
cliniques in order to show himself. 

Nothing definite is known in re- 
gard to the nature of the affection. 
Most observers at present agree that 
it is a trophic neurosis, an affection 
of trophic nerves or nerve-centers, 
hut where we are to look for the 
special seat of the disease, whether 




in the trigeminus or in the sympa- Fig. 114.— Left facial hemiatrophy. 

thetic, we do not know. Mendel 

lately found in a case which came to autopsy a definite neuritis in the tri- 
geminus. 

The disease is not dangerous in itself, and usually causes no special subjective 
disturbance, but it seems to be incurable. In cases at their beginning we can 
at most make an attempt to bring the disease to a standstill by a long-continued 
application of electricity. 



As an appendix it may be briefly mentioned here that there is a unilateral 
hypertrophy, which is also possibly connected with neurotrophic disturbances. 
We saw at Leipsic a ten-year-old boy, otherwise perfectly healthy, in whom a 
striking hypertrophy of the left side of his face and of the left arm had gradually 
developed. 



CHAPTER IY 

EXOPHTHALMIC GOITRE 

{Parry's Disease. Morbo di ilajani. Graves's Disease. Basedoitfs Disease) 

-ZEtiology. — The special group of symptoms to which the name of exophthal- 
mic goitre has been given, and whose three cardinal symptoms are acceleration 
of the pulse, goitre, and exophthalmus, was first carefully described in Germany, 
in the year 1840, by the Merseburg physician Basedow, although similar but less 



910 



DISEASES OF THE NEEVOUS SYSTEM 



precise observations had been published in England by Graves five years earlier. 
[Parry, in England, was the first accurately to describe the disease in 1786, and 
it was also recognized by Flajani in Italy in 1800. — jK.] 

In the aetiology of the disease all those factors play a part which are important 
in the aetiology of neuroses in general. In many cases a hereditary predisposition 
can certainly be discovered. The disease has been repeatedly seen in several 
members of the same family. We have ourselves seen severe exophthalmic goitre 
in two sisters. Furthermore, exophthalmic goitre is also quite frequent in those 
families in which there is a hereditary predisposition to neuroses in general — 
epilepsy, the psychoses, or hysteria. Among the exciting causes we must first men- 
tion great mental excitement — grief, terror, anger. Sometimes real injuries, as 
well as these " psychical injuries," seem to have an influence on the development 
of the disease — that is, great general bodily concussion, such as a fall. Many 
authors have laid considerable weight on diseases of the female sexual organs, but 
the importance of this factor seems to us to be exaggerated. It is certain, how- 
ever, that the first symptoms of exophthalmic goitre often develop at the period 
of pregnancy. 

The influence of sex upon the origin of the disease is plain, since women, 
especially somewhat anaemic, " nervous " women, are much more frequently 
affected than men. Exophthalmic goitre usually appears in middle life, while it 
is seen only exceptionally in children and old people. 

Symptomatology. — Of the three cardinal symptoms of exophthalmic goitre- 
named above, of which, of course, one or another is often absent or only slightly 
developed, the acceleration of the pulse is the most constant and usually the ear- 
liest. The frequency of the pulse averages 100 to 120, sometimes only 80 or 90 r 
but in other cases even 140 or 160. It is not alike at all times, but has many 
variations — the symptoms lasting for long periods and also coming on in single 
paroxysms. In sleep the frequency of the pulse, as we have ourselves confirmed,, 
is sometimes almost normal, and sometimes also rapid, but usually less so 
then when the patient is awake. A very vigorous action of the heart, and 
as a rule the subjective feeling of palpitation, are usually associated with the 
acceleration of the pulse. There is a vigorous pulsation of the carotids, and 
sometimes of the smaller arteries. We do not discover any qualitative changes 
of the pulse. The pulse is usually quite regular, but arhythmia has been excep- 
tionally observed. In some cases the patients surfer from pronounced angina 
pectoris. 

Physical examination of the heart in many cases shows nothing especial, ex- 
cept an accelerated and violent action of the heart, but we sometimes find, as 
we can affirm from several cases in our own experience, a manifest hypertrophy 
of the left ventricle, and also dilatation of the heart, and even actual valvular 
disease. In the diagnosis of the latter some caution is necessary, because func- 
tional heart murmurs, especially at the base of the heart, are often present in 
exophthalmic goitre. 

The goitre usually develops somewhat later than the first symptoms in the 
heart. In many cases it is entirely absent, or present only in a slight degree. The 
swelling of the thyroid gland is generally only exceptionally very marked. 
There are sometimes decided variations in it in the course of the same case. The 
comparative softness of the tumor, the frequent and strong pulsations in it, and 
the loud vascular murmurs, which are often but not always heard, and which 
arise in the dilated vessels of the thyroid gland, are characteristic of the goitre in 
Basedow's disease. By laying the hand on it we can often feel the thrill and 
pulsation. 

The exophthalmus, the protrusion of the eyeballs from their orbits, is always 
bilateral, although it is sometimes more marked on one side than on the other 



EXOPHTHALMIC GOITEE 



911 




(see Fig. 115). In many cases it is entirely absent; in others it may attain so high 
a degree that an actual " dislocation of the eyeball " has been described. In the 
marked degrees of exophthalmus there is often a peculiar staring expression to the 
countenance. This is due chiefly to the unusual size of the palpebral fissure and 
to the less frequent winking than normal (Stellwag's sign). A peculiar symptom, 
first described by Graefe, is also worthy of mention. On raising and, still plainer, 
on lowering the eyes, the corresponding associated movements of the upper eye- 
lid, which are always present under normal conditions, are absent. This " Graefe 
symptom " may sometimes be one of the earliest signs of the disease, and may 
therefore be x>f diagnostic value; but we must maintain, after much personal 
experience, that it is on the whole rare, and that it may often be wholly absent 
even in the severest cases of the disease. Disturbances of the pupils and of ac- 
commodation are unknown in exophthalmic goitre, but paralyses of the external 
ocular muscles sometimes oc- 
cur, and we have ourselves 
repeatedly observed anoma- 
lies in the movements of the 
eyeball, especially temporary 
strabismus. We might men- 
tion one symptom, which Mo- 
bius first noticed, and which 
we also have repeatedly but 
not constantly seen, especially 
in patients with rather marked 
exophthalmus. It consists in 
the fact that one eye very soon 
deviates outward if we have 
the patient converge the eyes 
strongly, as in fixation of a 
near object — " insufficiency of 
convergence." Inflammatory 
processes in the eye are some- 
times seen, which are probably 
due to the fact that the upper 
lid can not so well protect the 
protruding eye. 

Besides the chief symptoms 
of exophthalmic goitre thus 
far described, we must also 
mention a list of other symp- 
toms which come under our observation, both in the typical cases and still more 
often in anomalous cases — the so-called " formes frustes " of the French. Among 
them are some nervous symptoms, especially a peculiar tremor to which Marie first 
called attention. This tremor affects the whole body, or the extremities alone ; it 
shows at times temporary remissions and exacerbations, and it may be so severe 
as to form the patient's chief complaint. A moderate tremor of the fingers and 
hands is one of the most constant symptoms of exophthalmic goitre. In a case 
under our observation marked tremor was one of the first symptoms of the dis- 
ease. It may become so violent at times that there are even spasmodic twitchings- 
in the extremities and in the muscles of the face. We may also mention headache, 
vertigo, weakness of memory, and sleeplessness. The peculiar nervous anxiety 
and the irritable disposition of the patient are, however, very frequent, and in 
fact very characteristic, in many cases of the disease. The anxiety and the haste 
in all movements, in speaking, etc., often show themselves, even during the physi- 



Fig. 115.— Patient with 
goitre). 



(Personal observation.) 



;xophtkaImus, 



912 



DISEASES OE THE NEKVOUS SYSTEM 



cian's examination, in so striking a way that they must be regarded as not unim- 
portant factors in diagnosis. The easily occurring flushing of the face, the 
marked subjective feeling of heat, and the hot hands,, from which many patients 
suffer, are probably due to vaso-motor disturbances. Objective elevations of tem- 
perature up to 100° or 101.5° (38°-38.8° C.) have also been repeatedly confirmed 
by others (Eulenburg) and by ourselves. A marked increase of the sweat pro- 
duction, which in rare cases is only unilateral, is often associated with the feel- 
ing of heat. On the other hand, one of our patients complained of a constant 
dryness in the mouth. 

Of symptoms which are referred to other organs we must first considei some 
disturbances on the part of the respiration. The respiration is usually moderately 
accelerated, and many patients complain of dyspnoea and of a feeling of oppres- 
sion in the chest. In one case we saw at times deep spasmodic inspirations; in 
other cases a peculiar dry, " nervous cough " appears, such as we not infrequently 
see in patients with goitre. There are also symptoms on the part of the digestive 
organs. Paroxysmal vomiting is common, and in severe cases it may become so 
persistent, distressing, and uncontrollable as to constitute one of the chief dan- 
gers of the disease. In one of our female patients the disease began with an 
attack of almost uncontrollable vomiting lasting for several weeks. We less fre- 
quently see peculiar paroxysmal sero-mucous or even bloody diarrhoea. We have 
once seen severe jaundice. Finally we must mention certain disturbances in the 
skin : vitiligo has often been observed, and also diffuse brownish pigmentation of 
the skin or chloasma-like pigment-spots and urticaria. It is a noteworthy fact, 
first discovered by Vigouroux, that the galvanic resistance of the skin is remark- 
ably small in patients with exophthalmic goitre. This condition is probably due to 
the fact that the skin is made wet by the profuse sweating, and also, perhaps, to 
some form of atrophy of the skin. A very rare but dangerous occurrence, of 
which we ourselves have seen a striking example, is an apparently spontaneous 
g;angrene of the extremities. In our case, which ended fatally, the gangrene 
affected the right leg. 'Not the slightest anomaly could be made out in the ves- 
sels at the autopsy. 

The general nutrition of the patient suffers in most cases ; a certain degree of 
ansemia and emaciation is often present. In severe cases, especially in those of 
rapid development, there is often in a very short time a high degree of emacia- 
tion associated with much general weakness. Muscular atrophy frequently de- 
velops, chiefly in certain regions — the arm or leg muscles. We may mention, in 
conclusion, that in many, though not in all, female patients disturbances of 
menstruation (especially amenorrhoea) occur. In a few cases peculiar atrophic 
-conditions have also been found in the genitals and the breasts. 

Special complications are not very common in exophthalmic goitre. We may 
mention as most important that other neuroses (hysteria, epilepsy) and true 
psychoses may also occur with exophthalmic goitre. The complication with dia- 
betes, or, as a rule, more properly, with alimentary glycosuria, is also of interest. 
Tabes has also been found associated with exophthalmic goitre. [Myxoedema 
and acromegaly may also be present. — K.] , 

Pathological Anatomy and Pathogenesis. — Although all the symptoms of 
exophthalmic goitre point to an affection of the nervous system as a cause of the 
disease, as we see from the symptomatology, the results of pathological investiga- 
tions are still very meager. There is a class of cases in which changes in the sym- 
pathetic, and especially in the lowest cervical ganglion, are said to have been pres- 
ent; but the pathological significance of the discovery is not placed beyond all 
doubt; and in other cases nothing abnormal at all could be found in the sympa- 
thetic. The theory that all the symptoms of exophthalmic goitre are derived 
from a disturbance of the sympathetic also meets many difficulties and contradic- 



EXOPHTHALMIC GOITEE 



913 



tions. If we regard only the three cardinal symptoms, we can bring the accelera- 
tion of the pulse, and perhaps the exophthalmus, into harmony with the theory of 
irritation of the sympathetic; but not the goitre, which is dne to a dilatation of 
the vessels. The theory of a paralysis of the sympathetic explains the goitre, and 
also the exophthalmus — if we assume as the cause of the latter a dilatation of the 
vessels in the back of the orbit — but again the acceleration of the pulse remains 
unexplained. The experiments by Tilehne, in which symptoms said to be similar 
to those of exophthalmic goitre were produced by dividing the restiform bodies in 
young rabbits, have had up to the present time no bearing upon human pathology, 
since the restiform bodies have been found as a rule to be perfectly normal in 
autopsies of patients with exophthalmic goitre. The theory of the disease ad- 
vanced by Mobius is by far the most probable and the most in accord with our 
present scientific views. According to this, exophthalmic goitre is due to a pri- 
mary morbid change in the function of the thyroid gland, either from the abnor- 
mally great formation of certain irritating substances in the gland, or from the 
imperfect destruction of such substances. At any rate, the peculiar contrast be- 
tween the symptoms of cachexia strumipriva (vide supra, myxoedema) and those 
of exophthalmic goitre is striking. In cachexia strumipriva there are absence of 
the thyroid, and then thickening of the skin, slow pulse, motor and mental slow- 
ness, but in exophthalmic goitre there are general emaciation and atrophy of the 
skin (diminished electrical resistance), tachycardia, mental irritability, tremor, 
etc. The results of thyroidectomy in exophthalmic goitre (vide infra) also 
favor the view that a change in the function of the thyroid gland is the main 
feature of the whole symptom-complex. [Overdoses of thyroid gland will give 
rise to certain symptoms like those of exophthalmic goitre (nervousness, tachy- 
cardia, etc.), while even small doses of the gland may aggravate the symptoms if 
given to a patient with exophthalmic goitre. — K.] 

Course and Diagnosis. — The course of the disease is in most cases very chronic, 
and it may extend over years and years, but there are also more acute cases with a 
rapid development of all the symptoms. We may often see considerable variation 
in the intensity of the symptoms. All the symptoms of the disease may often al- 
most wholly disappear, to recur after the lapse of years. In other cases, especially 
of the milder form, there is not complete recovery, but there is a permanent arrest 
of the disease. In general, the cases beginning in youth give a more unfavorable 
prognosis than those arising in later years. Complete recoveries have certainly 
been observed, but they are not very common, although marked improvement in 
all the symptoms is by no means rare. In some acute and apparently very severe 
cases especially we have seen almost complete recovery ; there was usually only a 
certain amount of exophthalmus after all the other symptoms had disappeared. 
The disease sometimes terminates fatally with the signs of general weakness and 
finally paralysis of the heart, but more frequently from complications in the heart 
or lungs. 

In fully developed cases of exophthalmic goitre a positive diagnosis can almost 
always be made without difficulty. The peculiar facial expression, altered by 
emaciation and exophthalmus and associated with goitre, often permits the recog- 
nition of the disease at the first glance; but the diagnosis is often very uncertain 
in the milder, undeveloped cases. In many patients with slight or even marked 
goitre we find some " Basedow symptoms " without being able to call it actually 
" Basedow's disease." If there be no evident goitre, we must be very slow in our 
judgment, but absence of exophthalmus with other plainly developed symptoms 
is often seen. On the other hand, when there really is exophthalmus it is one of 
the most unequivocal symptoms. In all doubtful cases we should consider care- 
fully the mode of onset and the associated symptoms, especially emaciation, tre- 
mor, general nervous irritability, the feeling of heat, the tendency to sweating, etc 
58 



914 



DISEASES OF THE NEEVOTJS SYSTEM 



Treatment. — In the first place we must consider the general treatment of the 
patient. Physical and mental rest, good food, and the avoidance of all stimulants 
— such as alcohol or strong coffee — and the cautious use of cold-water cures, espe- 
cially sponging, salt baths, etc., may cause a decided improvement of the condi- 
tion. For anaemic patients we prescribe iron, alone or in combination with small 
doses of arsenic. A course at the springs at Franzensbad, Schwalbach, Pyrmont, 
Elster, and Cudowa, is also sometimes attended with good results. Residence in 
mountainous regions or by the sea often seems to act still more favorably. 

Of other remedies, electricity is first to be mentioned, especially the application 
of galvanism to the neck — the so-called galvanization of the sympathetic at the 
inner border of the sterno-mastoid. The slowing of the pulse, which sometimes 
comes on at once ("vagus irritation," or mental quieting!), is striking. Vigou- 
roux praises faradization of the sympathetic and of the goitre as the best method 
of treatment. Among internal remedies we may recommend atropine or tinc- 
ture of belladonna, and ergot or ergotine. We believe we have repeatedly seen 
good results from the latter. Many physicians reject the use of preparations 
of iodine as without benefit, but we- have ourselves at times seen decidedly good 
results from the long-continued use of small doses of iodide of sodium, etc. 
The administration of preparations of thyroid gland, however, are not to be 
advised, both for theoretical and practical reasons [vide supra]. Digitalis 
has often been prescribed for the palpitation, but usually without any good result. 
With great exophthalmus the eyes must be protected from external injuries. The 
occasional severe symptoms on the part of the digestive organs (vomiting, diar- 
rhoea) must be treated symptomatically, by ice, opium, and champagne. 

In view of the above-mentioned theories as to the nature of exophthalmic 
goitre, partial extirpation of the goitre has of late been frequently tried. Very 
favorable results have been reported by different physicians, but, on the other 
hand, there have of course been some sad experiences. In general we should 
advise the operation only in severe cases where all other methods of treatment 
had proved of no avail. 



DISEASES OE THE SPIXAL MEXIXGES 



915 



III.— THE DISEASES OF THE SPINAL CORD 



CHAPTER I 
DISEASES OF THE SPINAL MENINGES 

1. Acute Inflammations of the Spinal Hentnges 

etiology and Pathology. — Isolated acute inflammation of the spinal me- 
ninges is very rarely primary, so far as we know, but inflammatory processes in 
the neighborhood quite frequently involve the meninges, or a spinal meningitis 
occurs as one symptom of a general cerebro-spinal meningitis. This latter con- 
dition is seen chiefly in the idiopathic, generally epidemic, cerebro-spinal menin- 
gitis — a specific infectious disease, which has already been described in detail 
in a previous chapter. A tubercular spinal meningitis is also very often 
combined with tubercular inflammation of the cerebral meninges, but, since the 
symptoms of the latter are usually in the foreground of the picture, we will treat 
of tubercular cerebro-spinal meningitis in the section on diseases of the cerebral 
meninges. Secondary cerebro-spinal meningitis is sometimes seen in the course 
of certain other infectious diseases, and is then probably to be regarded as a 
special localization of the specific poison of the disease. This is the explanation 
of the occurrence of acute spinal and cerebral meningitis as a sequel of croupous 
pneumonia, and also of its occurrence in pyaemic and septic diseases, and, very 
rarely, in typhoid fever and the acute exanthemata. We must mention, finally, the 
occurrence of a purulent cerebro-spinal meningitis as a sequel of empyema, pul- 
monary gangrene, etc., which, although very rare, we have repeatedly noticed. 
In these cases the infection of the meninges also results from the primary foci of 
disease, but the channel of infection is not yet exactly known. Perhaps the 
intercostal nerves are the media of communication. 

In all the cases so far mentioned we have chiefly an inflammation of the pia 
mater, a so-called lepto-meningitis ; the dura mater is not implicated in the dis- 
ease at all, or only to a slight degree. The condition is different in those inflam- 
matory processes which gradually invade the meninges from the neighboring 
parts outside the cord. Thus we very often see circumscribed inflammations on 
the outer surface of the dura (pachymeningitis) in caries of the vertebrae, and 
these inflammations often invade the inner surface of the dura, or more rarely 
reach the pia mater. Acute purulent peripachymeningitis is a very rare disease ; 
it is a purulent inflammation of the connective tissue between the dura mater 
and the vertebral column, which is always of secondary origin. We have seen 
a very characteristic case of this sort in the course of a puerperal pyaemia. The 
inflammation had spread from a purulent inflammation of the pelvic cellular 
tissue, through the foramina of the vertebral canal, and had finally set up a 
purulent inflammation on the outer surface of the dura, extending up to the 
cervical cord. We meet with an inflammation of the pia mater chiefly in diseases 
of the spinal cord, from an extension of the process, as the pia is involved to a 
greater or less extent in many cases of myelitis. 

We do not know with certainty whether other influences, especially injuries 
and exposure to cold, can lead directly, as has often been claimed, to inflammation 
of the spinal meninges. 



916 DISEASES OE THE NERVOUS SYSTEM 



We need to say but little in regard to the pathological anatomy of acute spinal 
meningitis. The changes in purulent inflammation of the pia mater have been 
described in the chapter on epidemic meningitis. Precisely the same conditions 
are found in the other forms of acute leptomeningitis. The changes in pachy- 
meningitis are completely analogous. The dura mater is traversed by dilated ves- 
sels, and therefore is reddened; it is also thickened, and on its internal or ex- 
ternal surface (pachymeningitis interna or externa, or peripachymeningitis) 
there is usually found a purulent or a sero-purulent exudation. 

Symptoms. — An accurate distinction between acute inflammations of the pia 
mater and those of the dura mater can not be made clinically. The symptoms 
of the disease include the symptoms of any primary disease present, the general 
symptoms, such as fever, etc., and in addition the necessary consequences which 
the presence of a disturbance of the meningeal circulation and of the meningeal 
exudation exerts on the cord and nerve-roots. These consequences are due both 
to a mechanical compression of the parts named, and often probably to an inva- 
sion of the substance of the cord itself by the inflammation. To these is added 
the frequent combination of spinal symptoms with the symptoms of a co-existing 
cerebral meningitis. 

The symptoms of acute spinal meningitis are already known to us from the 
description of epidemic meningitis (see page 111). Recapitulating them briefly, 
we may mention chiefly the very severe pain in the back, the great sensitiveness of 
the vertebral column, and the stiffness of the back and neck. To these may be 
added usually symptoms of irritation on the part of the nerve-roots: eccentric 
pains in the trunk and the extremities, hyperesthesia of the skin and of the 
deeper parts, symptoms of direct or reflex motor irritation, muscular tension, 
contractions, etc. The cutaneous and tendon reflexes are often, but not always, 
much diminished or abolished in consequence of the lesion of the nerve-roots. 
There are at times disturbances in the passage of urine and f seces. If, in the later 
course of the disease, there are actual paralysis and anaesthesia, they are usually 
a sign of a more marked implication of the cord itself. 

Diagnosis. — From the symptoms named, we can in many cases make a diag- 
nosis of spinal meningitis. Of course a meningitis is found often enough on the 
autopsy-table whose symptoms during life were completely obscured by other se- 
vere general symptoms, while, on the other hand, with severe constitutional symp- 
toms the symptoms of meningitis may be illusory, as in typhoid fever or pyaemia. 
Fuller information as to the seat and the extent of the inflammation is afforded 
by considering the most painful parts of the vertebral column, the predominance 
of pain and cutaneous hyperesthesia in the arms (cervical region) or legs (lum- 
bar region), etc. When the meningitis involves the upper portion of the cord 
and the medulla there may also be disturbances of respiration, symptoms in 
the pupils, and anomalies in the innervation of the heart. We can decide as 
to the form of the meningitis, whether purulent or tubercular, only by a con- 
sideration of the history, the other morbid symptoms, and the course of the 
disease. 

Prognosis. — We have seen an undoubted recovery, in severe cases, only in epi- 
demic cerebro-spinal meningitis, and in the sporadic cases of idiopathic menin- 
gitis, which are probably identical in aetiology. In all other cases reported with 
a favorable termination the diagnosis may be doubted, for in general the rule 
is certain that, in extensive acute purulent leptomeningitis and pachymeningitis 
the prognosis is almost absolutely unfavorable, whether it be secondary to another 
infectious disease or arise from propagation from some neighboring focus of 
inflammation. We may, perhaps, make an exception of certain mild, circum- 
scribed cases, which do not come to suppuration, but these are always uncertain 
in regard to diagnosis. 



DISEASES OE THE SPINAL MENINGES 



917 



Treatment. — In regard to treatment we must refer entirely to what has been 
said under epidemic and tubercular meningitis. 

2. Chronic Spinal Leptomeningitis 

Although chronic leptomeningitis (usually wrongly termed chronic spinal 
meningitis) once played quite a large part in the diagnosis and pathology of dis- 
eases of the spinal cord, we must at present assert that its occurrence as an inde- 
pendent disease is exceedingly rare. Most of the reported cases of chronic men- 
ingitis were published at a time when the diagnosis of many diseases of the cord 
itself was still perfectly impossible, and when the thickenings and opacities of 
the meninges were much more striking at the autopsy than far more essential 
changes in the substance of the cord itself, which could be made out only by a care- 
ful microscopic examination, and not by the naked eye. In recent years only 
a very few cases have been published which can be regarded, at least with some 
reason, as primary chronic meningitis. It is especially hard to determine this 
since syphilitic disease of the spinal meninges (vide infra) shows almost precisely 
the same anatomical appearance. Clinical experience is also entirely against the 
idea of the frequent occurrence of chronic spinal meningitis. Among many cases 
of spinal disease we shall scarcely be induced even to assume the probability of 
the existence of primary chronic meningitis. 

The case is different with secondary chronic leptomeningitis. This, in the 
first place, is, in rare cases, the termination of an acute meningitis. Secondary 
leptomeningitis may certainly be detected, especially in epidemic meningitis. 
We also find chronic meningitis frequently as a secondary affection in primary 
diseases of the cord and the vertebrae. Thus, for example, in old cases of chronic 
spinal disease, associated with atrophy, such as tabes dorsalis, progressive muscu- 
lar atrophy, etc., the pia is almost always quite opaque, thickened, and often 
united to the cord and the dura by very many firm adhesions, while a cloudy 
sero-gelatinous exudation is found in the meshes of the arachnoid. All these 
anomalies, however, are of a secondary nature, and have no clinical significance ; 
for the same changes, though rarely so marked, are quite often found in old 
people, where they are analogous to the equally frequent opacities of the cerebral 
meninges, the pleuritic adhesions, etc., and where, during life, they have not 
caused the slightest symptoms of spinal disease. 

The symptoms which have been set down as characteristic of leptomeningitis 
correspond precisely to those of acute meningitis, except, of course, that they are 
relatively less intense, and that the course of the disease is more protracted. 
Pain and stiffness in the back and neck, abnormal painful sensations and pares- 
thesia in the extremities, a girdle sensation, and finally paresis, anaesthesia, and 
vesical disturbances, are the leading features of the type of disease as constructed, 
in whose fabrication there have been, at any rate, many confusions with myelitis, 
spinal syphilis, spondylitis, beginning tabes, multiple neuritis, etc. In the few 
cases confirmed by autopsy the clinical picture resembled in some degree, from 
the intention tremor of the arms and the spastic symptoms in the legs, that of 
multiple sclerosis. It is strange that often there were scarcely any shooting pains 
during life in spite of marked meningeal changes. 

It is clear that under such circumstances no special rules for the diagnosis or 
even the treatment of chronic spinal meningitis can be given. Given a case, we 
would try local applications to the vertebral column; painting with iodine; dry, 
or, exceptionally, in strong patients, wet cups; also protracted tepid baths, 90° 
to 95° (26°-28° R.), or cautious cold-water treatment; and finally the use of the 
galvanic current. Of internal remedies, iodide of potassium would be most indi- 
cated. We may refer to the description of the treatment of myelitis in regard to 
all further details. 



918 



DISEASES OF THE NERVOUS SYSTEM 



3. Pachymeningitis Cervicalis Hypertrophica 

Pachymeningitis cervicalis hypertrophica was first fully described, as a spe- 
cial yet very rare form of disease, by Charcot in 1871, and later by his pupil 
JofTroy. iEtiologically, it is still utterly obscure. Alcoholism, exposure to cold, 
and injury have been alleged to cause it. ~No small number of cases seem to have 
some connection with syphilis. 

Anatomically, the disease is characterized by a chronic and often very con- 
siderable thickening of the dura, almost always, as it seems, in the cervical por- 
tion of the cord, while the pia takes but a comparatively small part in the affec- 
tion. The dura may attain a thickness of six or seven millimetres, and usually 
appears composed of a number of concentric layers. Histologically, the hyper- 
trophy consists of a new growth of dense connective tissue. The clinical symp- 
toms of the disease arise from the fact that, first, the penetrating nerve-roots, 
and later on the cord itself, undergo a considerable mechanical compression. If 
this is of high degree and persistent, there are, as a necessary result, secondary 
degenerations of the motor nerves and muscles, and a secondary descending de- 
generation of the pyramidal tract in the cord. 

The clinical symptoms are easily understood from this. The disease almost 
always begins with severe pain, which shoots from the neck into the occiput and 
the arms. Besides this, there are paresthesia and a numb feeling in the arms and 
hands. Rarely there is an eruption of herpes. All these symptoms depend upon 
the irritation of the posterior roots. 

After this first period of the disease (periode douloureuse of Charcot) has lasted 
some two or three months, the second period begins — the period of paralysis. 

An atrophic paralysis in the upper 
extremities gradually develops, 
mainly as a result of the compres- 
sion of the anterior motor roots. 
This affects, in a remarkable man- 
ner, chiefly the distribution of the 
ulnar and median nerves, while the 
distribution of the radial on both 
sides usually remains free. The 
hand, therefore, assumes a charac- 
teristic position (Fig. 116), as a re- 

Fig. 116.-Position of the hand in pachymeningitis SIU * °f tn< 3 contracture of the an- 
cervicalis hypertrophica. (From Charcot.) tagonistic extensors. The paralyzed 

muscles rapidly become atrophic and 
show a marked reaction of degeneration. In this stage there may also be partial 
anaesthesia of the skin. 

If the compression of the cord advances, the motor fibers for the lower ex- 
tremities, which pass through the cervical cord, must necessarily at last be in- 
volved sympathetically — the third period of the disease. The result of this is a 
spastic paralysis of the lower extremities — that is, a paresis or paralysis with 
increased tendon reflexes, but of course without muscular atrophy, because the 
trophic centers for the muscles of the legs, in the anterior cornua of the lumbar 
cord, remain perfectly intact. The compression of the cervical cord, however, 
may finally lead also to anaesthesia of the lower extremities, to paralysis of the 
bladder, and bed-sores, under which symptoms death ensues; but, on the other 
hand, it must be mentioned that probably cases of recovery, or at least of actual 
improvement in pachymeningitis cervicalis hypertrophica, may occur even after 
it has lasted for years. 

The diagnosis of the disease is based first upon the fact that the affection be- 




DISEASES OE THE SPINAL MENINGES 



919 



gins with pains in the arms, and upon the later appearance of the characteristic 
paralyses. It may easily be confused with tumors in the cervical cord and with 
cervical spondylitis. Amyotrophic lateral sclerosis is distinguished, however, by 
the absence of disturbances of sensibility, by the bulbar symptoms, and by the 
fact that the functions of the bladder remain intact. 

Treatment can do little directly, and it must be chiefly symptomatic. Baths, 
iodide of potassium, and electricity are most used. Joffroy recommends the appli- 
cation of the actual cautery to the neck. 

4. HEMORRHAGE INTO THE SPINAL MENINGES 

(HcematorrhacMs. Meningeal Apoplexy. Pachymeningitis spinalis Ticemorrliagica interna) 

Large haemorrhages into and between the spinal meninges are of rare occur- 
rence. They arise chiefly from traumatic influences, from concussion or fracture 
of the vertebral column, or from direct injuries of the meninges, such as stabs or 
gun-shot wounds. In a few cases great physical exertion may also lead to a me- 
ningeal apoplexy. Diseases of the vertebrae, caries, and carcinoma, may also lead 
to a haemorrhage from the erosion of a vessel. The frequent little meningeal haem- 
orrhages which appear as a complication of meningitis, in haemorrhagic diseases, 
in the course of severe general infectious diseases, septic infection, typhoid fever, 
and small-pox, and as a result of severe general convulsions, very rarely have any 
clinical significance. Finally, it may be mentioned that aneurism of the aorta or 
its branches may rupture into the vertebral canal. 

The clinical symptoms of meningeal haemorrhage are almost always sudden 
and " apoplectiform," but are unattended by any disturbance of consciousness. 
Their intensity depends entirely upon the degree of compression which the nerve- 
roots and the cord undergo from the effused blood. The symptoms of irritation 
usually predominate — severe pain in the back, paraesthesia, and neuralgic pains in 
the extremities; and also symptoms in the motor distribution, tension, tremors, 
and contractures of the muscles. With large haemorrhages, symptoms of paraly- 
sis, partial anaesthesia, disturbances of the bladder, symptoms of unilateral 
lesion, etc., may ensue, but the different types of the disease of course vary with 
the seat of the haemorrhage. On the whole, the diagnosis of meningeal haemor- 
rhage can but rarely be made with any certainty, unless suggestive aetiological 
factors precede and the symptoms and manner of beginning are especially char- 
acteristic. 

The course is quite favorable in many cases if the blood be rapidly reabsorbed, 
but sometimes a permanent disturbance of function is left. 

In regard to treatment, complete rest and the energetic local use of ice are 
chiefly to be recommended, and also local blood-letting — dry cups, or leeches, 
where there are severe initial symptoms of irritation. Under some circumstances 
we may try to remove a part of the blood by lumbar puncture, and thus relieve the 
pressure on the cord. [When the diagnosis of haemorrhage into the meninges is 
reasonably certain, an attempt should be made to relieve the condition by opening 
the spinal canal and removing the clot. — K.] If permanent disturbances be left, 
they should be treated by the ordinary methods — iodide of potassium, baths, and 
electricity. 

We must here speak of pachymeningitis interna hemorrhagica as a special 
form of disease, which usually occurs at the same time with haematoma of the 
cerebral dura mater {vide infra), and is precisely analogous to it in its aetiology 
and pathological anatomy. Encapsulated collections of blood are found on the 
inner surface of the dura; these often have a considerable circumference, and 
contain blood already disintegrated, detritus, haematoidine crystals, etc., since 
they are usually of old standing. Besides this, there are also the signs of a fibri- 



920 



DISEASES OF THE NERVOUS SYSTEM 



nous inflammation — as in the cerebral dura — which, according to the opinion of 
most observers, is the primary process, so that the haemorrhages into the newly 
formed false membrane are secondary. The symptoms of the affection — which 
has been observed chiefly in the chronic insane (general paralytics) and drunk- 
ards — are rarely pronounced, and consist chiefly of pain in the back, stiffness of 
the vertebrae, and some signs of compression on the part of the nerve-roots and 
the cord; but we can very rarely make a definite diagnosis. 



CHAPTER II 

PRELIMINARY REMARKS ON" THE LOCALIZATION AND TOPICAL 
DIAGNOSIS (SEGMENTAL DIAGNOSIS) OF DISEASES OF THE 
SPINAL CORD 

The pathological processes that take place in the spinal cord may be divided 
into two groups, according to their localization. In the first group the anatomical 
changes are limited with remarkable regularity to definite neurone territories 
which are associated both anatomically and physiologically. These diseases are 
called system diseases, since the entire group of functionally associated neurones 
is called a " system." We may, in all probability, conceive that these affections 
arise in one of two ways: either certain neurone systems in some individuals 
have from the outset a congenital (inherited) weak and morbid predisposition, 
and, in consequence thereof, they are not able to perform their functions, but 
atrophy prematurely ; ' or, that certain external, usually toxic, influences exert 
their morbid action, not on the whole nervous system or fortuitous circumscribed 
parts thereof, but only on certain definite neurones (cells or fibers) — " elective 
injuries." The latter hypothesis finds a fitting and instructive example in the 
behavior of many well-known poisons (curare, strychnine, morphine, lead, etc.), 
which injure only certain very definite neurones and parts of nerves, while they 
leave all other neurones completely intact. According as the disease involves one 
or more neurone systems we speak of simple or combined system diseases. Spinal 
muscular atrophy, amyotrophic lateral sclerosis, etc., are due to disease of the 
motor neurones in the cortico-muscular tract; they are simple system diseases. 
Hereditary ataxia, on the other hand, is an example of a combined system dis- 
ease, since in this usually not only certain peripheral sensory neurones but also 
motor neurones undergo simultaneous degeneration. Since the processes of many 
neurones extend, on the one hand, from the spinal cord or spinal ganglia into 
the peripheral nerves, and, on the other, from the cord to the brain, and vice 
versa, we can not, strictly speakng, class the systematic neurone diseases with 
diseases of the spinal cord in their limited sense. Only for practical and, in 
part, purely conventional reasons do we consider the system diseases in this 
section. i 

In distinction from the system diseases there is a second group of diseases of 
the spinal cord where either there is no such limitation of the anatomical process 
to definite neurone territories, or the limitation is only very slight. In these cases 
the disease extends a greater or less distance transversely and longitudinally in 
the cord, forming either one large focus of disease of irregular outline, or many 
smaller, irregularly disseminated foci. To this group, the unsystemic, diffuse 
diseases of the spinal cord, belong all the traumatic destructions, also the haem- 
orrhages, new growths, and inflammations of the spinal cord (myelitides), mul- 
tiple sclerosis, etc. 



SPINAL LOCALIZATION 



921 



The diagnosis of diseases of the spinal cord is usually, first of all, a topical 
diagnosis. From the symptoms present in the individual case we try to deter- 
mine first that place in the spinal cord where an affection must be situated to 
explain the given symptoms. By appraising all the existing symptoms of dis- 
ease, and also all the functions that are still in normal activity, we can deter- 
mine whether the disease is limited to one definite neurone system or whether it 
must spread diffusely over a larger portion of the spinal cord. Only after the 
topical diagnosis of the disease is thus established do we try to form a judgment 
as to the nature of the disease by connecting it with well-known typical forms 
of disease or by considering the whole course of the disease and any accompany- 
ing symptoms. 

The topical diagnosis naturally presupposes an accurate knowledge of the 
functions of all the different parts of the spinal cord — a knowledge which at 
present we by no means possess, but we know at least the distribution of the 
motor and sensory functions in the different portions of the cord in their main 
outlines, and upon this basis we can often determine, at least with approximate 
certainty, the localization of the disease, the so-called segmental diagnosis, in the 
transverse lesions of the spinal cord. 

1. In regard to the localization of motor functions we know definitely that the 
motor fibers of the anterior roots all arise from the ganglion-cells of the anterior 
cornua. To each individual muscle belongs a group of cells in the anterior 
cornu of the cord, from which the corresponding motor nerves, which innervate 
the muscle, arise. These different muscle nuclei, however, apparently do not lie 
simply beside and above one another, but they encroach upon one another, so that 
naturally their accurate definition becomes difficult. Furthermore, the fibers of 
one muscle nucleus do not always pass out from a single anterior root, but often 
from two or more roots. The following summary of the arrangement of the 
spinal muscle nuclei in the different segments of the spinal cord has been com- 
piled by the aid of the well-known tables of Allen Starr, Kocher, and others, but 
it can be regarded as only an approximate expression of the actual conditions. 
Many details will be changed and many gaps filled by later investigations. The 
muscles printed in italics derive the main part of their nerves from the corre- 
sponding spinal segment. 



Segments or Anterior Roots 
1st Cervical Segment. 



2d Cervical Segment. 



3d Cervical Segment. 



Muscles 
Small muscles of the neck. 

(Obliquus capitis superior et inferior, rectus capitis posti- 
cus major et minor.) 
Sterno-hyoideus. ) 

Sterno-thyroideus. y Ramus descenclens hypoglossi. 

Omo-hyoideus. ) 

Thyro-hyoideus. 

Trapezius. 

Sterno-cleido-niastoideus. 

Rectus capitis anticus major. 
Longus colli. 

Complexus major et minor (trachelo-mastoideus). 

Cervicalis ascendens. 

Splenius capitis et colli. 

Sterno-cleido-mastoideus. 

Trapezius. 

Rectus anticus major. 
Longus colli. 
Complexus. 
Cervicalis ascendens. 
Splenius. 
Trapezius. 



922 



DISEASES OE THE NEKVOUS SYSTEM 



Segments or Anterior Roots 
4th Cervical Segment, 



5th Cervical Segment. 



6th Cervical Segment. 



7th Cervical Segment. 



8th Cervical Segment. 



1st Dorsal Segment. 



2d to 12th Dorsal Segment. 
2d to 11th Dorsal Segment. 
7th to 12th Dorsal Segment. 
1st Lumbar Segment. 



Muscles 

Splenius, trachelo-mastoideus, longus colli. 

Scaleni. i 

Diaphragma (N. phrenicus). 

Levator scapulae. 

Supra-spinatus. 

Infra-spinatus. 

Deltoideus. 

Biceps, supinator longus. 
Ehomboidei. 

Rhomboidei (N. dorsalis scapula?). 

Supra- et infraspinatus (N. supra-scapularis). 

Deltoideus (N". axillaris). 

Biceps. ) 

Coraco-brachialis. > N. musculo-cutaneus. 

Brachialis interims. ) 
Supinator longus et brevis. 
Diaphragma. 

Pars clavicularis pectoralis majoris. 
Serratus anticus major. 
Teres minor. 
Latissimus dorsi. 

Serratus anticus major (N*. thoracicus longus). 

Pectoralis major et minor. 

Latissimus dorsi. 

Subscapularis. 

Teres major. 

Triceps. 

Pronator teres et pronator quadratus. 

Biceps, brachialis internus. 

Pars clavicularis pectoralis majoris. 

Extensors of the hand and fingers. 

Scaleni. 

Extensors of the hand. 

(Radiales externi, s. extensor carpi radialis longus et 

brevis, ulnaris externus, s. extensor carpi ulnaris.) 
Flexors of the hand. 

(Radialis internus, s. flexor carpi radialis, ulnaris internus, 

s. flexor carpi ulnaris.) 
Extensors of the fingers. 
Pronators of the forearm. 
Portio sterno-costalis pectoralis majoris. 
Latissimus dorsi. 
Subscapularis, teres major. 

Long extensors of the fingers. 

(Extensor communis digitorum, extensor pollicis longus et 

brevis, extensor indicis.) 
Long flexors of the fingers. 

(Flexor digitorum sublimis et profundus, flexor pollicis 

longus.) 
Small muscles of the hand. 

Small muscles of the hand and fingers. (Interossei, 

thenar, hypothenar.) 
Long extensors of the thumb. 

Dilatator pupilloz (to N. sympathetica, vide p. 905). 
Back muscles. 
Intercostal muscles. 
Abdominal muscles. 



Lowest abdominal muscles. 
Quadratus lumborum. 



Ilio-psoas 
Sartorius. 



SPINAL LOCALIZATION 



923 



Segments or Anterior Roots 
2d Lumbar Segment. 

3d Lumbar Segment. 



4th Lumbar Segment. 



5th Lumbar Segment. 



1st Sacral Segment. 



2d Sacral Segment. 



3d Sacral Segment. 

4th Sacral Segment. 

5th Sacral Segment and Coc- 
cygeal Segment. 



Muscles 

Cremaster. 
Ilio-psoas. 

Ilio-psoas (psoas, iliacus interims). 
Sartorius. 

Adductors of the thigh. 
Pectineus. 

Extensor cruris quadriceps. 
Obturator externus "? 
Gracilis, adductores. 

Glutceus medius et minimus. 

Semimembranosus, semitendinosus. 

Biceps femoris. 

Tensor fasciae lata?. 

Dorsal extensors of the foot and toes. 

Piriformis. ~\ 

Gemelli. r \ 0utward rotators of the thi - b - 

Quadratus femoris. J 

Dorsal extensors of the foot and toes. 

(Tibialis anticus, peronei, extensor digitorum communis.) 

Plexors of the foot (gastrocnemius, soleus). 

Flexor digitorum communis, flexor hallucis longus. 

Tibialis posticus. 

Small muscles of the foot. 

Erection. 

Perineal muscles. 

Ejaculation (ischio-cavernosus, bulbo-cavernosus). 
Sphincter et detrusor vesical. 
Sphincter ani, levator ani. 



Considering the muscles with regard to their function, we obtain the follow- 
ing table of the motor functions of the spinal segments : 



Cervical Cord 

1st Cervical Segment : Turning the head. 
Bending the head backward. 

2d and 3d Cervical Segments : Bending the 
head forward. Raising the shoulders. 

4th Cervical Segment : Inspiration. Drawing 
the shoulders backward. 

5th Cervical Segment : Raising and outward 
rotation of the upper arm. Flexion and 
supination of the forearm. 

6th Cervical Segment : Adduction and in- 
ward rotation of the upper arm. Exten- 
sion and pronation of the forearm. 

7th Cervical Segment : Flexion and extension 
of the hand. 

8th Cervical Seg- ) Flexion and extension 
ment : y of the fingers. Move- 

lst Dorsal Segment : ) ment of the thumb. 



Lumbar Cord 

2d and Sd Lumbar Segment: Flexion and 

adduction of the thigh. 
4th Lumbar Segment: Extension of the lower 

leg. 

5th Lumbar Segment : Abduction and inward 
rotation of the thigh. Flexion of the lower 
leg. 

1st Sacral Segment : Extension and outward 
rotation of the thigh. Dorsal extension of 
the foot. 

2d Sacral Segment : Plantar flexion of the 

foot. Toe muscles. — Erection. 
3d Sacral Segment : Ejaculation. 
4th Sacral Segment : Bladder. 
5th Sacral Segment : Rectum. 



If there is disease of the anterior horns of the gray matter (poliomyelitis, 
syringomyelia, hsematomyelia) or compression of the anterior motor roots, the 
muscles paralyzed will correspond directly to the affected segments; but with 
more extensive transverse disease (myelitis, tumors, compression) of course 



924 



DISEASES OF THE NEKVOTTS SYSTEM 



those muscles will also be paralyzed whose nuclei lie below the seat of the lesion, 
since the fibers of the pyramidal tract leading to them will be interrupted. 
Erom what has already been said (page 851), we? may readily distinguish the 
nuclear or root paralyses from the pyramidal (lateral) tract paralyses by the 
greater atrophy, and especially by the electrical reaction of degeneration, 

2. The distribution of the sensory conducting path to the different segments 
of the spinal cord corresponds in general to the territories of distribution of the 
sensory fibers arising from each spinal ganglion {vide page 796 et seq.) ; but since 




Fig. 117.— Distribution of the sensory root-areas from the lumbo-sacral plexus (from Thorburn). 1 

the outgoing posterior root-fibers are mixed with one another in the plexuses, 
■each region of the skin is supplied by sensory fibers from at least two and prob- 
ably three spinal segments, or from two or three posterior spinal roots. The 
accompanying diagram, devised by Kocher (Table 1), gives, as far as our present 
knowledge admits, a good representation of the extent of the different root terri- 
tories. We must be prepared for individual variations. We see that in the arms 
the radial region is innervated from the upper (fourth and fifth) roots of the bra- 
chial plexus and the ulnar region from the lowest roots (first, and probably second 



Fig. 2. Fi 9 l 

Distribution of the Areas of the Sensory Roots upon the Surface of the Body 

(from Kocher). 
Red : Area of the cervical roots (C. 2 to C. 7). 
Yellow : Area of the dorsal roots (D. 1 to D. 12). 
Green : Area of the lumbar roots (L. 1 to L. 4). 
Blue : Area of the sacral roots (S. 1 to S. 4). 



SPINAL LOCALIZATION 



925 



dorsal roots). If we conceive of the arm raised horizon-tally with the thumb 
directed upward, we can in a way imagine a horizontal segmental division of the 
arm according to the different sensory-root areas. On the trunk the segmental 
arrangement of the different sensory root-areas is very plain; although the seg- 




Fig. 118. Fig. 119. 

Lesion at the level of the second lumbar segment. Lesion at the level of the third lumbar segment. 



ments do not run parallel to the ribs and intercostal nerves, but they are strictly 
horizontal. In the legs Kocher's diagram fails to give the area of distribution of 
the fifth sensory lumbar root. We therefore add for comparison the diagram 
given by Thorburn for the distribution of the sensory root-areas from the lumbo- 




Fig. 120. Fig. 121. 

Lesion at the level of the fifth lumbar segment. Lesion of the first sacral segment. 



sacral plexus (Fig. 117). The two diagrams differ considerably from each other, 
so that further investigations are very desirable. Figs. 118 to 124 (from work 
conducted in the author's clinique by L. R. Muller) show summarily the distribu- 



926 



DISEASES OF THE NERVOUS SYSTEM 



tion of the anaesthetic (shaded) areas of the skin in transverse lesions of the 
spinal cord at different levels of the lumbo-sacral cord. 

In subsequent chapters we will return to many details in regard to the sig- 
nificance of disturbances of sensation in accurate- segmental diagnosis. We 
can here speak of only two important points. Symptoms of sensory irritation are 
regarded in spinal diseases almost exclusively as root symptoms, due to an irrita- 




Fig. 122. 

Lesion of the second sacral segment. 



Fig. 123. 

Lesion of the third sacral segment. 



tion of the affected posterior roots by pressure, laceration, etc. Such symptoms 
of irritation, therefore, are seen chiefly in diseases which arise in the coverings 
of the spinal cord (the vertebrae and the spinal meninges). Then we must also 
refer once more to the circumstance mentioned on page 799, that the tracts for 

the conduction of sensations of pain and 
temperature after their entrance into 
the cord probably go at once to the gray 
matter of the posterior horns, while the 
simple sensations of touch are conducted 
to the brain through the white posterior 
columns. If we find, therefore, in spinal 
diseases the so-called dissociated anaes- 
thesia, especially anaesthesia for pain and 
temperature with retained sensibility for 
touch, we may be quite certain that there 
is a central lesion in the posterior gray 
cornua, such as is found especially in 
syringomyelia, injury of the cord, and 
central glioma. 

[Brissaud and other recent French 
writers lay much stress upon the differ- 
ence between the sensory areas supplied by 
the spinal roots (radicular metamerism) 
and the sensory areas supplied by the dif- 
ferent spinal segments (spinal metamerism). The former have already been de- 
picted. It is claimed that the latter areas surround the limb, their boundaries be- 
ing perpendicular to its long axis. They correspond, therefore, to areas covered by 




Fig. 124.— Lesion of the fourth sacral segment. 



SPINAL LOCALIZATION 



927 



a glove, a sleeve, a stocking, etc. (geometrical anaesthesia).' The determination of 
the areas of anaesthesia may therefore be of importance in deciding whether dis- 
ease affects merely the spinal roots or the substance of the cord. Dejerine, how- 
ever, denies any spinal metamerism, and various German observers claim that 
in syringomyelia, where the central gray matter is affected, the areas of anaes- 
thesia correspond to the root distribution as given above, and are not arranged 
in bands about the limb; that there is no difference between radicular and 
spinal metamerism, and that lesions of any spinal segment cause practically the 
same distribution of anaesthesia whether the roots or the central gray mat- 
ter be involved. The question is still unsettled, and further study is neces- 
sary. — K.] 

3. The presence or absence of certain reflexes may also aid the segmental 
diagnosis. Of course the conditions here are often very ambiguous, since the 
reflex may be absent either from an interruption of its particular centripetal or 
centrifugal roots or from an interruption in any part of the reflex arc itself. The 
centripetal and centrifugal portions of the reflex arc are not always necessarily 
at the same level. Our knowledge is by no means absolutely definite as to the po- 
sition of the reflex arc itself. The statements as to the relation of definite segments 
of the cord to certain reflexes therefore refer in general only to afferent (centripe- 
tal) posterior nerve-roots involved in such reflexes. The assumption that the 
transmission of the irritation to the appropriate motor ganglion-cells takes place 
in the same corresponding segment of the spinal cord, is warranted at most for 
certain simple mono-muscular reflexes (patellar reflex, abdominal reflex, etc.). For 
more extensive reflexes (general flexion reflex in the leg, etc.) we must assume from 
the outset that the reflex process spreads over many segments of the spinal cord. 

We have set forth the relations of the spinal segments (or posterior roots) to 
the different reflexes in the following table, which represents our present knowl- 
edge of the subject, although it is still very uncertain: 



Biceps tendon reflex. 

Triceps tendon reflex. 

Tendon reflexes in the forearm. 

Upper abdominal reflex. 

Middle and lower abdominal reflex. 

Cremaster reflex. 

Patellar reflex. 

Glut seal reflex. 

Plantar flexor reflex. 

Achilles tendon reflex. 



5th cervical segment? 
6th cervical segment % 
7th and 8th cervical segments' 
8th and 9th dorsal segments. 
10th to 12th dorsal segments. 
1st to 3d lumbar segments. 
2d to 4th lumbar segments. 
4th and 5th lumbar segments. 
1st and 2d sacral segments. 
2d sacral segment % 



Many details as to the behavior of the reflexes in different spinal diseases will 
be mentioned in later chapters. We may here state briefly that in general, the 
absence of a reflex points to a lesion of the corresponding segment of the spinal 
cord. Transverse diseases above any given reflex arc are usually (but not always, 
vide infra) associated with a pronounced increase of the reflex. In diseases of 
the lumbar cord the tendon reflexes in the lower extremities are therefore lost as 
a rule, while in diseases of the dorsal and cervical cord they are usually much 
increased. 

4. At this point we must mention some important anatomical relations be- 
tween the position of the different portions of the spinal cord and the surround- 
ing vertebras. It is well known that the lower end of the spinal cord extends only 
to the level of the second lumbar vertebra. The vertebral canal below this point 
is filled partly by the filum terminale, but chiefly by the bundles of roots of the 
cauda equina. The greatest breadth of the cervical enlargement is at the level of 
the fifth and sixth cervical vertebrae. The dorsal cord begins at the level of the 



928 



DISEASES OE THE NERVOUS SYSTEM 



— 1 c 



second dorsal vertebra, the lumbar cord at the level of the tenth dorsal vertebra. 
The lumbar enlargement attains its greatest circumference at the eleventh dorsal 

vertebra. The position of the conus terminalis cor- 
responds to the upper half of the second lumbar 
vertebra. 

The topical relations between the different 
spinal segments and spinal roots and the bodies 
of the vertebras are also of great practical impor- 
tance. Since the spinal segments are shorter in 
the vertical direction than the bodies of the verte- 
brae, the spinal roots, from above downward, must 
travel farther and farther downward to reach their 
corresponding intervertebral foramina. The ac- 
companying diagram from Gowers (Eig. 125) 
makes this relation plain. A lesion of the eighth 
dorsal segment, for example, lies opposite the body 
of the seventh, and not of the eighth dorsal verte- 
bra; but since the spinous process also has a de- 
scending direction, the lesion must be sought at the 
level where we can feel the seventh or even the 
sixth spinous process. These relations have great 
practical significance for any operative procedure, 
but we must also remember that there may be indi- 
vidual variations from the rule. 



10 

11 
12 

L.I 



1 D 



~7l 















1 L 



CHAPTER III 

DISTURBANCES OF CIRCULATION, HEMOR- 
RHAGES, TRAUMATIC LESIONS, AND 
FUNCTIONAL DISTURBANCES OF THE 
SPINAL CORD 



1 s 



5 

Co. 



Fig. 125.— Diagram to explain the 
relation between the points 
where the different spinal roots 
are given off from the cord and 
the different vertebral bodies 
and spinous processes. 



1. Disturbances of Circulation. — Our knowl- 
edge as to the occurrence and as to the clinical sig- 
nificance of pure disturbances of circulation in the 
spinal cord is very slight. Most that is stated in 
regard to them in the older descriptions of the 
pathology of the spinal cord corresponds much more 
to theoretical hypotheses than to the actual ob- 
jective facts. 

It goes without saying that a complete anaemia 
of the spinal cord must destroy its function; this 
fact is best illustrated by the well-known experi- 
ment of Stenson: if we compress the abdominal 
aorta of an animal, and thus cut off the blood-sup- 
ply to the lumbar cord almost completely, a paraly- 
sis of the posterior portion of the body very rapidly 
ensues. Embolic (or thrombotic) obstruction of 
the aorta also leads to flaccid paralysis of the legs in 
man, but this paraplegia is to be referred to anae- 
mia of the peripheral nerves and muscles, and not 
to any change in the spinal cord, as we must main- 



DISTURBANCES OF CIRCULATION, HEMORRHAGES, ETC. 929 



tain after a personal observation upon this point. The spinal cord is abundantly 
-supplied with blood by the spinal arteries coming from the vertebral artery. 
Some precisely analogous observations have been made in man in the rare cases 
of obstruction of the aorta by emboli or thrombi. Pronounced spinal symptoms 
in general anaemia, which may be referred to a co-existing anaemia of the cord, 
are rare, and at any rate are of much less clinical prominence than the important 
results of a co-existing cerebral anaemia (vide infra). In only a few cases has para- 
plegia been seen after a great general loss of blood, as after metrorrhagia or intes- 
tinal haemorrhage. The severe spinal symptoms sometimes occurring in pernicious 
anaemia are due to combined columnar degeneration in the cord (vide infra). 

All statements as to the occurrence and clinical significance of hyperaemia of 
the spinal cord are still more dubious. We do not know whether there is active 
.hyperaemia of the cord. The hyperaemia from stasis, in general disturbances of 
the circulation, in which certainly the spinal cord often takes part, causes no 
especially marked symptoms. 

2. Haemorrhage into the Substance of the Spinal Cord — Spinal Apoplexy — 
Haematomyelia. — Primary haemorrhage into the spinal cord is as rare as haemor- 
rhage into the brain is common. It is due most frequently to traumatic influ- 
ences (fall on the buttocks, blow on the back, etc.). We will return to this 
traumatic haematomyelia later. The sudden onset of spinal paralysis has also 
been seen after great physical exertion, and this is probably due to a spinal 
apoplexy. It is possible, but it is not yet absolutely certain, that primary vas- 
cular disease (small aneurisms) may favor the occurrence of haemorrhage in such 
•cases. Small capillary spinal haemorrhages are not infrequently seen as a second- 
ary complication in tumors of the cord, and in inflammatory affections such as 
myelitis, epidemic meningitis, etc., and in the general haemorrhagic diathesis, as 
in scurvy or severe general infectious diseases, and after great congestion, convul- 
sions, etc. E. Schultze has also found haemorrhages into the gray matter of the 
posterior horns in new-born infants who have come into the world asphyxiated 
after difficult labor, and these haemorrhages may perhaps be of some significance 
in later life. 

Anatomical experience in regard to primary spinal apoplexy is still quite 
■slight. The commonest situation for spinal haemorrhage is the gray matter, either 
in the cervical or the lumbar enlargement. If the haemorrhage be abundant, we 
find the substance of the cord destroyed to a great extent. The apoplectic center 
usually extends principally in the long axis of the cord. The blood is still fluid 
in fresh cases. Later on it undergoes all those changes which are fully described 
in the chapter on cerebral apoplexy. It is not improbable that some cases of 
syringomyelia may be referred to a primary haemorrhage into the spinal cord. 

The symptoms of spinal apoplexy must in the first place depend entirely upon 
the seat and extent of the haemorrhage. The sudden, apoplectiform onset of the 
symptoms is always characteristic. It usually begins with severe pain in the 
back, followed very speedily by more or less widespread paralysis, anaesthesia, 
vesical disturbances, etc. Since the haemorrhage is usually situated in the gray 
matter, the localization of the muscular paralyses and the form of sensory dis- 
turbance (dissociated anaesthesia !) often show the peculiarities attendant upon 
such a lesion. Haemorrhage into one half of the cord sometimes shows very 
definite symptoms of unilateral lesion (vide infra). Thus in some cases of 
haemorrhage into the cervical cord, in particular, Minor has observed the fol- 
lowing symptom-complex : partial atrophic paralysis of one arm, spastic paralysis 
of the leg on the same side, partial anaesthesia (just as in syringomyelia) in the 
extremities of the opposite side. 

The course of haemorrhage of the cord may in many cases be comparatively 
favorable. If the blood be absorbed, and essential paths of conduction be not per- 
59 



930 



DISEASES OF THE NERVOUS SYSTEM 



manently destroyed, the symptoms of paralysis gradually pass away, and recovery 
or at least improvement and an arrest of the symptoms follow. In many cases, 
of course, the severe type of spinal paralysis develops, with bed-sores, cystitis, etc., 
and this, after a longer or shorter time, leads to death. 

We must always be very guarded in making a diagnosis of spinal haemorrhage. 
We can do so with some probability only when the symptoms begin in a pro- 
nounced apoplectiform manner, and when definite serological factors (trauma) 
are to be made out; but, as we shall see later, central softening without actual 
haemorrhage may follow trauma and cause precisely the same symptoms as 
haematomyelia. We should also not forget that many forms of acute myelitis, and 
even chronic spinal affections (especially spinal syphilis), may also show a re- 
markably sudden onset or at least may suddenly become worse. The distinction 
between genuine spinal apoplexy and meningeal haemorrhage is often difficult. 
Initial symptoms of marked sensory irritation favor meningeal haemorrhage, while 
the occurrence of symptoms pointing to an affection of the gray matter, especially 
the combination of atrophic muscular paralysis with partial anaesthesia (thermo- 
anesthesia, analgesia), warrants the suspicion of central haematomyelia. 

Treatment. — If we have the rare opportunity to be able to interfere at the 
beginning of the symptoms, we should prescribe a perfectly quiet position in bed, 
local use of ice, and eventually ergotine. Later on the treatment should be 
directed according to the methods generally in use in spinal paralysis. 

3. Traumatic Lesions of the Spinal Cord. — In spite of the protected position 
of the spinal cord, it is often the seat of severe acute traumatic lesions. Frac- 
tures and dislocations of the vertebrae are the most frequent, and these may give 
rise to considerable injury of the spinal cord by the dislocation of the vertebrae, or 
by the projection of a fragment of bone. Dislocations occur most frequently in 
the cervical region (between the atlas and axis or very often between the fifth and 
the sixth cervical vertebrae). The upper vertebra in such cases is usually dis- 
located forward. The spinous process of the lower vertebra therefore projects 
backward, while the spinous process of the dislocated vertebra is pushed forward. 
The head is bent forward. Every movement of the head is painful, and is there- 
fore anxiously avoided. Fractures are very often situated in the middle cervical 
vertebrae or at the twelfth dorsal and first lumbar vertebrae. 

Besides the indirect lesions of the cord by displaced vertebrae, the action of 
the injury (fall on the back, etc.) may also extend immediately to the spinal cord. 
In many cases there may be at the moment of the injury a temporary distortion 
of the vertebral column associated with local laceration of the cord; but some- 
times severe traumatic lesions of the cord occur without any vertebral injury. 
These consist of haemorrhages, which are usually central (haematomyelia {vide 
supra), or traumatic softening, which is also usually central. Haemorrhage and 
softening may also be associated. Some writers hold that an effusion of cerebro- 
spinal fluid may sometimes cause laceration and injury of the tissues. The dif- 
ferent actions of the traumatic force are, of course, very often associated; thus 
we not infrequently see, in particular, above and below the destruction of the 
cord caused by a vertebral lesion, central haemorrhages, or softening in the an- 
terior and posterior horns. 

Gun-shot wounds of the cord are quite frequent, in which the bullet either 
penetrates the cord itself or produces injury of the vertebrae and haemorrhage, 
which involve the cord indirectly. Stabs and incised wounds of the cord have 
been repeatedly seen. The point of a knife or sword may penetrate the spinal 
canal from behind through the soft parts and cause a partial section or at least 
a contusion of the cord. In such cases a secondary " traumatic inflammation n 
may be added to the direct injury. 

The symptomatology of injuries of the spinal cord follows the general rules 



DISTURBANCES OF CIRCULATION, HEMORRHAGES, ETC. 931 



for the localization of disease of the cord laid down in the previous chapter. 
There is usually at first a pronounced and often complete motor paralysis of the 
lower extremities. There is also anaesthesia, and very often vesical and rectal 
paralysis. In many severe cases the secretion of urine seems at first much 
diminished or wholly wanting. If the spinal roots be affected there are severe 
shooting pains and paresthesia. Above the limit of total cutaneous anaesthesia 
we sometimes find a zone with dissociated anaesthesia (analgesia and thermo- 
anesthesia). This symptom points to a haematomyelia or a central softening 
in the corresponding posterior cornu of the gray matter above the seat of 
the special lesion (vide supra). The reflexes are usually diminished at first, but, 
later, if the injury be above the reflex arc, they are increased; but if the arc 
itself be broken, they are permanently absent. This rule, however, undergoes an 
interesting exception, since we often find after severe injury of the cervical cord, 
and especially after a complete transverse lesion thereof, a flaccid paralysis of the 
lower extremities and complete absence of the tendon, and more rarely of the 
cutaneous, reflexes (Bastian, Thorburn, Brums, and others). To explain this 
striking fact we must suppose that the reflex path in the lumbar cord has also un- 
dergone some disturbance, either from the initial general concussion or from its 
separation from all the higher parts in the brain. With the loss of reflex is often 
associated paralysis of the bladder and rectum. We often see in men, especially 
after injury of the cervical cord, a more or less complete and persistent erection 
of the penis, which is probably due to a direct or reflex irritation of the nerves 
of erection. In injuries of the cervical cord particularly, we often see a great and 
general increase of temperature, up to 110° or 112° (43°-44° C), especially in 
severe and rapidly fatal cases; this is of physiological interest, and agrees with 
the results of experiments. On the other hand, there are also, especially in 
injuries of the dorsal cord, as it seems, great falls of temperature, down to 90° or 
86° (32°-30° C). 

The further course of the affection differs very much. In the worst cases death 
ensues in a few hours or days. In other cases the patients recover from the first 
" shock," but permanent paralysis remains, which may sooner or later lead to 
death from the ensuing sequelae, cystitis and bed-sores ; but we often see partial 
improvement and a cessation of all the symptoms. Although certain functional 
disturbances remain permanently, life is not further endangered. Finally, in 
comparatively mild cases, there may be a complete recovery. 

The very characteristic injuries of the conus terminalis and the cauda equina 
yet demand special mention. The conus terminalis is sometimes crushed in 
fracture of the first lumbar vertebra. The symptoms consist of paralysis of the 
bladder, rectum, and sexual functions, with anaesthesia of the skin over the sa- 
crum and about the anus, perineum, and genitals (cutaneous branches of the last 
sacral nerves, compare Fig. 117, page 924). If the injury extends higher there 
are also sensory disturbances on the posterior aspect of the lower extremities, and 
paralysis in the region of the sciatic (see Figs. 118-124, pages 925, 926). A pre- 
cisely similar type of disease, however, also develops from injury of the cauda 
equina (for example, from fracture of the lowest end of the vertebral column or 
fracture of the sacrum), since injury of the root-fibers of the sacral and coccygeal 
plexuses must of course cause the same symptoms as injury of the corresponding 
spinal segments themselves. In such cases we also see the peculiar distribution of 
the sensory disturbances and the paralyses localized in the sciatic region, especial- 
ly the double peroneal paralysis that is so very characteristic. The differential 
diagnosis between an affection of the cauda and a lesion of the lowest portion of 
the cord is not always easy, but it is of practical importance, especially in regard 
to the question of any surgical interference. Besides the consideration of the 
chief point of action of the injury, we must consider especially that symptoms 



932 



DISEASES OF THE KEBVOUS SYSTEM 



of severe sensory irritation (shooting pains, paresthesia) favor in general an 
affection of the cauda, while the existence of dissociated disturbance of sensa- 
tion is of value in assuming a (central) disease of the spinal cord. 

The treatment of the primary affections belongs to the domain of surgery; 
especially any attempt to lay open the vertebral canal, in order, if possible, to re- 
lieve the existing pressure on the cord by reducing the dislocation of the verte- 
brae or the splinters of bone. In most cases, particularly in all cases where the in- 
jury is confined to the cord, we have to confine ourselves to putting the patient in 
a proper position on a water-bed, and guarding as carefully as possible against 
bed-sores and cystitis. Locally, the constant application of ice is most to be 
recommended. We can expect but little from local blood-letting, inunctions with 
mercurial ointment, etc. If the first acute stage pass off favorably, the treatment 
of any paralytic symptoms remaining follows the ordinary rules (baths and 
electricity) . 

4. Diseases of the Spinal Cord after a Sudden Reduction of the Atmospheric 
Pressure [Caisson Disease]. — In bridge-builders and others, who have worked for 
hours under water in the so-called " caissons," under an external pressure of two 
or three atmospheres, we sometimes observe peculiar nervous symptoms after 
they leave the caisson — that is, on the sudden reduction of the atmospheric pres- 
sure. These symptoms do not come on immediately after the change to the ordi- 
nary atmospheric pressure, but usually some minutes or even half an hour later. 
They progress very rapidly, so that in a few hours at the latest the disease is 
fully developed. Besides the frequent mild and transitory symptoms of pain in 
the ears and haemorrhage from the ears, articular and muscular pains in the back 
and the extremities, slowing of the pulse and vomiting, vertigo, tinnitus, dis- 
turbances of vision and speech, clouding of consciousness, or even complete men- 
tal confusion, there are also more persistent and severe disturbances of motil- 
ity and sensibility, which point unequivocally to an affection of the spinal cord. 
Usually the spinal symptoms affect the lower extremities chiefly ; more rarely they 
also involve the arms. Paralysis of the diaphragm has also been observed. The 
type of disease differs much in its details; as a rule the symptoms of spastic 
paraplegia predominate, but in other cases there are marked disturbances of sen- 
sation or co-ordination. The bladder is often involved ; there is usually retention 
of urine. The patient sometimes recovers in a few weeks, but in other cases the 
condition terminates fatally in a comparatively short time — in a few weeks or 
months. Anatomical investigations (Leyden, F. Schultze, von Schrotter, and 
others) show in such cases a disseminated but extensive affection in the dorsal 
cord, chiefly in the posterior columns and the posterior portions of the lateral 
columns. The nervous tissue in the diseased parts is completely destroyed, and 
instead of it is found detritus and a collection of large, round, fatty granular 
cells. Haemorrhages into the cord, which might perhaps be expected, have not 
been seen. The cause of these small multiple foci of softening is to be found in 
the occurrence of many gas emboli. During the workman's stay in the compressed 
air the blood absorbs an abnormal amount of gas, especially nitrogen (Hoppe- 
Seyler, P. Bert, and others). With too sudden a return to the ordinary con- 
ditions of atmospheric pressure, bubbles of gas form in the blood, and, in case they 
can not be thrown off fast enough by the lungs, they lead to numerous emboli in 
the smaller vessels with their consequences. The anatomical arrangement of the 
vessels seems to be the reason why the embolic foci are situated chiefly in the 
dorsal cord. 

The treatment is the same as in acute myelitis. The prophylactic measures to 
be employed in a given case are of course very important. The onset of morbid 
symptoms can be certainly avoided by the cautious and slow reduction of the 
atmospheric pressure. [No person suffering from any disease, especially of the 



DISTURBANCES OF CIRCULATION, H JEALORRH AGE S, ETC. 933 



heart or kidneys, no one addicted to alcohol, and no old or very stout person, 
should enter a caisson. It is probably safer not to enter a caisson fasting. Be- 
ginners should remain in the caisson a comparatively short time — not over an 
hour. Tor more experienced workmen a day's work should not exceed four 
hours, divided into two shifts with four hours' interval. Great precautions 
must also be taken against cold. The process of " unlocking " must be slow, 
at least five minutes for each atmosphere of pressure. It is said that when the 
symptoms first come on they may be averted by restoring the victim to the 
caisson or to a cabinet capable of affording increased atmospheric pressure. Fluid 
extract of ergot (a drachm [gramme 4.0] every hour for a few doses) is said to 
give great relief at the outset. — K.] 

5. Functional Disturbances (Spinal Irritation — Spinal Neurasthenia). — In 
practice we very often see cases where the patient complains of a set of symptoms 
which are in all probability of spinal origin; but since all the objective signs of a 
severe spinal affection are entirely absent, and since the whole development and 
further course of these cases oppose the theory of a coarse anatomical disturbance 
in the cord, we have a right to regard them as mere " functional disturbances," 
and thus to express their relation to certain injurious ^etiological influences, and 
their comparative freedom from danger. It is often very hard to judge as to the 
special origin of the symptoms. The hypothesis of " fine molecular changes " and 
also the hypothesis of " abnormal vaso-motor influences and disturbances of the 
circulation " are forms of speech without any actual basis. In very many cases — 
though of course not in all — the influence of a morbid imagination and of men- 
tal anxiety is very evident. The spinal symptoms are also very often associated 
with certain cerebral symptoms, so that the former are only a part of a general 
neurasthenia. We must therefore refer to the description of the latter. 

If we look for the cause for the development of the disease, we find, as a rule, 
one or more of those injurious factors, which have an undoubted influence in 
the development of almost all the neuroses : severe and persistent emotional ex- 
citement, mental and physical over-exertion, improper methods of living, poisons, 
such as alcohol and nicotine, and sexual excesses, such as masturbation, etc. 
Besides these there is very often a hereditary predisposition, a congenitally weak 
resistance of the nervous system, which is often further enfeebled by a poor 
state of the general nutrition. Finally, a hypochondriacal disposition is of great 
significance, as it causes not only an abnormally increased attention to the symp- 
toms, but also an abnormal hyperaBsthesia to all subjective sensations, and even 
the development of new subjective sensations. The constant anxiety about the 
dreaded results of any excesses committed (especially with many patients the 
fear of the supposed effects of previous masturbation) is often much more injuri- 
ous than the excesses themselves. Hypochondriacal dread, too, usually plays the 
largest part in the spinal neurasthenic conditions frequent among physicians 
(tabophobia). 

The symptoms of the morbid conditions in question usually begin gradually. 
The patient begins to complain of weakness and fatigue in walking, and also very 
often of pains in the back and loins, and not infrequently in the extremities also. 
In spite of the vivid description which the patients give of their pain, they usually 
have to admit, if questioned about it closely, that the intensity of the pain is 
really not very great. Besides the pain there are usually many forms of pares- 
thesia — numbness, formication, cold feelings, etc. The more the patient knows, 
or at least believes he knows, of the symptomatology of spinal diseases from 
reading and from associating with other patients, the more detailed are his com- 
plaints. Disturbances of the bladder are usually present only in a slight degree, 
but still they do occur. They often depend merely upon the disturbance of 
the involuntary reflex mechanism, clue to the added factor of increased voluntary 



934 



DISEASES OF THE KEKVOUS SYSTEM 



attention. There are very often sexnal disturbances (pollutions, sexual weakness, 
etc.), which are usually to be referred to former excesses, especially to masturba- 
tion or to the hypochondriacal condition of the patient. 

If we make a physical examination of the patient we can not discover definite 
signs of a spinal affection. In some of the cases we find an increased sensitive- 
ness of the vertebras on pressure, which may be limited to a few definite spots, 
a symptom to which the name of " spinal irritation " is often given ; but we often 
fail to find this tenderness of the vertebrae. Nothing abnormal is to be discovered 
in the pupils or the reflexes. The tendon reflexes are sometimes quite lively and 
sometimes weak. The sensibility is objectively perfectly normal; neither can we 
discover actual paresis or atrophy of the muscles. Vaso-motor disturbances, 
however, are often seen : abnormal coldness, pallor or redness of the hands, tend- 
ency to sweating, etc. The manifold cerebral symptoms, that are usually present 
at the same time, will be mentioned in the description of neurasthenia. The 
condition of the general nutrition in many patients remains unchanged, but, of 
course, some become pale, thin, and weak. 

The diagnosis of functional disturbances of the spinal cord is usually not 
difficult, as we have said, and it may often be made from the history, from the 
patient's whole outward behavior, and from the manner of his complaints ; but we 
can not lay too much stress upon the injunction that a careful physical examina- 
tion should always be made, in order to avoid confusion with an incipient serious 
disease. We shall repeatedly call attention in what follows to the symptoms which 
must chiefly be observed for this purpose. 

In regard to prognosis and treatment we will refer to what is said in the chap- 
ter on neurasthenia. 



CHAPTEE IV 

THE PRESSURE PARALYSES OF THE SPINAL CORD 

(Slow Compression of the Spinal Cord, especially in Caries and Carcinoma of the Vertebrae) 

^Etiology. — Many pathological processes in the vicinity of the spinal cord 
exert a gradually increasing pressure upon it, and thus inhibit the conduction of 
nervous irritation, and even cause coarse organic changes in the substance of the 
cord. The seat of such affections is in the first place in the membranes of the 
spinal cord. In the chapter on meningitis we have already mentioned the com- 
pressing action of the masses of inflammatory exudation on the nerve-roots and 
the cord, and we have learned to recognize, especially in pachymeningitis cervi- 
calis hypertrophica, a characteristic example of a gradually increasing compres- 
sion of the cervical cord. Precisely similar conditions are found in the not very 
rare meningeal tumors, whose special pathology will be described in connection 
with the tumors of the cord itself. 

By far the most frequent pressure paralyses of the spinal cord, and hence the 
most important practically, are caused by certain diseases of the vertebrae, and 
first of all by chronic caries of the vertebrae (spondylitis, Pott's disease, spondyl- 
arthrocace).* There is no longer any doubt that in almost all cases vertebral 
caries is of tubercular origin — a local tuberculosis of the vertebrae. Although 



* la the kyphoscolioses of the vertebral column, not due to spondylitis, but caused by abnormal 
mechanical conditions or conditions of growth, there are practically never any symptoms of compres- 
sion in the cord, even in very pronounced cases. In these cases the cord manifestly shows quite a 
great adaptability. 



THE PEESSUEE PAEALYSES OE THE SPINAL COED 935 



these facts were formerly rendered very probable by the histological conditions of 
the process, and by its frequent relation to other unquestionable tubercular dis- 
eases, such as phthisis, miliary tuberculosis, and tubercular meningitis, they 
have of late been confirmed beyond a doubt by the almost invariable discovery 
of tubercle bacilli in the cheesy nodules of the vertebral caries. Tubercular 
spondylitis occurs at almost any age; it is rare only in old people. It often de- 
velops in children, but it is almost as frequent in adults. The serological signifi- 
cance of injuries, such as a fall or a blow, which are often mentioned by the 
patients themselves or their parents, is in most cases doubtful, but not wholly to 
be ignored. As a rule vertebral caries apparently develops quite independently as 
a primary disease. Of course we can very often succeed in finding serological 
factors rendering tubercular disease likely — the tubercular habit, hereditary 
tendency, or previous tubercular disease elsewhere, such as phthisis, pleurisy, 
other affections of the bones, etc. 

Cancer of the vertebrae, as well as caries, leads to pressure paralysis of the 
spinal cord; but it is relatively much rarer than caries, it develops chiefly in 
older persons, and it occurs only as a secondary new growth in cancer of other 
organs — the breast, the stomach, the oesophagus, etc. Sarcoma is the chief pri- 
mary tumor of the vertebrae ; but it may also involve the vertebrae secondarily by 
extension from growths in the vicinity. 

We must mention here briefly, as very rare causes of compression of the spinal 
cord, aneurism of the aorta, which gradually erodes the vertebrae, echinococci in 
the vertebral canal, exostoses of the vertebrae, [myeloma,] and syphilitic new 
growths. 

Pathological Anatomy. — Vertebral caries is by far most frequent in the dorsal 
portion of the vertebral column (dorsal spondylitis), less frequent in the cervical 
portion (cervical spondylitis), and rarest in the lumbar por- 
tion (lumbar spondylitis) and in the sacrum (sacral spon- 
dylitis). It usually extends over several adjacent vertebrae, 
or more rarely two separate foci of disease are seen. The 
process itself, the details of which can not be discussed here, 
probably always begins in the spongy substances of the bod- 
ies of the vertebrae. We see here, on section, in incipient 
cases, roundish, pale reddish, or yellowish nodules, which 
consist of newly formed fungous tissue — that is, tubercular 
granulation-tissue. The bony substances become more and 
more destroyed by the invasion of the new growth, which it- 
self shows the characteristic tendency of all tubercular new 
growth to cheesy degeneration. Thus there is often an ex- 
tensive destruction of the bodies of the vertebrae, which later 
on involves the vertebral processes also, the intervertebral 
disks, and the other articular connections between the differ- 
ent vertebrae. 

There are essentially two factors to be considered in re- 
gard to the question which chiefly interests us here — that is, in regard to the occur- 
rence of compression of the spinal cord. In the first place, it is clear that the com- 
plete or partial destruction of the bodies of one or even more vertebrae, and of their 
articular connections, can not remain without influence upon the position of the 
other adjacent vertebrae. In fact, we very often see dislocations of the vertebrae 
as a result of it, usually by the pushing backward of the partly destroyed verte- 
bra by the movements of the vertebrae above and below the diseased portion on one 
another (see Fig. 126). There arises, on the one hand, a contraction of the ver- 
tebral canal, and with it often a very considerable limitation of the space for the 
cord; and, on the other hand, that characteristic projection of the spinous pro- 




C 



Fig. 126. — Schematic 
representation of ver- 
tebral displacement in 
spondylitis. The point 
of compression of the 
cord, at the level of 
the second dorsal ver- 
tebra, is at C. 



936 



DISEASES OE THE jSTERYOUS SYSTEM 



cesses in the region of the diseased portion of the vertebral column which forms 
the so-called Pott's boss — the angular kyphosis (Eig. 127, page 938). In very- 
slight degrees of the disease there is only a trifling projection of one or more- 
spinous processes, but in other cases it gradually becomes an extensive deformity 
of the vertebral column, which strikes us at the first glance ; but it must be espe- 
cially borne in mind that in very many cases of vertebral caries, where the body 
of no vertebra is wholly or mainly destroyed, there is no knuckle formed at alL 
The line of the spinous processes in such cases preserves completely its normal 
external form. 

The second factor, which is very often to be considered in the mechanism of 
compression of the cord, is the formation of tubercular granulation tissue or of 
foci of cheesy pus on the posterior surface of the bodies of the vertebras. Since 
the inflammatory tubercular new growth involves the periosteum, there are often 
formed here large collections of cheesy pus, which are situated beneath the peri- 
osteum, raise it, and push it out far into the vertebral canal. Still more com- 
monly, the tubercular new growth directly involves the outer surface of the dura, 
and forms here extensive cheesy masses which of course may also cause a com- 
pression of the cord. The inner surface of the dura at the corresponding parts 
is usually a little injected, but otherwise perfectly normal. A direct invasion of 
the inner surface of the dura or of the pia by the tubercular process through the 
dura is rare. 

If now a greater or less contraction of the vertebral canal has arisen from- 
dislocation of the vertebras, or from the projection inward of the cheesy purulent 
masses into the canal, the consequences of pressure on the spinal cord itself are 
not long wanting. In cases where there has been much displacement of the verte- 
bras or an abundant formation of cheesy purulent masses on the outer surface of 
the dura with considerable narrowing of the vertebral canal, the direct and purely 
mechanical injury of the nervous elements certainly plays a part ; but we not 
infrequently see during life marked paraplegia in vertebral caries, where the 
autopsy shows only a comparatively slight narrowing of the vertebral canal, usu- 
ally from granulations on the outer surface of the dura mater. In such cases 
there are a number of other factors, for the most part also of a mechanical nature, 
which lead to destruction of the substance of the cord. In the first place the com- 
pression of the epispinal lymph-space causes a stasis of lymph (Schmaus) in the 
periadventitial and also in the periganglionic lymph-spaces and in the lymph- 
spaces between the axis cylinders and the medullary sheaths. The retained 
lymph has a mechanical and probably a toxic action on the nerve elements. We 
also see not infrequently thrombosis of the small afferent arteries, causing 
anaemic necrosis of their respective vascular territories. It is hard to decide 
how much effect may be ascribed to direct compression of the vessels ; and equally 
hard to say whether toxines from the tubercular nodules may perhaps reach the 
substance of the cord, and there exert an injurious action. In no case, however,, 
have we a right, in our opinion, based upon a comparatively large number of cases 
seen in hospital and private practice, to speak of a " compression myelitis."" 
Myelitis — that is, inflammation — always implies agents of inflammation at the 
place of inflammation, and of that there is no suggestion in compression of the 
cord. The histological changes at the point of compression (vide infra) are not 
of an inflammatory nature, but they may all be explained by the above-mentioned 
mechanical factors. 

If we find a greater narrowing of the vertebral canal, the spinal cord is also 
smaller at the point of compression. If the narrow part correspond to a bend in 
the vertebral column, we can very often see a marked angle of bending on the 
anterior surface of the cord. The whole configuration of the cord and the ar- 
rangement of the nervous elements may be considerably disturbed and distorted 



THE PKESSUKE PAKALYSES OF THE SPINAL COED 937 



mechanically. The consistency of the cord at the part' affected, the extent of 
which seldom exceeds a few centimetres, is usually diminished; the cord is soft 
and may be easily bent. In old cases only do we find the cord itself harder than 
normal and sclerosed (vide infra). It is very remarkable, however, that often, 
as we have repeatedly seen, marked symptoms of paralysis may be present during 
life without finding any coarse mechanical lesion of the cord in the cadaver, so 
that the cord may have an almost perfectly normal appearance. As in the periph- 
eral nerves, so in the spinal cord, a moderate pressure is manifestly enough to 
excite a partial break in the conduction, without being at the same time neces- 
sarily associated with an actual mechanical destruction of nervous elements. On 
careful microscopic examination of the cord, we find in such cases, in spite of the 
existence of a complete paraplegia during life, that most of the nerve-fibers are 
still completely preserved, and that there are only here and there a few lacunas, 
corresponding to circumscribed lymph-spaces (vide supra), and to single fibers 
which have been destroyed. This discovery is especially interesting because it 
makes us understand the possibility of recovery, even in apparently severe cases 
(vide infra). 

If we take a portion from the soft place of compression for examination in the 
fresh state, we find usually many, sometimes (in old cases) only a few, granular 
cells, according to the amount of disintegrated nerve-medulla, the remains of 
which are taken up by the white blood-corpuscles (the wandering cells), and prob- 
ably also by the glia cells. If we make stained cross-sections of the hardened cord, 
we see under the microscope no signs of hyperemia, or accumulation of cells about 
the vessels, and only exceptionally a little hemorrhage; but we do find, besides 
many still preserved nerve-fibers, other fibers, which are involved in the disinte- 
gration or are already destroyed. Very commonly the changes are distributed in 
the form of nodules. We find groups of greatly swollen axis-cylinders, or of axis- 
cylinders torn off and rolled up in a spiral. The medullary sheaths are every- 
where involved in the disintegration, until they blend with the disintegrated axis- 
cylinders. The products of disintegration developing everywhere serve, as was 
said above, to form the granular cells. The ganglion-cells and the glia also show 
signs of disintegration. We not infrequently find the so-called corpora amylacea, 
whose origin is still somewhat obscure. If the destruction of the nervous tissue 
have advanced to a certain degree, there is in the later stages, as in all analogous 
processes, a secondary implication of the neuroglia. ISTow follows an increase 
of the interstitial connective tissue. Its proliferations, which take the place of 
the destroyed nervous tissue, seem broad and thick — at first loose, but later firm 
and fibrillary. Thus it happens that in old cases we find nothing at the point of 
compression but a loss of nerve-fibers in the cord, and instead a firm fibrous tissue. 
We can sometimes notice processes of regeneration in the nerve-fibers (vide 
infra) . In general the changes are much more marked in the white matter of the 
cord than in the gray. 

Finally, after every protracted compression of the cord we find an ascending 
and descending secondary degeneration of certain systems of fibers in the cord 
(vide infra). 

We need not go more fully into the details of compression of the cord from 
other causes, since the results, as far as they are of a purely mechanical nature, 
are precisely the same. In cancer of the vertebras there may also be dislocations 
of the vertebral column after the destruction of some of the vertebras, but usually 
the compression depends upon the direct growth of the newly formed tissue into 
the dura. In these cases the compression of the nerve-roots in the intervertebral 
foramina is also of importance. 

Clinical History. — 1. The Pressure Paralyses in Vertebral Caries. — Many 
cases of spondylitis run their course without involving the cord, or at least they 



938 



DISEASES OF THE NEKVOUS SYSTEM 




/ 



involve it only in quite a subordinate fashion. In other cases the symptoms of 
disease of the vertebrae exist for a long time alone, until at last, slowly or sud- 
denly, the signs of compression of the cord are added to them. Finally, in a 
third group of cases, the vertebral disease is so latent that only the cord symp- 
toms are prominent in the type 
of the disease, and the disease of 
the vertebras is easily entirely 
overlooked. 

Usually the symptoms of the 
developing primary disease, the 
affection of the vertebras, precede 
the appearance of the first cord 
symptoms by some time. The 
patient feels a dull pain at a 
definite part of the spine, which 
is increased by movements of 
the trunk, by bending or straight- 
ening up. Many patients notice 
the stiffness of the vertebral col- 
umn of themselves, and some- 
times even a beginning deform- 
ity. In characteristic cases we 
notice at once, on examining the 
vertebral column, an angular 
kyphosis (gibbus, Fig. 127) of 
considerable extent or limited 
to a few vertebras; but some- 
times there is only a slight prom- 
inence of a single vertebra, and 
not infrequently there is exter- 
nally no change in the formation 
of the vertebral column. The 
tenderness on pressure on the 
spinous processes is also not a 
constant symptom; it may be 
very pronounced, but it is not 
infrequently absent even in 
marked kyphosis. The first cord 
symptoms usually consist of pain- 
ful sensations, which are not con- 
fined to the place of the disease, 
but spread out along the course 
of the nerve-paths. These pains 
are due to the compression and 
the consequent irritation of the nerve-roots, and therefore extend, according to 
the seat of the affection, into the shoulders and arms, into the lateral portions of 
the trunk, or into the lower extremities. The initial pains are most frequently 
felt in the region of the lower ribs or of the epigastrium, corresponding to the 
most frequent situation of vertebral caries in the lower dorsal vertebras. They are 
sometimes very severe, and then they usually have a pronounced neuralgiform 
character, or they may be more dull, pressing, dragging, etc. Besides the special 
pains, there are also many forms of paresthesia, such as formication, cold feel- 
ings, and burning feelings. 

The disturbances of motility begin to appear at the same time with these 




Fig. 127. — Angular kyphosis in vertebral caries. 
(Personal observation.) 



THE PKESSUKE PAKALYSES OF THE SPINAL COED 939 



symptoms or soon after them. A stiffness and weakness arise which, impede the 
gait more and more, usually not in both legs at once, but first in one and then in 
the other, although, as a rule, both legs are soon involved. This paresis increases 
rapidly or slowly, and it may finally go on to a complete motor paralysis. If the 
seat of the affection be in the dorsal vertebrae, as it usually is, or if it be in the 
lumbar vertebrae, the paralysis affects the lower extremities only, and the arms, 
of course, remain intact; but in cervical spondylitis the arms are usually first 
and chiefly affected. Only on great compression of the cervical cord is the con- 
duction of the fibers passing through it for the lower extremities impaired, and 
then there are also disturbances of function in these. Ataxia of the legs is not 
very common, but it certainly does occur in compression of the cord. The ataxia 
of course is usually concealed by the co-existing paresis of the muscles or the ex- 
isting spastic conditions. We see ataxia most frequently in the stages of devel- 
opment or recovery of compression paralyses. 

Disturbances of sensibility are quite often found, independently of the pains 
and paraesthesiae above mentioned, but in many cases of pressure paralysis they 
are present in only a comparatively slight degree. It seems that the sensory 
nerves resist pressure more than the motor nerves, just as in the pressure paraly- 
ses of peripheral nerves; but possibly their position in the gray matter of the 
posterior cornua protects them better from the above-mentioned mechanical in- 
juries than is the case, for example, with the motor fibers in the pyramidal tract. 
The fact is that often, even in complete motor paraplegia, there is little if any 
diminution of sensibility, and that marked anaesthesia is rare, and is seen only in 
the last stages of the disease. We find most frequently a slight blunting of sen- 
sibility equally to all forms of sensation, especially to the sense of pain, in other 
cases partial disturbances of the sense of temperature with the sensibility to 
touch and pain well preserved, sometimes partial anaesthesia of the sense of 
pressure, etc. The different parts of the skin not infrequently act differently, so 
that we find portions with quite normal sensibility, as well as very anaesthetic 
portions. There may also be hyperaesthetic areas of the skin (especially at the 
upper boundary of the disturbance of sensation), particularly with marked hyper- 
esthesia to pain (pin-pricks). 

The condition of the reflexes is interesting. If the seat of the compression be 
above the reflex arc, which we must assume to be in the lumbar cord for the re- 
flexes of the lower extremities, we should expect that the reflexes would persist, 
and in many cases even be increased, corresponding to the decline in the inhibi- 
tory influences coming from above. The latter takes place in most cases with the 
tendon reflexes. The increase of the tendon reflexes, and the coincident increase 
of muscle tonus, may reach so great a degree in many cases of compression of the 
•dorsal and cervical cord as to show in the lower extremities the pronounced type of 
spastic rigidity and spastic paralysis. The legs are then found in a rigid tonic ex- 
tension, with the knees pressed firmly together, or there is spastic contracture of 
the flexors and adductors. All passive movements of the legs can be performed only 
with the greatest difficulty, and the attempt often causes a general tremor of the 
leg. All the tendon reflexes (patellar reflex, adductor reflex, ankle clonus, etc.) are 
much increased, but we must remember that even in apparently flaccid paraplegia 
the reflexes are sometimes quite lively. In cervical spondylitis the tendon and 
periosteal reflexes in the arms are also increased sometimes, but in other cases, if 
the reflex arc be injured, they are absent. Where the seat of the compression is 
above the lumbar cord, the cutaneous reflexes sometimes show considerable vigor, 
but their increase is much less frequently decided than is the increase of the 
tendon reflexes. In severe pressure paralyses in the dorsal cord the cutaneous 
reflexes are sometimes diminished. They are rarely entirely absent, but one must 
understand testing them, and must employ long-continued cutaneous irritation, 



940 



DISEASES OF THE NEKVOUS SYSTEM 



such as pinching and pricking, in different parts of the skin in order to provoke 
them (vide supra, page 839). [In spastic conditions the Babihski reflex is usu- 
ally found. — K.] In many cases of total compression of the cervical cord we 
find a flaccid paraplegia with absence of the tendon reflexes in the legs, just as 
in traumatic total transverse lesion of the cervical cord. In these cases we shall 
usually be able to find secondary changes in the lumbar cord on careful examina- 
tion (vide page 931). 

Disturbances of the rectum and bladder occur in almost all severe cases of 
pressure paralysis. The difficulty of micturition is often an early symptom of the 
disease ; later on there is complete retention of urine, and, in the more advanced 
stages of the disease, there is usually incontinence. With this the danger of the 
development of cystitis becomes very great. The bowels are usually constipated, 
but sometimes there is also incontinence of fasces. 

Trophic disturbances are often found in the paralyzed parts. If there be 
severe symptoms of sensory irritation there may sometimes be eruptions of her- 
pes, corresponding to the course of the nerves. More frequently there are chronic 
disturbances in the nutrition of the skin in severe and long-continued cases. It 
becomes dry, the epidermis scales off, and the nails become brittle. Bed-sores 
form very easily in severe cases on the sacrum, on the buttocks, on the inner side 
of the knees, and on the heels, especially when the patient has insufficient care. 
The muscles retain their normal volume and their normal electrical excitability 
in many cases as long as their trophic center remains uninjured; but sometimes, 
even when the point of compression is above the lumbar cord, there is a great 
flaccidity (vide supra) and atrophy of the muscles of the legs, although the elec- 
trical reaction of the nerves is normal, or at most a little reduced in quantity. 
In cervical spondylitis with lesion of the cervical cord or of the anterior cervical 
roots there may be atrophic paralysis in the arms. If there be compression of 
the lumbar cord there is atrophic paralysis of the leg muscles. We have already 
learned to recognize the peculiar type of nervous symptoms in disease of the 
lowest portion of the cord or of the cauda equina (page 931). We sometimes see 
the same type in caries of the upper lumbar vertebras with compression of the 
conus, or in caries of the sacrum with compression of the cauda equina. The 
points to be noticed in distinguishing between affections of the conus and affec- 
tions of the cauda have already been mentioned on page 931. 

Thus we see, under some circumstances, in compression of the cord, the whole 
group of symptoms arising which are the necessary consequence of the break 
in conduction in the spinal cord, and which we shall likewise meet again in vari- 
ous other spinal affections, especially in myelitis and in tumors. The intensity 
and number of the symptoms must, of course, vary very much in the different 
cases. If the compression be quite slight, there are only mild symptoms of sen- 
sory irritation and slight paresis. One of the earliest and most constant signs 
of a compression of the cord, in the dorsal or cervical region, is a decided increase 
of the patellar reflex. We sometimes find it at a time when there is scarcely a 
single other cord symptom present. If the compression increases, the paresis 
becomes more marked, the disturbance of sensibility is greater, and vesical dis- 
turbances arise, until finally the complete type of an entire transverse interrup- 
tion of conduction in the cord is developed. The precise limitation of the symp- 
toms, especially the distribution of the sensory disturbance, follows the rules 
already given (page 920). There is only rarely, however, a complete transverse • 
destruction of the spinal cord in vertebral caries. The conduction of sensory 
impressions, at least, is usually not wholly abolished. The time required for the 
development of the symptoms of spinal compression differs very much. They 
sometimes attain a considerable height in a short time, and sometimes they de- 
velop only after a course of months. Variations in the intensity of the symptoms. 



THE PEESSUEE PAEALYSES OF THE SPINAL COED 941 



are frequent, and they point perhaps to a corresponding variation in the severity 
of the compression. 

In regard to the result of pressure paralyses in vertebral caries, spondylitic 
processes without doubt can recover, which is by no means in contradiction to 
their character as a local tubercular process. In this connection the fact is of 
great practical importance that even the pressure paralyses may be completely 
restored, as far as the cause of the compression can be removed by the absorption 
of inflammatory and tubercular new growths, so that a complete and permanent 
recovery may take place even after the paralysis has lasted for some months, or 
a year, or even a year and a half. Such recoveries have been seen in a consider- 
able number of cases by others and also by ourselves. They are explained in part 
by the restoration of function in fibers which were rendered merely incapable of 
conduction by pressure, but not completely destroyed (page 937), and in part per- 
haps in old cases by the occurrence of regeneration. Fickler has made the inter- 
esting observation in the author's clinique that the ends of the pyramidal fibers in 
the lateral tract may grow out above an old compression, pass around the scar of 
the compression through the anterior fissure, and enter the cord below it to their 
anterior horns. 

Although, according to this, the prognosis in a part of the cases of pressure 
paralysis from spondylitis is comparatively good, still many other cases terminate 
unfavorably. The cause lies either in the occurrence of dangerous sequelae of 
the paralysis, such as bed-sores, cystitis, or pyelo-nephritis, with fever and in- 
creasing general weakness ; or in the development of other tubercular diseases, 
especially phthisis, or more rarely miliary tuberculosis or tubercular meningitis, 
which prove fatal. In some cases there is a stationary paralytic condition, since 
the vertebral disease recovers and sclerosis ensues in the cord, which is capable 
of no further change. 

2. The Pressure Paralyses in Cancer of the Vertebrae. — In pressure paralysis 
from cancer of the vertebras, which is not very rare, the spinal affection may 
seem to be primary, especially when the primary growth (breast, etc.) has not up 
to that time caused any very striking clinical symptoms. The first symptom is 
usually pain, both in the region of the new growth and radiating in neuralgic 
form. The pain becomes distressing if the tumor grows about and compresses the 
posterior roots ("paraplegia dolorosa"). The other spinal symptoms are pre- 
cisely analogous to those in compression of the cord by vertebral caries, and 
therefore they need not be described again in detail. Changes in the shape of 
the vertebral column sometimes occur, but we only rarely find a characteristic 
angular gibbus, as in vertebral tuberculosis. The general cancerous cachexia is 
usually soon apparent. The course is in general more rapid than in caries. The 
disease rarely lasts more than nine to eighteen months before its invariably 
fatal end. 

Diagnosis. — The frequency of the pressure paralyses of the spinal cord admon- 
ishes us to examine the vertebral column carefully in every case of spinal disease, 
especially if the case in question can not be referred to one of the special types of 
systemic diseases (vide infra). We should look especially for the stiffness of spe- 
cial parts of the vertebral column on movements of the head or trunk, and also for 
the pronounced tenderness of single vertebrae to pressure, and, finally, as a most 
important and most certain sign, for the deformity of the vertebral column, the 
marked projection of a single spinous process, or the formation of an evident 
angular kyphosis. If we find such a Pott's boss the diagnosis is easy, and we can 
then at any rate refer the existing cord symptoms to a compression of the cord 
caused by a disease of the vertebra 1 . 

The diagnosis is more difficult if the signs of an affection of the vertebrae be 
not evident. It must once for all be stated that vertebral caries does not inva- 



942 



DISEASES OF THE NERVOUS SYSTEM 



riably and necessarily result in a manifest knuckle, and that even the tender- 
ness of the vertebrae to pressure is sometimes very slight in spondylitis. In such 
cases the examination of the vertebral column must be repeated frequently, 
since even slight anomalies obtain a diagnostic value if constantly present; and 
the whole course of the disease is also to be considered. The most characteristic- 
features of a compression of the cord are its beginning with symptoms of sensory 
irritation, the persistent and more or less severe pain in the back, the preponder- 
ance of symptoms of motor paralysis with comparatively little disturbance of sen- 
sibility, and finally the frequent asymmetry of the symptoms on the two sides, 
which may even recall the type of the so-called " unilateral lesion " of the spinal 
cord (vide infra). Sometimes the cause of the spinal symptoms is at first obscure r 
and later on in the disease a marked anomaly of the vertebral column develops. 

If the diagnosis of an affection of the vertebrae be certain, the next question is 
as to the nature of it, especially whether we have to do with a spondylitis, or with 
a cancer of the vertebrae. Since spondylitis is by far the more frequent disease, 
we must always think of that first, especially in young people predisposed to 
tuberculosis, and where we have the formation of a pronounced angular kyphosis. 
In cancer of the vertebrae the coarser changes in the form of the vertebral column 
are generally less marked. This develops usually in older people, after the age 
of forty, and is manifested, as we have said, by the great intensity of the initial 
symptoms of sensory irritation. The discovery of a primary nodule of cancer (in 
women the breasts require particular examination) and, as we ourselves have- 
seen, the appearance of a cancerous swelling of the inguinal lymph-glands, may 
serve to support the diagnosis. Finally, a certain stress is to be laid on the well- 
known general habit of patients with cancer, on the peculiar cancerous cachexia, 
and on the whole course of the disease. 

In regard to the distinction between caries of the vertebrae and sarcoma of the 
dura mater, see the chapter on tumors of the spinal cord. 

The place of compression is, in the majority of cases, to be recognized by the 
evident localization of the disease of the vertebrae. In other respects the same 
rules hold for localization which we have given in detail in the second chapter of 
this section (page 920 et seq.). 

Treatment. — In regard to the special treatment of spondylitis, especially the 
orthopaedic treatment, we must refer to the text-books of surgery. The most 
benefit is to be expected from the various contrivances for extension of the spinal 
column. It can not be denied, and we have ourselves several times seen, that 
such extension sometimes produces a decided diminution of the pressure on the 
cord, which is followed by a remarkably rapid improvement of certain symptoms 
of paralysis. Such observations are strongly in favor of our theory that the ac- 
tion of vertebral caries is usually purely mechanical. Very often, however, we 
have had to admit that the extension apparatus was of no benefit or only of tempo- 
rary benefit, or that it even materially aggravated the patient's distress. In 
vertebral caries with co-existing spinal symptoms we must therefore use extension 
of the vertebrae, plaster jackets, etc., with caution. Surgical interference to re- 
move dislocated vertebrae, compressing masses of pus, etc., , has been repeatedly 
tried in vertebral caries, sometimes with benefit, but often without success. In 
most cases we shall be limited to a general symptomatic and dietetic treatment. 
Persistent rest in bed, on the back, is of the greatest importance, and it must 
always be strongly advised. Several cases of complete recovery from severe pres- 
sure paraplegia, which we have had under our own observation, were due to this 
alone. The most careful treatment of the general condition (fresh air, good food, 
cod-liver oil, arsenic, iron, etc.) of course also demands attention. We have seen 
very unfavorable action from Koch's tuberculine. Local applications to the verte- 
bral column are much used — dry cups, painting with iodine, and especially the hot 



ACUTE AND CHRONIC MYELITIS 



943 



iron. The use of the latter in spondylitis has even to-day warm advocates, and, 
in fact, deserves to be tried, the procedure with Paquelin's thermo-cautery being 
especially easy; we make some three or four eschars on each side of the diseased 
vertebrae. 

Among other remedies we may mention stabile galvanization at the point of 
pressure, and the electrical treatment of the paralyzed extremities ; also the use 
of baths, especially salt -baths. In regard to the symptomatic treatment, we will 
refer to the following chapter. 



CHAPTEE V 

ACUTE AND CHRONIC MYELITIS 

{Transverse Myelitis. Diffuse Myelitis) 

Definition and iEtiology of Myelitis. — " Myelitis " is the name we give to 
those inflammatory degenerative diseases of the spinal cord which develop pri- 
marily in the substance of the cord itself and lead to a more or less extensive 
destruction of the nervous elements. We know very little of the causes of these 
diseases, and of the precise nature and manner in which these causes exert their 
morbid influences. The name of myelitis has probably been used up to the pres- 
ent time for several quite distinct morbid processes, since it is often by no means 
easy to recognize the precise origin of the anatomical changes. At any rate, we 
must recognize this uncertainty in the definition of myelitis, and at least try as 
much as possible to keep separate the forms which surely do not belong in the 
same group. Thus we have said expressly in the previous chapter that the purely 
mechanical traumatic changes in the spinal cord are to be differentiated from 
true myelitis and that the inflammatory processes in these cases are at most sec- 
ondary. We must also emphasize the fact that anaemic necrosis of the cord from 
vascular obstruction (from primary endarteritis, thrombosis, or embolism of the 
vessels) does not seem to have the significance in the cord that it does in the 
brain, but that we must always bear in mind the possibility of its occurrence, and 
hold firmly to the fundamental distinction between such anaemic softening or 
infarction and primary degenerative inflammation. It is very difficult to deter- 
mine the position which syphilis holds in relation to the definition of myelitis. 
The distinction is, of course, easy in the rare cases where there is an actual 
gumma in the cord, but there are also a good many cases of apparently genuine 
degenerative myelitis in persons who have previously had syphilis. In these cases 
the anatomical findings often leave us in the lurch, if the question of the syphi- 
litic origin of the disease is to be answered with certainty. Even in cases where 
this origin is recognized, the way in which the syphilitic agent acts is still utterly 
obscure. Most stress is generally laid, of course, upon the " specific syphilitic " 
changes in the blood-vessels; but these criteria are not wholly unequivocal in 
their nature, and the question of the mutual relations between the disease of the 
vessels and the true parenchymatous changes still needs further discussion. It 
is, however, of great practical importance to know that syphilis apparently plays 
a considerable part in the aetiology of the spinal disease hitherto classed as mye- 
litis. The myelitis of the upper dorsal cord, which runs its course chiefly under 
the form of spastic spinal paralysis (q. v.), seems frequently to be due to previous 
syphilis. 

We can call only those processes genuine myelitis in which some excitants of 
inflammation act locally upon the substance of the spinal cord and cause diffuse 
inflammatory degenerative changes therein. Such genuine myelitides are decid- 



DISEASES OE THE NERVOUS SYSTEM 



edly rare, and little definite is vet known as to their causes. We sometimes 
see the disease develop in previously healthy persons, who are ignorant of any 
special harmful influence to which to attribute their illness. In other cases 
the blame is laid upon exposure to cold, repeated wettings, physical over-exer- 
tion (such as military maneuvers), etc. In women, the first symptoms of the 
disease sometimes follow childbed. These alleged causes, however, play ar 
most the part of an exciting cause. It is wholly out of the question that 
sexual excesses, as was formerly believed, can of themselves lead to anatom- 
ical disease of the spinal cord; the same is true of severe emotional disturb- 
ances. 

We may assume that the special cause of true acute myelitis is in all proba- 
bility some infectious germ. This has been maintained for some time in regard 
to acute poliomyelitis (q. v.) ; but the evidence is increasing in favor of the infec- 
tious nature of acute transverse myelitis also. Thus we have seen a case follow 
a felon, and staphylococci were found in the cerebro-spinal fluid, which was with- 
drawn by lumbar puncture. Eiirstner found pneumococci in the foci of inflam- 
mation in a case of acute disseminated myelitis. In short, it is probable that we 
shall obtain still clearer ideas of the aetiology of acute myelitis by continued in- 
vestigations. There is no doubt that infectious causes are to be considered in the 
rare cases of purulent inflammation of the cord (abscess of the cord) ; the same 
is true of the myelitides following acute infectious diseases (typhoid fever, 
small-pox, erysipelas, influenza, malaria, gonorrhoea, etc.). As to the causes of 
chronic myelitis — that is, of the " myelitic " transverse diseases of the cord 
which are chronic from the outset — our knowledge is the more uncertain since 
it is very hard strictly to define this morbid process. We will return to this 
point later. 

That secondary myelitis may arise by direct extension of the inflammatory 
process from the vicinity has been definitely determined only in acute purulent 
meningitis (especially the epidemic cerebro-spinal form) and tubercular menin- 
gitis. In the other cases formerly classed under this heading, we have to do. as 
has repeatedly been said, mainly with purely mechanical consequences. The 
hypothesis that neuritic processes may extend to the cord (ascending neuritis) 
we have already (page S86) characterized as doubtful and practically unim- 
portant. 

Pathological Anatomy. — Macroscopic examination of the cord in its fresh 
condition shows no marked pathological changes except in a small number of 
cases. At the first glance, the spinal cord often seems almost completely nor- 
mal, even if there have been severe spinal symptoms during life, and sometimes 
the opacities and adhesions of the pia, which often strike us at first, have no prac- 
tical importance. If we test the consistency of the cord carefully by touching it. 
of course a change in it often strikes the practiced examiner, since the cord over a 
definite extent is either softer and more flexible, or, on the other hand, harder and 
firmer, than normal. If we now make a number of cross-sections through the cord, 
we notice that the substance of the cord rises up more on section, that the outline 
of the gray matter is less distinct, and especially that the white matter is of a 
reddish-gray color, and that sometimes there is also a reddish, hyperaemic coloring 
of the gray matter. In some cases we can recognize small capillary haemorrhages 
with the naked eye. The more acute the disease the softer, as a rule, is the cord 
in the part diseased (" acute inflammatory softening "). If the disease is chronic 
or if some time has elapsed since the expiration of the acute initial stage, the cord 
in the diseased spot is denser, firmer, and sclerosed, and grayer in color on section, 
but it is not possible to determine precisely in the fresh cord the extent and degree 
of the disease. 

The changes are much more plainly visible if we harden the cord in chromic 



ACUTE AXD CHRONIC MYELITIS 



945 



acid, or Mutter's fluid," for at least eight or ten weeks. All the normal parts of 
the white matter of the cord assume a dark-green color, which is really due to the 
staining of the medullary sheaths by the chromic acid. The diseased portions, in 
which the medullary sheaths are mainly if not entirely absent, are thus often 
very sharply distinguished from the healthy, dark-green portions. Since similar, 
although less sharply defined, differences in color between healthy and diseased 
tissue are also noticed in the gray matter, the cross-section of the cord, well 
hardened in chromic acid, usually gives quite a correct idea of the extent of the 
disease. 

We obtain more precise disclosures, however, as to the form of the anatomical 
changes by microscopical examination. When made on the fresh, unhardened 
cord, it affords little information. The presence of numerous granular cells (vide 
infra) in fresh teased-out preparations is the only thing that is important, since 
they show with certainty the existence of a pathological change. If, however, we 
make thin cross-sections of the hardened cord, and stain them with carmine or 
some similar staining fluid, even the naked eye notices at once a marked difference 
between the diseased and the healthy tissue, since the former, which is almost 
always richer in connective tissue, has a much darker staining, and thus is dis- 
tinguished from the brighter normal tissue. The microscopic examination now 
shows that in the diseased parts the normal nerve-tissue has been almost wholly 
or at least partly destroyed. Only occasionally do we see nerve-fibers of normal 
appearance remaining here and there. In other places the fibers that are still 
visible are smaller and atrophied, and the axis-cylinders have in part lost their 
medullary sheaths, or are swollen. The changes in the ganglion-cells are harder 
to follow, but in more advanced cases they also show marked signs of destruction ; 
they are contracted, rounder, and have lost their processes. The increase of the 
neuroglia tissue corresponds to the destruction of the nerve-substance. The 
meshes of the neuroglia extend and swell, so that the space formed by the destruc- 
tion of the nerve-tissue is in great measure taken up by connective tissue. The 
older the process, the firmer and more fibrous is the connective tissue. The 
nuclei of the neuroglia increase in number, and we often find a very great increase 
in those peculiar, flat cells with many processes, first described by Deiters, and 
named after him — the so-called " Deiters' spider-cells." The fatty granular cells 
are also easily recognized in hardened preparations, provided they are not treated 
with alcohol. They lie in the interstices between the meshes of the neuroglia, 
and are especially numerous about the vessels. They are to be regarded either as 
white blood-corpuscles, or perhaps as endothelial cells from the sheaths of the 
vessels, which have taken up the fat from the disintegrated nerve-substance. If, 
therefore, the process be still fresh, or if it be still advancing, the fatty granular 
globules are to be met with in great numbers, while in old, sclerosed nodules, only 
a few of them, or scarcely any, are to be found. The changes in the vessels are 
usually very striking. They are often dilated and congested. Here and there 
there may be haemorrhages. The vascular walls are thickened, especially in old 
cases, and sometimes have become peculiarly homogeneous — " hyaline degenera- 
tion " ; and a large accumulation of nuclei, lines of fatty granular cells or peculiar 
epithelioid cells, may be found about the vessels. The so-called corpora amylacea 
are sometimes present in chronic cases in great numbers, and sometimes they 
are only scanty. Their significance and their genesis are still unknown. 

The extent of the whole process varies very much in different cases. We usu- 
ally find one main focus of myelitis, which extends in a diffuse manner over the 
greatest part of the transverse section of the spinal cord, and which may reach up- 



[* The formula for Midlers fluid is as follows : Two and a half parts of potassic hiehromate, one 
part of sodic sulphate, and one hundred parts of water. — K.J 
60 



946 



DISEASES OE THE XEKYOUS SYSTEM 



ward and downward for a space of five to ten centimetres or more. The dorsal por- 
tion of the cord is most frequently affected (dorsal myelitis), the upper half being 
usually most involved, but in some cases the lower half is chiefly affected- 
]STearly the whole of the dorsal cord is often the seat of a diffuse inflammatory 
affection, which, of course, differs in extent at different levels. In other much 
rarer cases the chief focus of disease is in the cervical cord (cervical myelitis), 
somewhat more frequently in the lumbar cord (lumbar myelitis). We often find 
small, distinct foci in the vicinity of the main focus. In all severe and long-con- 
tinued cases there develops later a systemic ascending and descending second- 
ary degeneration (vide infra). 

Acute disseminated myelitis has a special form of anatomical distribution 
It occurs in many small foci which may extend almost throughout the whole length 
of the cord. Individual columns of the cord, especially the posterior columns, 
are often chiefly affected. In rare cases, as has already been said, true purulent 
inflammation — that is, circumscribed abscess with purulent breaking down of 
tissue — has also been observed. 

The Individual Symptoms of Myelitis. — The course of transverse myelitis 
differs so much in different cases that it is impossible to give a picture of the 
disease which will be generally applicable. According as one or another part of 
the cord is involved, the clinical symptoms will relate chiefly to the sensibility or 
the motility, the trophic functions or the reflexes, and will be present in the upper 
or the lower extremities, or in both at once. The following description will, there- 
fore, be devoted first to the single symptoms, and will give the inferences which, 
according to the present state of our knowledge, may be drawn from their pres- 
ence as to the seat and the extent of the anatomical process ; not until then will 
we endeavor to distinguish the different clinical forms of myelitis. 

1. Symptoms of Motor Paralysis are not only the chief symptoms, as a rule, 
in well-developed myelitis, but are often the first sign of the beginning of the dis- 
ease. The patient feels at first only a slight weakness in one or both legs ; he gets 
tired more easily in walking, and begins to " drag " his legs after him. Sooner or 
later the motor weakness gradually becomes greater and increases to complete 
paralysis. The patient is then bed-ridden, and, finally, can not make the least 
active movement with his legs. The symptoms of paralysis in the arms are 
analogous. 

Since the chief paths for the conduction of voluntary motion are situated, as 
we have seen, in the lateral columns of the spinal cord, and especially in the 
lateral pyramidal tract, we conclude, in every spinal disease where symptoms of 
paralysis are present, that there is an interruption of this tract — that is, an 
implication of the posterior portions of the lateral columns. Since in transverse 
myelitis the whole cross-section of the cord is more or less involved, the paralysis 
also extends to the two halves of the body : motor paraplegia is the characteristic 
form of paralysis for transverse myelitis. Paraplegia of the lower extremities 
may of course arise wherever the myelitis is situated, whether in the lumbar, 
dorsal, or cervical region ; but the upper extremities necessarily remain entirely 
free in every dorsal or lumbar myelitis. The occurrence of paretic symptoms 
here, and the final development of a brachial paraplegia, point with certainty to 
an implication of the cervical region, to a cervical myelitis. If the symptoms of 
paralysis are not alike in the two corresponding extremities, but are more marked 
on one side than on the other, the anatomical affection must also be more intense 
on that side of the cord than on the opposite side. 

2. Symptoms of Motor Irritation of various sorts are often seen, both at the 
beginning and during the whole course of myelitis. Single twitchings come on 
spontaneously in the limbs, which are at the same time paralyzed, or at least 
paretic, and these twitchings are short and rapid or slow and persistent. The- 



ACUTE AND CHEOXIC PYELITIS 



947 



thighs are drawn up on the abdomen, or there are severe spasms of the extensors. 
The interpretation of these symptoms is not always easy. It is often particularly 
hard to decide whether they are the result of a direct irritation of motor fibers 
in the cord, or whether they represent reflexes (vide infra). The value of the 
symptoms of motor irritation for the localization of the disease is accordingly 
slight, but, of course, in these cases we must consider chiefly the motor tracts in 
the lateral columns. 

3. Ataxia. — There can be no doubt that actual ataxia also occurs in transverse 
myelitis, but it is rarely pronounced because the co-existing spastic or paralytic 
symptoms, which are almost always present, of course conceal the ataxia. We 
therefore see evident ataxic disturbances rather in slow cases which do not 
speedily become paraplegic, or sometimes not until the disease improves. In re- 
gard to the localization of the disease, we may usually conclude, when there is 
ataxia, that the posterior columns are involved. Very marked ataxia of the 
arms and legs occurs in the acute disseminated myelitis of the posterior 
columns. 

4. Distukbaxces of Sensibility. — The disturbances of sensibility usually ap- 
pear to a marked degree only in the later stages of the disease. At the outset we 
generally notice merely mild symptoms of sensory irritation in the legs, such as 
formication, prickling, numbness, a woolly feeling, etc., while severe pain is hardly 
ever present in transverse myelitis, and hence it always points rather to some 
affection of the vertebras or the meninges. In very acute myelitis there may be 
at first a severe local pain in the back. Slight diminution of sensibility is often 
to be made out early on careful examination, but, in many cases, the sensibility 
remains for a long time wholly, or almost wholly, intact, either because the locali- 
zation of the disease spares the sensory portions of the cord, or because the sen- 
sory paths of conduction are more resistant, or they can act vicariously for one an- 
other to a higher degree. The more carefully we examine, the earlier shall we be 
able as a rule to find at least partial disturbances of sensibility. The examination 
of the sensibility to temperature, especially, should never be neglected. Partial 
anaesthesia of the pressure sense, analgesia, etc., also occur. We must also pay 
attention to the not uncommon delayed sensibility to pain (page 793). In the 
further course of the disease, however, there are almost always more marked dis- 
turbances of sensibility, and finally frequently a complete anaesthesia. On the 
other hand, we see in many cases a striking hyperaesthesia to painf til stimuli, such 
as a pin-prick. 

From the presence of marked disturbances of sensibility we can conclude with 
certainty that there is an affection of the posterior col um ns, and especially of the 
posterior cornua of the gray matter. With marked analgesia and thernio-anags- 
thesia the latter are always involved. Disease of the lateral columns also may 
probably cause disturbances of sensibility (page 799). 

The disturbance of sensibility gives important service in estimating the height 
at which the affection in the cord is situated. If we search on the trunk for the 
line where the cutaneous sensibility becomes normal, we may from this determine 
the upper boundary of the myelitis in accordance with the data furnished on 
page 924; but since each cutaneous region, as has been said, is supplied with 
sensory fibers from at least two or three spinal segments, we must look for the 
upper boundary of the disease not simply in the segment corresponding to the 
upper boundary of the anaesthetic area, but one or two segments higher. In 
myelitis in the lumbar region the disturbance of sensibility reaches to the 
umbilicus, or even a little higher; in myelitis in the lower dorsal region it reaches 
about to the lower end of the sternum; in myelitis in the upper dorsal region to 
the level of the axilla?: and in ceiwical myelitis the sensibility of the upper ex- 
tremities is also impaired, but complete anaesthesia is very rare. 



948 



DISEASES OE THE KEKVOUS SYSTEM 



5. Cutaneous Reflexes. — As is generally assumed, the reflex arcs in the cord 
are found at about the same level as the centripetal sensory and the centrifugal 
motor fibers. They are also connected with fibers which come from above and 
have properties of reflex inhibition. If these fibers above the reflex arc are put 
into a state of irritation, the reflex is thereby impaired; but if the conduction 
be broken in these fibers, the reflex activity appears increased, the reflex comes on 
with a weaker irritation, and the contraction is more vigorous. If the reflex arc 
itself be broken at any point, the reflex must disappear. 

The data from the examination of the patient may generally be harmonized 
with this scheme, although, of course, the reality probably shows more compli- 
cated conditions. In extensive lumbar myelitis, by which the reflex path in the 
lumbar cord is broken, the cutaneous reflexes in the lower extremities must be 
diminished or absent. In these cases the loss of sensibility runs about parallel 
to the diminution of the reflexes. In dorsal and cervical myelitis, however, the 
reflex arc in the lumbar cord remains unimpaired, but the conduction of sensory 
impressions to the brain may very well be interrupted. In these cases the cutane- 
ous reflexes are retained, even when there is anaesthesia ; or, if the reflex inhibitory 
influences be removed, they are decidedly increased. [There is often dorsal ex- 
tension of the great toe on irritating the sole of the foot — the Babinski reflex. 
— K.] The cutaneous reflexes in the legs, however, may also be diminished or 
delayed in myelitis of the lower dorsal cord, in which case we must imagine as 
a rule a secondary loss of excitability of the fibers and cells presiding over the 
reflex, or perhaps an irritation of inhibitory fibers. It is often important in 
determining the seat of myelitis to examine the cremaster reflex, the abdominal 
reflex, etc. If the reflex paths described above (page 927) be interrupted, the 
reflexes of course must be absent. 

6. Tendon Reflexes. — The same rules generally hold in judging of the ten- 
don reflexes as are to be considered in judging of the condition of the cutaneous 
reflexes. We know that the reflex arc of the patellar reflex is at the level of the 
second to the fourth lumbar segments (page 927). If the entrance zones of the 
posterior sensory roots or the ganglion-cells in the anterior horns be diseased at 
this level, the patellar reflex must disappear. The Achilles tendon reflex and the 
ankle clonus have their reflex arcs in the sacral segments of the cord. The Achilles 
tendon reflex is always absent in extensive disease of the posterior columns and 
of the gray matter in the corresponding portion of the lumbar cord. The absence 
of the tendon reflexes in the lower extremities is therefore one of the most impor- 
tant points besides the other symptoms for the diagnosis of a myelitis of the lum- 
bar cord. In almost all inflammations above the lumbar cord — that is, in dorsal 
and cervical myelitis — there is, however, a very decided increase of the tendon 
reflexes, the result, as we must suppose, of the loss of the reflex inhibitory influ- 
ences. We have much reason to assume that the fibers which influence the condi- 
tion of the tendon reflexes run chiefly in the lateral columns (pyramidal tract) of 
the spinal cord, but that they are not identical with the fibers of the lateral pyram- 
idal tracts which serve for voluntary motion (see the chapter on spastic spinal 
paralysis). We may therefore assert that, with a considerable increase of the ten- 
don reflexes in the lower extremities, the seat of the myelitis must be above the 
lumbar cord — that is, in the cervical or dorsal cord — and that in these cases we 
have to suppose that the lateral columns are chiefly implicated. In cervical 
myelitis the tendon reflexes in the upper extremities are often considerably in- 
creased. 

We have already said, on page 840 et seq., what is necessary in regard to the 
different signs of the increased tendon reflexes, the exaggerated patellar reflex, 
ankle clonus, the periosteal reflexes, etc. The peculiar character which the 
paralysis of the legs assumes from a considerable simultaneous increase of the 



ACUTE AND CHBONIC MYELITIS 



949 



tendon reflexes (spastic paraplegia) will be described more fully in the chapter 
on "spastic spinal paralysis " (vide infra). 

7. Disturbances in the Bladder and Eectum. — Disturbances in micturition 
are one of the commonest symptoms of myelitis. The first manifestation is usu- 
ally a difficulty in micturition ; the patient has to strain and to wait longer before 
urinating. There may finally be a complete retention of urine from paralysis of 
the detrusor urinae. In the later stages of the disease, however, there is usually a 
paralysis of the sphincter vesicae, and consequently more frequent desire to 
micturate, and finally incontinence of urine. The disturbances of the bladder 
give no points for the localization of myelitis, since they may occur with disease 
at any level of the spinal cord ; but we believe we are right in assuming that they 
always permit us to decide that the posterior columns of the cord are involved. 

The clinical significance of disturbances of the bladder in myelitis, and in 
many other diseases of the cord, apart from the great distress and discomfort for 
the patient, lies in the fact that they very often — almost always in severe cases — 
give rise to the development of cystitis. In retention of urine the use of the 
catheter, by which inflammatory irritants are often brought into the bladder, in 
spite of all attempts at disinfection, leads to decomposition of the urine and to 
cystitis ; but where there is also incontinence, the imperfect closure of the sphinc- 
ter and the constant presence of stagnating and decomposing urine in the urethra 
are the causes of the entrance of these irritants into the bladder. If cystitis have 
developed, it may be followed under some circumstances by pyelitis and purulent 
pyelo-nephritis (q.v.), which conditions are often the immediate cause of death 
from the sequelae connected with them, such as fever — sometimes associated 
with chills — general weakness, and emaciation. 

Defecation is also disturbed in many cases of myelitis. There is usually con- 
stipation at first, which may depend either upon weakness of the intestinal peri- 
stalsis, or upon paresis of the abdominal muscles. Sometimes the constipation 
reaches such a degree that the bowels move only at intervals of one or two weeks. 
In many severe cases there is finally incontinence of faeces, as a result of paralysis 
of the sphincter ani. We can give no details as to the localization of the nerve- 
tracts in the cord which take part in defecation. 

We have yet to note that micturition and defecation are often aroused reflexly 
in an abnormal fashion where there is increased reflex irritability. On irritation 
of the skin over the thighs, the perineum, the gluteal region, etc., there is often an 
involuntary contraction of the bladder, associated with loss of urine. 

In conclusion, we may mention, as an addendum, that the sexual functions are 
often considerably disturbed in many cases of myelitis, and finally they may be 
wholly lost. 

8. Trophic Disturbances. — The trophic condition of the paralyzed muscles 
affords extremely important points for diagnosis. In cervical and dorsal myelitis 
the trophic centers in the lumbar cord for the muscles of the legs remain intact ; 
the paralyzed muscles, therefore, retain essentially their normal volume, and espe- 
cially their normal electrical excitability. Even in such cases the muscles are 
sometimes flabbier and of less girth than under normal conditions, but this 
depends partly on the decline in the general nutrition, and partly perhaps on the 
lack of movement, the " atrophy of inactivity." Only occasionally do we find 
more marked muscular atrophy, but without reaction of degeneration; but if 
we find in myelitis a marked atrophy, with reaction of degeneration in the muscles 
of the lower extremities, we can from this draw a definite conclusion that the 
anterior gray cornua or the fibers of the anterior roots in the lumbar cord are 
affected (see page 851). In an analogous fashion degenerative atrophy with 
reaction of degeneration in the muscles of the upper extremities points to an 
affection of the anterior gray matter in the cervical cord. 



950 



DISEASES OE THE NEKVOTJS SYSTEM 



Trophic disturbances in the skin are also frequent. We often find the skin 
dry, hard, with a scaly epidermis, and the nails thickened and brittle. Excep- 
tionally there are eruptions of herpes, urticaria, etc. Yaso-motor disturbances 
also occur. Sometimes the paralyzed extremities show a mottled, cyanotic redden- 
ing, and feel cold. Slight oedema is quite frequently present in the paralyzed 
parts. Disturbances of the sweat secretion are not infrequent. We find either 
that it is absent or that there is a great increase in it, so that the paralyzed parts 
are constantly moist. All these symptoms have no value at present for the special 
topical diagnosis. 

The frequent occurrence of bed-sores in the sacral region, over the glutaei, or 
more rarely over the trochanters on the feet or the inner side of the knees, is of 
great practical importance. Although trophic and vaso-motor influences may play 
a part in their origin, still their ultimate cause is always to be found in external 
conditions, pressure, uncleanliness, etc. The more faulty the care of the patient 
is, the easier bed-sores arise. With completely paralyzed and anaesthetic patients, 
with incontinence of urine and faeces, of course they sometimes can not be wholly 
and permanently avoided, even with the most careful management. The extent 
which a bed-sore may reach is sometimes absolutely frightful. A large part of 
the sacrum may be laid bare, after the overlying soft parts and the periosteum 
have become gangrenous and been thrown off. 

9. Disturbances in the Eegion of the Cerebral Nerves are entirely absent 
in most cases of transverse myelitis. In rare cases of cervical myelitis the pro- 
cess may gradually extend upward and give rise to bulbar symptoms. We some- 
times see changes in the pupils in cervical myelitis, such as inequality and spinal 
myosis ; and finally myelitis has been repeatedly combined with an optic neuritis. 
In general, however, any co-existing cerebral symptoms always require a special 
explanation. They are either co-existent from the same cause (for example, 
syphilis), or, instead of an ordinary transverse myelitis, there is multiple scle- 
rosis, or some other disease. 

Different Forms of Myelitis. Acute and Chronic Myelitis. — The whole pic- 
ture of transverse myelitis in its different forms may be constructed from the 
symptoms described in detail in the preceding paragraphs. We can usually 
determine without difficulty, at least approximately, the seat and extent 
of the disease. If we group the chief symptoms of the different forms of mye- 
litis together, according to the location of the disease in the cord, they are 
as follows: 

Cervical Myelitis. — Paraplegia of the legs, combined with more or less ex- 
tensive disturbances in the upper extremities, and eventually disturbances of 
sensibility over a like extent. At times atrophy of single muscular regions in the 
arms. Xo marked atrophy in the legs. Increased tendon reflexes and spastic 
symptoms in the legs and often in the arms. Cutaneous reflexes in the legs re- 
tained, and sometimes even increased. Disturbances of the bladder and rectum. 
Sometimes changes in the pupils. 

Dorsal Myelitis. — Upper extremities free. Motor, and eventually sensory, 
paraplegia of the legs, without degenerative atrophy. Increased tendon reflexes 
and pronounced spastic symptoms in the legs (especially in myelitis in the upper 
dorsal cord) ; cutaneous reflexes retained, sometimes increased. Disturbances 
of the bladder and rectum. 

Lumbar Myelitis. — Upper extremities free. Motor, and eventually sensory, 
paraplegia of the legs. Cutaneous and tendon reflexes in the legs diminished or 
absent. Under some circumstances degenerative muscular atrophy in the legs 
with reaction of degeneration. Disturbances of the bladder and rectum. In 
myelitis of the lower sacral cord the paralysis is confined chiefly to the distribu- 
tion of the sciatics and the bladder and rectum. The disturbance of sensation is 



ACUTE AND CHRONIC MYELITIS 



951 



found on the posterior aspect of the thighs, the buttocks, and the genitals (page 
925). 

The above division of the different forms of myelitis refers only to the 
different locations of the disease and the difference in symptoms thereby pro- 
duced, so that we must further discuss the division of myelitis into an acute 
and a chronic form. This division is made solely by observing the course of the 
disease, or from the statements in the history of the case as to duration; but 
we must bear in mind that this refers only to the first stage of the disease, to 
the rapidity with which the myelitic symptoms develop at the start. In most cases 
of genuine primary myelitis the myelitic symptoms come on very suddenly, lead in 
a very short time (sometimes in a few days or a few weeks) to the most complete 
paralysis (paraplegia, vesical paralysis, anaesthesia, bed-sores, etc.), and advance 
irresistibly, causing death in a short time (from four to twelve weeks). Such 
cases are, of course, called acute transverse myelitis. "We sometimes see, how- 
ever, the disease beginning acutely, and rapidly developing a more or less com- 
plete paraplegia, which after some time remains entirely stationary, or at least 
shows only extremely slight further changes. Such cases must also be classed 
definitely as acute myelitis, although they present later a chronic type of spinal 
disease, which sometimes lasts for many years ; but they are also undoubtedly cases 
of acute myelitis, ending in relative recovery — that is, in recovery with a scar or 
defect in the cord. We can call only those cases actual chronic myelitis which 
are chronic from the first — that is, which begin slowly and progress gradually — 
but such forms of actual chronic myelitis are very rare, for the not very rare 
cases which seem to belong under this heading during life usually prove at the 
autopsy, at least as far as our experience goes, to be something different — multiple 
sclerosis, tumor, combined columnar or systemic disease, etc. We might rather 
speak of chronic myelitis in those cases which have an acute initial stage, and 
then take later a chronic progressive course. At any rate, in our definition of 
chronic myelitis we must pay especial attention to the clinical course and an 
accurate history, for the pathological lesions alone can not be conclusive. The 
pathologist can not determine whether a given transverse sclerosis of the cord 
is the result of a process chronic from the first or of a long-past acute process. 

We can not give at present a definite picture of acute disseminated myelitis. 
We would be most ready to suspect this form of myelitis if an acute type of 
spinal disease developed apparently primarily or especially as a sequel of some 
previous acute infectious disease, and if it indicated an isolated or combined 
columnar affection rather than a transverse affection. Acute ataxia with loss of 
tendon reflexes and evident vesical disturbances, or a combination of ataxia with 
paresis and spastic symptoms, have been most frequently observed. 

Eecovery from acute myelitis is perhaps not impossible, but it is certainly 
very rare. We know of no case that recovered completely where the diagnosis 
could be made with certainty. The cases reported where a recovery is claimed 
are usually cases of pressure paralysis, multiple neuritis, poliomyelitis, etc. 
We may speak somewhat more frequently of relative recovery if the severe initial 
■symptoms subside in part and change to a mild, stationary, morbid state. The 
fatal termination of acute or chronic myelitis is the result of the general weak- 
ness which finally sets in; or it comes from cystitis or pyelo-nephritis, both of 
which are often combined with pysemic conditions ; or from extensive bed-sores ; 
or finally from some complication, such as tuberculosis or acute diseases. 

Diagnosis. — The diagnosis of diffuse transverse myelitis is always made by 
considering the whole group of symptoms prominent in the individual case. The 
possibility of a compression of the cord must be excluded by a careful examina- 
tion of the vertebral column, and by consideration of the course of the disease. 
We must also be sure that the existing symptoms do not correspond to a definite 



952 



DISEASES OE THE NERVOUS SYSTEM 



typical disease, or a systemic disease, but that they can agree only with the 
assumption of a diffuse transverse disease at a certain point in the cord, to be 
made out accurately according to the symptoms. The further decision, as to 
whether this diffuse transverse disease is a myelitis, may be made quite positively 
in acute cases or cases beginning acutely, but in cases chronic from the outset 
it can hardly ever be made definitely, for precisely the same type of disease may 
sometimes be produced by multiple sclerosis (q. v.), by new growths in the cord 
(glioma), and finally by combined systemic disease. In the description of all 
these diseases we will once more return to the likeness sometimes observed be- 
tween them and transverse chronic myelitis. 

Treatment. — Although our therapeutic endeavors are rarely crowned with per- 
manent and complete success, still in many cases we can relieve the suffering and 
delay the end. 

We can try to meet the causal indication in cases where the history or the 
examination shows evidence of the existence of previous syphilis (page 943). 
Even if the connection between previous syphilis and myelitis can not be as- 
sumed with absolute certainty — and usually it can not — still we must always try 
inunction thoroughly, using half a drachm to a drachm (grammes 3-5) of mer- 
curial ointment a day. We give twenty to thirty grains (grammes 1.5-2.0) of 
iodide of potassium daily at the same time. We sometimes see decided improve- 
ment from this; but in some cases, of course, the result is uncertain, or the treat- 
ment seems to exert even an unfavorable influence upon the disease. In the 
latter case we must stop it at once. 

Of the other methods of treatment the chief are electricity, baths, and cold- 
water cures. We alternate these. New attempts at cure raise the patient's cour- 
age and hope afresh. 

Electricity may give symptomatic improvement in many cases, but of course 
it causes recovery only exceptionally, at most. In severe and hopeless cases, how- 
ever, it is at least the best means of consoling the patient. The constant current 
has the greatest therapeutic value. We use large electrodes placed on the verte- 
bral column, and pass not too strong a stabile or slowly labile current through the 
cord for about four or five minutes, chiefly through the region where we suppose 
the seat of the disease to be. We usually take the ascending current, and alter- 
nate with the two poles on the diseased part. We should avoid reversals and great 
variations in the strength of the current. We associate with this peripheral gal- 
vanization, and often faradization of the muscles and nerves of the paralyzed ex- 
tremities. Single symptoms sometimes deserve special attention — faradization of 
the skin in anaesthesia, galvanization of the bladder in vesical weakness, etc. The 
sittings should take place daily or every other day. If we would be successful, the 
treatment must be kept up persistently for months. 

The treatment of myelitis by baths, if prudently used, may also be of evident 
service. Even simple tub-baths, such as can be had in almost every household, 
do good service under some circumstances. The chief rules are never to make the 
baths too warm — about 88° or 95° at most (25°-28° R.) — to limit them at first to 
ten or fifteen minutes, and to give them at first not oftener than three or four 
times a week. Sometimes hot baths (95°-100° F. [28°-30° R.] or more) seem 
to act well, but in other cases they certainly are injurious. If the baths are well 
borne, they may be employed daily. We should be most cautious in incipient and 
still advancing cases. The best action of the simple warm bath is seen in chronic 
myelitis with predominant spastic symptoms. In these cases the duration of the 
baths may be increased to on hour or more. Sometimes the bnths work still 
better when certain substances are added, especially if we use salt-baths, which 
are made by the addition of five or ten pounds of common salt (Stassfurt salt), 
or four to six pounds of brine salt, or one to three quarts of brine to the water. 



ACUTE AND CHRONIC MYELITIS 



953 



By introducing carbonic acid into the water through a perforated tube in the floor 
of the tub we can easily make artificial carbonic-acid salt baths. 

If we can send patients in easy circumstances to a health-resort, the carbonic- 
acid thermal salt springs at Oeynhausen and !N auheim are most suitable for this 
purpose, also the baths at Kissingen, Wiesbaden, and Baden-Baden, the thermal 
baths of Ragatz, Teplitz, Wildbad, and Gastein, the mud-baths in Elster, Marien- 
bad, etc. 

A methodical cold-water treatment sometimes gives quite good results ; but in 
these cases we should wholly avoid all the more heroic treatments, such as douches, 
violent rubbing, and very cold baths, and employ only short, cool, full or half 
baths or packs or mild cold sponging. Hydrotherapeutics are usually combined 
with electricity. 

We can expect but little success from internal treatment, but it can not be 
dispensed with in practice. A trial of strychnine (subcutaneously or by the 
mouth) is most to be recommended, and also ergotine, nitrate of silver, and espe- 
cially iodide of potassium. Salicylate of sodium may be tried in fresh acute cases. 

The general hygienic and symptomatic treatment is very important. If the 
first symptoms of a beginning spinal disease show themselves, we should urgently 
advise the patient to take the best possible care of himself (avoiding all physical 
over-exertion), and to enjoy mental rest. The diet should be strengthening but 
easily digestible. Large amounts of spirits, much smoking, much tea and coffee, 
etc., are to be avoided. If the patient becomes bedridden, we must employ the 
utmost care to get a good bed in order to guard against bed-sores. In severe 
cases, especially where there are disturbances of sensibility, a water-cushion is 
most desirable. The patient's position must also be frequently changed, and the 
sacral region must often be washed and rubbed. Every incipient bed-sore must 
be very carefully treated by Peruvian balsam ointment (1 to 30), iodoform, 
salicylate plaster, or mercurial plaster, which acts very well, in order to 
prevent its spreading. When the bed-sore is very extensive the continuous bath 
is the best remedy. 

If there is retention of urine and the patient has to be catheterized, the most 
extreme care must be employed in cleaning and disinfecting the catheter, or else 
cystitis will develop in a few days. If it does, it is best in severe cases to wash 
out the bladder regularly with boracic-acid solution, permanganate of potassium, 
and like remedies. In milder cases we may try chlorate of potassium internally, 
fifty to seventy-five grains a day (grammes 3-5), salol, urotropine, or balsams. 
If there is complete incontinence it is advisable to introduce a permanent cath- 
eter (sonde a demeure) into the bladder — that is, a JSTelaton's catheter, which lies 
in the bladder and is fastened to the thighs by strips of plaster. The urine runs 
away through a rubber tube, and we avoid the constant wetting of the skin and 
linen. In men, good urinals are often perfectly satisfactory, but in women, their 
application usually causes great difficulties. 

Constipation must be met according to the general rules. We should be as 
sparing as possible with cathartics at first, and try to make an appropriate diet 
and enemata suffice. If there is severe pain, subcutaneous injections of morphine 
are unavoidable, but we always delay this as long as possible, although finally we 
let the dose of morphine be unlimited in hopeless cases. 



954: 



DISEASES OF THE KEKVOUS SYSTEM 



CHAPTEK VI 



MULTIPLE SCLEROSIS OF THE BRAIN" AND SPINAL CORD 

(Disseminated Nodular Sclerosis. Sclerose en plaques) 

.ZEtiology and Pathology. — Multiple sclerosis of the central nervous system 
is a special chronic form of disease, whose anatomical basis consists in the devel- 
opment of numerous disseminated "sclerotic nodules" (vide infra) in the brain 
and cord. We know practically nothing as to its aetiology, for the significance of 
exposure to cold, over-exertion, and mental emotions, sometimes given as causes of 
the disease, is wholly doubtful. It is also very improbable that syphilis plays any 
part in the aetiology of multiple sclerosis. P. Marie claims to have seen the dis- 
ease come on very frequently as a consequence of some acute infectious disease 

(typhoid fever, scarlet fever, etc.), 
and therefore he suspects that the dif- 
ferent foci of disease have an infec- 
tious inflammatory origin; but our 
own experience does not permit us to 
confirm this, nor does our experience 
pronounce in favor of a relation be- 
tween multiple sclerosis and chronic 
intoxication, as Oppenheim supposes; 
on the contrary, in the majority of 
our own observations we could find ab- 
solutely no material external cause, in 
spite of careful inquiry. We are 
therefore disposed to regard the dis- 
ease as of endogenous nature, as a 
multiple gliosis due to congenital ab- 
normal predisposition. The anatom- 
ical data also harmonize very well 
with this view. Any injury preceding 
the development of the disease, acute 
diseases, intoxications, emotional dis- 
turbances, etc., would therefore act at most as exciting causes. If, however, a 
" disseminated myelitis " should actually at any time follow an acute disease and 
lead to the formation of multiple, sclerotic nodules in the nervous system with 
corresponding symptoms, this would be an affection similar to multiple sclerosis, 
but yet essentially different. 

A hereditary predisposition seems to be present in only a few cases. The 
affection occurs chiefly in youth, somewhere between the ages of eighteen and 
thirty-five, but we have ourselves seen one case, which came to an autopsy, in a 
man of sixty. The disease also occurs in children. ISTo material distinction has 
been made out as to sex. 1 

In regard to the development of the different sclerotic nodules, nothing defi- 
nite has been established at present as to their genesis. The suspicion has re- 
peatedly been uttered that the disease is due to primary changes in the vessels, 
but no proof of this can be given. » The nodules are in part easy to recognize with 
the naked eye, from their gray color, and we can also feel an increased resistance. 
They are scattered over the whole central nervous system. Their favorite seats 
in the brain are the centrum ovale, the walls of the lateral ventricles, and the 
corpus callosum; but on careful examination we usually find many nodules in the 
gray matter of the central ganglia and the cortex; the nodules are also quite 




Fig. 128. — Distribution of the sclerosed nodules on 
the surface of the pons. 

(From Leube.) 



MULTIPLE SCLEKOSIS OF THE BRAIN AND SPINAL CORD 955 






abundant, as a rule, in the pons, less frequent in the medulla, and very abundant 
and variously distributed in the cord (see Figs. 128 and 129), chiefly in its 
white substance. Examined microscopically, the nodules consist of an abundant, 
reticulated, fibrillary neuroglia tissue, in which the nerve-fibers are lessened in 
number, but, as a rule, not wholly destroyed; on the contrary, we usually find 
many axis-cylinders preserved in the nodules, as Charcot first 
found and as has often been confirmed since by other observers. 
This fact is important clinically, because it explains why multi- 
ple sclerosis only rarely or only in its advanced stages leads to 
complete paralysis. It also indicates, as it seems to us, that the 
process does not start from the nervous tissue, but from the 
interstitial neuroglia tissue. It also explains the remarkable 
fact that the ordinary secondary degenerations are almost al- 
ways absent, in spite of the presence of many nodules in the 
spinal cord. In the vessels we usually notice thickening of the 
walls, which may be surrounded by neuroglia cells. The author 
regards these changes as of secondary nature. Fatty granular 
cells are often to be found in fresh cases. 

Clinical History. — From the variations which the number 
and the localization of the nodules show, it may be understood 
from the outset that a picture of the disease which repre- 
sents all cases can not be drawn; but many cases show so 
characteristic a group of symptoms that the diagnosis can 
often be made with considerable certainty. We will first 
describe this typical form of disease, for the knowledge of 
which we must thank Charcot chiefly, and then we will add 
some remarks upon the cases which differ from this type 
(" formes frustes "), which are by no means very rare. 

The symptom of the typical cases of multiple sclerosis 
which we must first mention is an extremely striking dis- 
turbance of motion which manifests itself either as actual 
ataxia or as the so-called " intention tremor." This " tremor " 
was apparently the reason why multiple sclerosis was repeat- 
edly confounded in former years with paralysis agitans, al- 
though the two diseases have not the slightest resemblance one 
to the other. The one fact that the motor disturbance of mul- 
tiple sclerosis comes on only exceptionally when at rest, but 
almost always on voluntary movement, affords an effectual 
distinction. Moreover, the motor disturbance of multiple scle- 
rosis can be called an actual tremor only in part of the cases. 
Such a true oscillatory tremor is often seen, for example, 
in the arms when the patient tries to hold them out unsup- 
ported, but the tremor, in distinction from that of paralysis 
agitans, seems to occur less in the fingers than in the larger 
joints. We have scarcely ever seen oscillatory tremor in the 
legs in multiple sclerosis. In purposive movements there is 
rarely a true oscillatory tremor in the arms, but rather an 
ataxic motor disturbance — that is, an uncertainty and an ex- 
cursive movement, which is especially plain when the patient 
tries to touch a given point with his forefinger, to put the tips of the forefingers 
together, to bring a glass of water to the mouth, to pour water from one test-tube 
into another, etc. In the legs the ataxia usually occurs precisely as in tabes 
dorsalis (as in putting the heel on the other knee). We sometimes see consider- 
able wavering and shaking of the head when unsupported. The ataxia of the 






Fig. 129. — Example 
of disease of the 
cord in multiple 
sclerosis. The dark 
portions are the 
parts diseased. 



956 



DISEASES OE THE NERVOUS SYSTEM 



trunk is usually very evident. If we make the patient stand with the feet to- 
gether, it usually causes a marked swaying of the whole body. This swaying is 
often much greater when the patient shuts his eyes. We therefore find " Rom- 
berg's system" in multiple sclerosis precisely as in tabes dorsalis (q. v.). If the 
patient with multiple sclerosis is excited, his uncertainty and unrest usually be- 
come greater. 

In two other muscular regions the motor disturbance often makes itself mani- 
fest in a very characteristic way— in the muscles of articulation (tongue) and the 
muscles of the eye. Even on protruding the tongue we sometimes see an uncer- 
tainty of movement, but the disturbance is still more evident when the patient 
speaks. Many patients with multiple sclerosis, though of course not all, show 
a very characteristic disturbance of speech. The speech is slow, monotonous, 
scanning, indistinct, and sometimes finally almost unintelligible. The patient 
sometimes pronounces almost every syllable, or even every sound, separately, thus : 
" S-w-al-low." We sometimes notice that the voice often breaks into a falsetto. 
There can hardly be a doubt that this disturbance of speech indicates the presence 
of sclerotic nodules in the pons and medulla, and that the anomaly of motion 
at the bottom of it is analogous to the ataxia of the arms and legs described 
above. The nystagmus sometimes seen in multiple sclerosis, especially when 
looking to one side, is also nothing but ataxia of the ocular muscles ; but we must 
confess that we have seen manifest nystagmus in multiple sclerosis much less fre- 
quently than might be expected from the statements of some writers. 

Besides ataxia and intention tremor, actual paresis or even paralysis of the 
muscles may be wholly absent or may be only a late symptom. At any rate, in 
spite of marked ataxia the gross strength of the arms and legs may be very well 
preserved for a long time. The thing, however, which, in addition to the ataxia, 
gives the motor disturbance of multiple sclerosis its special stamp is the almost 
constant increase in the reflexes, and the associated spastic symptoms. In the 
upper extremities the spastic symptoms are less prominent, but even here we 
almost always find very vigorous tendon and periosteal reflexes on striking the 
lower ends of the bones of the forearm or the tendon of the biceps or triceps. In 
the lower extremities we see not only a marked patellar reflex and a very in- 
tense and persistent ankle clonus, but often an evident hypertonicity of the mus- 
cles, or even a pronounced tonic rigidity of both legs. 

It is the spastic symptoms which materially affect the patient's gait. If they 
are comparatively slight the gait is simply uncertain, wavering, stumbling, and 
ataxic, although even here the stiffness and jerkiness of the spastic gait is usually 
plainly to be seen (" spastic-ataxic gait"). The ataxia of the gait is due (un- 
like the ordinary tabetic gait) not to the uncertainty of the legs, but to the 
swaying of the whole body, as in cerebellar ataxia. If the spastic symptoms are 
more prominent, the gait also becomes more spastic, but the individual steps are 
always quick and long on account of the absence of paresis. In many cases with 
slight ataxia and marked hypertonicity of the muscles the gait is almost purely 
spastic. Only when paresis of the legs ensues does the gait become more dragging 
and labored, with slow, stiff steps (" spastic-paretic gait ")'. The ataxia is then 
of course no longer very noticeable. 

It is not easy to explain the occasion of all these motor symptoms of multiple 
sclerosis thus far described, but we may certainly say this : that the persistence 
of the axis-cylinders in the sclerotic nodules mentioned above explains the fact 
that there is so often in multiple sclerosis not a real paralysis, but only ataxia 
(intention tremor) and spastic symptoms (increased tendon reflexes). The gen- 
eral tendency is to refer the ataxia to nodules in the posterior columns or in the 
superior leminiscus, and the spastic symptoms to nodules in the lateral tracts. 
The occasion of the oscillatory tremor is still wholly unknown. 



MULTIPLE SCLEEOSIS OF THE BRAIN AND SPINAL COED 957 



Other symptoms besides the motor symptoms just mentioned are much less 
common in multiple sclerosis. It is especially noteworthy in respect to diagnosis 
that disturbances of sensation and of the bladder are usually quite subordinate. 
On careful testing we of course find not infrequently in some places slight or tem- 
porary diminution of the cutaneous sensibility or insignificant disturbances of 
micturition, but such symptoms are not part of the characteristic picture of mul- 
tiple sclerosis. The cutaneous reflexes usually show no special disturbances, but 
we have so frequently found certain reflexes absent, especially the abdominal re- 
flex, that we must ascribe to this symptom a certain significance in diagnosis. 

A number of cerebral symptoms are far more important, although they are 
present only in a part of the cases. First to be mentioned are the not uncommon 
ocular disturbances. The disturbances of vision are the most important; these 
may be either a simple diminution of the acuteness of vision or a contraction of 
the visual field and disturbance of the color sense. These symptoms are due 
to an atrophy of the optic nerve, which as a rule appears first in the temporal half 
of the papilla. The disturbance of vision only rarely goes on to complete blind- 
ness. The atrophy of the optic nerves may sometimes develop from an optic 
neuritis. Motor disturbances of the eyes are also not uncommon, and sometimes 
they may even be the first noticeable symptom of the disease. The paralysis 
almost always affects the external ocular muscles only, and usually causes diplopia. 
It may affect one or both eyes, and sometimes there is associated paralysis. Re- 
flex immobility of the pupils is hardly ever seen. 

Of other cerebral symptoms we may mention headache and especially ver- 
tigo. The latter is often a very early symptom of the disease. It may be parox- 
ysmal or persistent. In the course of the disease there often appears a certain 
mental weakness, an imbecility, which sometimes increases to marked dementia. 
Conditions of melancholy or exaltation are much rarer. We must also mention 
the occurrence of apoplectiform attacks as a symptom which is often important 
in diagnosis. After slight prodromal symptoms, such as headache and vertigo, 
loss of consciousness and hemiplegia come on quite suddenly. With this the face 
is usually red, the pulse is frequent, and the temperature may rise to 104° or 106° 
(40°^41° C). After a day or two the consciousness gradually returns, and the 
hemiplegia soon disappears. Epileptiform attacks are much rarer. We saw these 
repeatedly in a typical case; they were mainly unilateral, and were followed by 
a hemiplegia which soon passed away. The precise cause of these attacks is still 
wholly unknown. We know only that they are not due to complicating gross 
changes in the brain, but that they arise merely from functional conditions of 
paralysis or irritation. Finally, we must mention an interesting symptom not 
infrequently observed in multiple sclerosis, which may also be of value in diag- 
nosis — namely, the so-called impulsive laughing and crying. In many patients 
these emotional manifestations occur very frequently and in an uncontrollable 
fashion, either almost spontaneously or especially upon the slightest occasion. 
Not infrequently the two manifestations pass almost directly into each other. 

In regard to the general course of typical cases, the disease develops very slowly 
and gradually. Motor symptoms, tremor, uncertainty of movements, and disturb- 
ances in gait, usually appear in the extremities first. The patient often com- 
plains at the same time of occasional headache and vertigo. The speech gradually 
becomes more indistinct, the intelligence weaker, and the other symptoms of the 
disease described above develop. The affection almost always lasts for years and 
years. Variations in the course, temporary improvement, and new relapses are 
common. It would even seem in mild cases as if there were sometimes a recovery 
or at least an arrest of the symptoms, but in general we must always regard 
the prognosis as very unfavorable. We often see the condition rapidly grow 
worse, especially after the above-mentioned apoplectiform attacks. The last stage 



958 



DISEASES OE THE NERVOUS SYSTEM 



is characterized by the gradually increasing disturbance of the general nutrition, 
and, finally, by paralysis and bed-sores. Death ensues from intercurrent diseases, 
from the increasing weakness, or sometimes in an apoplectiform attack. 

Unusual Forms. — Besides the typical form of multiple sclerosis described, 
there are often, as we have said, cases that vary from the type (" formes frustes "). 
We will mention briefly the following possibilities : 

1. The disease may be very latent. We saw one case in which, for a long 
time, the only symptom was a complaint of slight headache and vertigo. Finally, 
there was a transitory apoplectiform attack, several months later an epileptiform 
attack, and a few days after that death took place. The autopsy showed a com- 
pletely developed multiple sclerosis. 

2. Sometimes the disease appears under the exact type of a chronic myelitis. 
The cerebral nodules cause no symptoms, they are present, perhaps, only in small 
numbers, and the spinal nodules cause a gradually increasing paraplegia of the 
legs, with vesical disturbance, loss of sensibility, etc. We have notes of several 
autopsies of multiple sclerosis in which, during life, the diagnosis of a simple 
transverse myelitis had been made (vide supra, page 951). 

3. Cases have been repeatedly known where multiple sclerosis has appeared 
under almost the exact type of a spastic spinal paralysis (vide infra). In these 
cases many nodules were situated in the lateral columns of the cord. If the spas- 
tic symptoms be combined with muscular atrophy (nodules in the anterior gray 
cornua), the disease may even simulate the type of an amyotrophic lateral scle- 
rosis, with at times co-existing bulbar symptoms (vide infra.) If multiple scle- 
rosis be localized to an unusual extent in the pons and medulla, the symptoms of 
a chronic bulbar paralysis may be prominent. 

4. Much less frequently the type of the disease may resemble tabes (immobile 
pupils, ataxia, pain). We do not know whether absence of the patellar reflex has 
been seen in undoubted multiple sclerosis. There are, however, combinations of 
multiple sclerosis and gray degeneration of the posterior columns (syphilis?). 

5. It sometimes happens that multiple sclerosis is the reason for a slowly de- 
veloping hemiplegia, which may then be falsely regarded as cerebral, while the 
autopsy shows several nodules in the corresponding side of the cord and pons. 

6. In some cases the mental disturbances (dementia) are so prominent that 
there is the pronounced picture of paralytic dementia with disturbances of 
speech, etc. 

Diagnosis.— In all such atypical cases the diagnosis of multiple sclerosis is 
sometimes quite impossible, or at best it can be made with a fair amount of proba- 
bility only when some, at least, of the characteristic symptoms of the disease are 
present besides the anomalous symptoms. The circumstance, indeed, that the 
anomalous cases will not properly fit the moulds of any other form of disease, 
should make us think of the possibility of a multiple sclerosis ; for in these 
anomalous cases, of course, there may be all possible combinations of symptoms. 

In typical cases, however, the diagnosis is easy, and often it can be made with 
absolute certainty. The slow development of the disease, usually without any 
discoverable cause, the comparative youth of the patient, the ataxia of the legs 
and the ataxia or tremor of the arms, the swaying of the body when standing 
with the feet together, the uncertain spastic-ataxic gait, the occasional absence 
of the abdominal reflex, the increased tendon reflexes in the arms and legs, the 
absence of any marked disturbances of sensation or of the bladder, in some cases 
also the disturbance of speech, the nystagmus, the impulsive laughing and crying, 
the slight mental weakness which often comes on later, and finally the occasional 
apoplectiform or epileptiform attacks — all these symptoms give a very character- 
istic picture, which is usually quickly recognized and correctly interpreted. It is 
hardly possible to confuse it with paralysis agitans (q. v.) if we remember the 



THE SO-CALLED PSEUDO-SCLEROSIS 



959 



characteristic attitude of the latter affection, the oscillatory tremor of the fingers 
when at rest, the rigidity of the face, etc. It is very seldom difficult to distin- 
guish it from true tabes dorsalis. It is easier to confuse multiple sclerosis with 
Friedreich's hereditary ataxia (q. v.) ; but the condition of the tendon reflexes is 
usually decisive; these are wholly absent in tabes and Friedreich's disease, but 
they are almost invariably increased in multiple sclerosis. It sometimes happens 
that hysteria assumes a form very similar to multiple sclerosis (tremor, ataxia, in- 
creased tendon reflexes, etc.), but in such cases we can usually arrive at a correct 
diagnosis by careful observation if we pay attention to the whole condition of 
the patient, the course of the disease, and the characteristic hysterical " stigmata." 
There is, however, a combination of multiple sclerosis and hysteria (especially 
hysterical hemianesthesia), as has been maintained especially by Charcot's pupils. 
The distinction between multiple sclerosis and the so-called pseudo-sclerosis will 
be stated below. 

Prognosis. — The most important features in prognosis have already been men- 
tioned. We have seen that an improvement in the symptoms is not uncommon, 
but that the final outcome of the disease, with perhaps a few exceptions, is un- 
favorable. The disease may last for many years. 

Treatment. — In the treatment we may make a trial of the same remedies that 
have been mentioned in the description of chronic myelitis. Absolute rest and 
good care, which many patients can obtain only in a good sanitarium, are often 
beneficial. We may also use galvanism, baths, and sponging, and internally 
iodide of potassium, ergotine, and nitrate of silver. The uncertainty of move- 
ment can sometimes be distinctly improved by methodical gymnastic exercises 
(see the following chapter). 

APPENDIX 

THE SO-CALLED PSEUDO-SCLEROSIS 

Cases of disease have been observed, first by C. Westphal and later by the 
author and others, the symptoms of which seemed to warrant the diagnosis of 
multiple sclerosis, but the autopsy proved wholly negative. The victims are 
usually young and often have a predisposition to nervous disease. The symptoms 
of the disease consist of a marked rapid or slow oscillatory tremor with wide ex- 
cursions, which sometimes occurs during rest, but which becomes unusually vio- 
lent on motion. The tremor affects the arms particularly, but also the trunk and 
legs. There seems to be no real ataxia as in multiple sclerosis. The tendon reflexes 
are increased and a distinct spastic rigidity may develop in the legs. The speech 
is sometimes quite as decidedly scanning as in multiple sclerosis. Nystagmus is 
usually absent. We have seen apoplectiform attacks in a pronounced form, and 
also impulsive laughing and crying. The face often has a peculiar rigid ex- 
pression. Certain mental disturbances are very characteristic, especially a 
marked tendency to outbursts of wrath and actual maniacal attacks. Signs of 
confusion and hallucinations are less common. The course may extend over many 
years. The disease seems to be incurable. Death ensues through increasing 
general weakness or in an apoplectiform attack. Anatomical investigation, as has 
been said, is essentially entirely negative, even with a careful microscopical ex- 
amination of the nervous system. 

The resemblance between the type of this " pseudo-sclerosis " and true mul- 
tiple sclerosis is evident ; nevertheless, now that we know the disease, we can often 
make the distinction. The chief points to bear in mind are the very marked true 
oscillatory tremor, the absence of real ataxia, and the mental disturbances just 
mentioned. 

The treatment of pseudo-sclerosis is the same as that of multiple sclerosis. 



960 



DISEASES OF THE NERVOUS SYSTEM 



CHAPTER VII 

TABES DORSALIS 

{Locomotor Ataxia. Gray Degeneration of the Posterior Columns. Posterior Spinal Sclerosis) 

We give at present the old name of tabes dorsalis, " consumption of the spinal 
cord," to a perfectly definite chronic disease of the central nervous system, whose 
chief, but by no means sole, anatomical basis is regarded as a primary systemic 
degeneration of the peripheral sensory neurones, and especially of their processes 
in the posterior columns of the spinal cord. The first description of tabes, which, 
of course, is defective in many respects, is found in a work of W. Horn in 1827. 
We must thank especially the investigations of Romberg in Germany, in 1851, 
and of Duchenne in France, in 1858, for a more comprehensive knowledge of the 
disease, and for a precise distinction between it and the other chronic diseases 
of the spinal cord. 

iEtiology. — But little that is definite was known until lately as to the cause of 
tabes dorsalis. Hereditary conditions play a very slight part in genuine cases, 
and even a general " neuropathic taint " can only rarely be made out in ataxic 
patients. Much weight in regard to aetiology was formerly laid upon previous 
exposure to cold. It can not be denied that sometimes the first symptoms of the 
disease follow some pronounced exposure to wet or cold, but much more fre- 
quently nothing of the sort can be made out. The case is similar with regard to 
physical and mental over-exertion, which were formerly made answerable for the 
origin of tabes. It is an utterly ungrounded assertion that sexual excesses may 
be the cause of tabes. Tabes may rarely develop as a result of acute diseases 
or somewhat more frequently as a result of injury (general concussion of the 
body from a fall, fractures, etc.) ; but we may ascribe to these factors merely 
the significance of an exciting cause. In these rare cases, too, it is hard to 
confirm the connection. The earlier teaching that tabes develops after " sup- 
pression of the foot-sweat " is manifestly due to a confusion of cause and 
effect. The absence of foot-sweat is not the cause, but a symptom of incipient 
tabes. 

The only serological fact which in our opinion is beyond any doubt is the 
relation of tabes to a previous syphilitic infection. This relation of the two dis- 
eases to each other was first confirmed in France by Fournier and in Germany by 
Erb, and in spite of the vigorous contradiction which the views of these observers 
at first met with on many sides, this theory of tabes is constantly acquiring more 
and more general recognition. 

The connection between tabes and syphilis can be confirmed, first of all, by 
statistics. Erb was able to find a history of syphilis, with secondary symptoms, 
in about 62 per cent, of his patients ; and Fournier, in 103 cases, found syphilitic 
antecedents as many as 94 times. Our own observations agree exactly with Erb's 
data, since 61 per cent, of our patients stated definitely that they had formerly 
suffered from syphilis. If we also reckon the cases where ;the patients admit a 
former sore but no secondary symptoms, the percentage becomes much gre^te 1 ' — 
90 per cent. In general it is worthy of note that, as a rule, in most cases of t^bes 
the previous syphilis has not had a great intensity. Only quite infreqnentlv do 
we find tertiary syphilitic symptoms as well as tabes; we have seen, for ex^mp^e, 
severe ulcers of the skin, gummatous periostitis, etc. The time between the in- 
fection and the beginning of the first symptoms of tabes varies very much; it 
may be from two to twenty years. 

The connection between tabes and previous syphilis also explains nntur^lb r a 
number of peculiarities in the occurrence of tabes, especially the fact that tabes 



TABES DOESALIS 



961 



is much commoner in men than in women, that it is particularly very rare in 
women of the better class, while it is found much more frequently in women of 
the lower classes, that it comes on particularly in middle life, that it is much 
more common in the higher classes and in urban populations than in the country, 
that certain classes (merchants, artists, officers) show a much larger percentage 
of cases of the disease than others (clergymen, teachers, etc.)- If we see, however, 
any cases of tabes which show striking differences in these respects, we can al- 
most always find evidence, even in such cases, of a previous syphilitic infection. 
Such individual cases therefore afford material for the most convincing proof of 
the connection between the two diseases. Thus we sometimes see tabes in per- 
fectly irreproachable women ; here we can almost always detect previous syphilis 
in the husband which has been transmitted to the wife. We ourselves and other 
observers have seen tabes arise in this way in both husband and wife. We may 
also find tabes in very young or very old persons, and then we can discover that 
syphilis was acquired at a very early or a very advanced age. A few cases of 
tabes occur in children, and are in all probability to be referred to hereditary 
syphilis. 

Although the connection between tabes and previous syphilis may be regarded 
as definitely established, the nature of this connection, on the other hand, is not 
yet fully explained. This much, of course, is certain, that tabes is not an ordinary 
tertiary syphilitic disease. Both its anatomical changes (vide infra) and the 
extremely slight effect of antisyphilitic treatment remove every doubt as to this. 
The connection between the two diseases must be of some other nature, and 
therefore we long ago expressed the opinion that tabes was due only to certain 
chemical poisons (toxines), which develop in the body from the action of the 
syphilitic infection. Such toxines may very well cause definite systems of fibers 
(vide infra) to degenerate, and their presence is also a good explanation of cer- 
tain clinical peculiarities of tabes, especially the paroxysmal occurrence of cer- 
tain symptoms (the so-called crises). Many of these crises, especially the gastric 
and intestinal crises, are very similar to toxic symptoms (vomiting, pain, pro- 
nounced general debility and weakness, etc.). Tabes and the closely allied gen- 
eral paralysis therefore stand in the same relation to syphilis as "post-syphi- 
litic nervous diseases," that the common " nervous sequelae " do to the acute infec- 
tious diseases — for example, as post-diphtheritic paralysis and ataxia do to previ- 
ous pharyngeal diphtheria. Of course this hypothesis does not afford a complete- 
ly clear insight into the nature of the tabetic process. Thus the constant advance 
of most (but of course not all) cases of tabes requires a further special explana- 
tion. We may perhaps imagine the process thus : that the toxines absorbed at 
first merely injure the affected nervous system (vide infra), but that the complete 
atrophy and cessation of function comes on gradually through the wear and tear 
associated with the normal functioning of the nervous elements. In this sense 
other external influences (fatigue and physical over-exertion, exposure to cold, 
injury) may be regarded as aiding the process. 

It can not at present be maintained that every tabes is of syphilitic origin, 
although we have never yet seen a typical genuine tabes in which syphilis could 
certainly be excluded; but it would not be impossible that other noxious influ- 
ences might cause the same systems of fibers to degenerate as in tabes, and thus 
produce a form of disease similiar to that of genuine tabes. Thus we know at 
present, from the investigations of Tuczek, that symptoms may develop in chronic 
ergot poisoning (ergotism) which are perfectly analogous to those of tabes and 
depend upon a corresponding disease of the posterior columns of the cord which 
can be demonstrated anatomically. These cases of " tabes," however, which are 
traced to some other cause, must later be distinguished from the post-syphilitic 
cases which constitute by far the great majority. 
61 



962 



DISEASES OF THE NEKVOUS SYSTEM 




Pathological Anatomy— As we have seen on page 796, the cell bodies of the 
peripheral sensory neurones lie in the spinal ganglia. The processes of the spinal 
ganglion-cells divide into two branches. One goes to the periphery of the body,, 
the cutaneous surface; it forms the so-called peripheral sensory nerve. The 
other process serves for the centripetal conduction of sensory irritations; it 

enters the cord through the 
a posterior roots and goes, as 

we have said above, either 
upward in the posterior col- 
umns or into the posterior 
gray cornua, there to connect 
with spinal sensory neurones 
of the second order. Upon 
this peripheral (first) sen- 
sory neurone system (spinal 
ganglion system), whose ana- 
tomical arrangement we 
have just briefly described, 
the (toxic) cause of tabes 
acts especially and causes it 
slowly, fiber by fiber or neu- 
rone by neurone, to degen- 
erate. In tabes, as in most 
other primary systemic dis- 
eases, we find that the evi- 
dent visible anatomical de- 
generation of the different 
neurones always begins in 
the prolongations, and the 
destruction of the cell body 
itself follows later, if at all, 
and is the last process. 
Since the prolongations of 
the spinal ganglion-cells are, 
first, the peripheral sensory 
nerves, and, second, the 
fibers in the posterior col- 
umns, and, in part, in the 
posterior horns of the spinal 
cord, we understand, with- 
out further explanation, that 
the anatomical process in 
tabes must manifest itself as 
a degeneration both in the 
peripheral nerves and in the 
posterior columns and pos- 
terior horns of the spinal 
cord. So far as we can at 
present appreciate the con- 
ditions, the spinal process of 
the neurone cells in the spinal ganglia seem to be affected earlier, more regu- 
larly, and more extensively than the peripheral process ; but it seems to us prob- 
able that there are individual differences in this respect, and that many differences 
in the course of the disease in different cases of tabes may be explained by 





Fig. 130.— Degeneration of 
tabes, a. Cervical cord 
(Personal observation.) 



e posterior columns in advanced 
b. Dorsal cord. c. Lumbar cord. 



TABES DOESALIS 



963 



such variations in the particular anatomical localization of the tabetic de- 
generation. 

If we examine the spinal cord of a patient who has died in the advanced stage 
of tabes, the smallness and thinness of the cord usually strike us at once. The 
pia mater is thickened and opaque, especially on the posterior surface. We often 
see the posterior columns appearing through the pia as a gray band extending the 
whole length of the spinal cord. On cross-section we notice that the smallness 
of the cord is due chiefly to the atrophy of the posterior columns, which is often 
very considerable. These no longer protrude at all backward, as they normally 
do, but seem flat and sunken. From their pronounced gray color they are very 
plainly distinguished on cross-section from the rest of the white matter of the 
cord. The posterior cornua of the gray matter, and the posterior nerve-roots, 
show exceptionally a considerable atrophy, and appear very small and thin and 
also of a gray color. 

Microscopic examination gives more exact information as to the extent and 
form of the degeneration. This shows (Fig. 130, a, b, c) that all portions of the 
posterior columns are not affected in like manner, but only those portions which 
contain the processes and collaterals of the posterior root-fibers, which therefore 
belong to the system of spinal ganglion neurones. The other tracts (short tracts, 
commissural fibers) are spared. The degeneration is almost always most intense 
in the lumbar cord ; here it affects chiefly the middle and posterior portions of the 
posterior columns, while the most anterior portion and the so-called dorso-median 
sacral bundle (Fig. 130, c) remain normal in almost all cases. These are indeed 
fibers which have another origin and do not belong to the spinal ganglion system. 
In the dorsal cord (Fig. 130, b) the posterior columns are almost completely de- 
generated. There are usually small normal areas still preserved in the posterior 
external and the most 

anterior portions. In ^\M^g//w \ 

the cervical cord (see f' I , s ^^^^ / 



areas " — that is, those 

portions in the columns of Burdach where fibers enter directly from the 
posterior nerve-roots, and from which fibers may be traced farther into 
the gray matter of the posterior cornua; but the so-called posterior external 
areas, and also two little antero-lateral areas, remain entirely, or at least 
for a long time, free from the disease, because these are also bundles of fibers 
which do not belong to the system of the spinal ganglia or posterior roots. If 
we examine cases of tabes in the earlier stages which happen to come to autopsy, 
we find in the posterior columns only a few root territories affected — that is, 
the fibers arising from individual spinal ganglia or posterior roots and lying near 
one another, while other root territories remain free from degeneration (Figs. 
131 and 132). A system of very fine fibers, entering through the posterior roots, 
is affected very early, as a rule. It branches outward immediately after the 
entrance of the roots, and occupies a small but very sharply defined territory at 
the point of the posterior cornua, between the posterior and lateral columns (the 
so-called zone of Lissauer). In all the affected root territories the degeneration 
slowly involves fiber after fiber. The order in which the different root territories 



Fig. 130, a) the so- 
called columns of Goll 
are chiefly affected, 
together with the pro- 
longation of the fibers 
from the root-zones of 
the lumbar cord, and 
also the " lateral root- 




Fig. 131.— Dorsal region. Fig. 132.— Lumbar region. 

Transverse section through the posterior columns of the cord in beginning 
tabes dorsalis. 



964 



DISEASES OE THE NERVOUS SYSTEM 



degenerate, after one another and in part at the same time with one another, is 
certainly not always the same in individual cases, as is evident from the varia- 
tions in the clinical course of the disease. As a rule, the neurones of the lumbar 
and lower dorsal spinal ganglia certainly degenerate first, and the neurone sys- 
tems of the cervical ganglia later. 

We must state, with reference to the participation of the gray matter in the 
disease, that the posterior cornua, as we have already said, are also found con- 
siderably affected, which is explained mainly by the atrophy of the posterior root- 
fibers which enter them directly. It also can not appear strange that the medul- 
lated fibers found in Clarke's columns seem very much reduced in number, since 
they also are direct processes of the posterior root-fibers. The cells of the col- 
umns of Clarke remain normal. The ganglion-cells of the posterior horns, which 
belong to the second sensory neurones, also remain normal, and no changes are 
found in the processes of these cells in the lateral columns. The lateral and ante- 
rior 'columns of the cord usually remain unaltered (vide infra). 

On the other hand, the peripheral sensory nerves — that is, peripheral pro- 
cesses of the spinal ganglion-cells — are by no means spared. In all cases of tabes 
which have been carefully examined thus far, we find in the peripheral nerve- 
trunks (sciatic, crural, etc.), and usually still more in the finer branches of the 
sensory nerves, a considerable number of degenerated centripetal fibers (Dejerine, 
Oppenheim and Siemerling, and others). We regard this degeneration as precise- 
ly analogous to the disease of the posterior columns and by no means a secondary 
degeneration. Like the degeneration of the posterior columns, it also is an ex- 
pression of the primary disease of the peripheral sensory neurone system. In 
regard to the cell-bodies in the spinal ganglia, those certainly are well preserved 
for a long time, at least in regard to their external aspect, but finally we may find 
more or less definite changes in them, although hardly ever complete atrophy. 

The anatomical process of tabes is by no means limited exclusively to a 
chronic degeneration of the first sensory neurone system. Other neurones and 
neurone systems may also be involved in the disease. The occasional affection of 
the trigeminal neurones is of course wholly analogous to the degeneration of the 
sensory spinal neurones ; but other regions sometimes become degenerated, espe- 
cially the optic nerve, more rarely the vagus and acoustic, and also certain motor 
regions, especially the ocular nerves, other peripheral motor nerves, the pyramidal 
lateral tract, etc. We will return more fully to these " complications," or, to 
speak more correctly, to these rarer localizations of the tabetic process, in the 
clinical portion of this chapter. If we consider, however, that the whole neurone 
territory of the spinal ganglia evidently contains neurones of very different 
physiological importance (fibers for the conduction of the different qualities of 
sensation, for the co-ordination of movement, for the innervation of the bladder 
and rectum, for reflex processes, etc.), and that also other most diverse neurone 
territories may be involved in tabes, we can understand that tabes can be termed, 
not a simple, but far more properly a " combined systemic disease" 

The form of the tabetic affection consists of a primary degenerative atrophy of 
the nerve-fibers, and a corresponding secondary increase of the connective tissue. 
The gray color of the posterior columns is due to the loss of the medullary 
sheaths. Since the destruction of the nerve-fibers advances but very slowly, we 
find only a few fatty granular cells. In old cases we find numerous corpora 
amylacea, whose origin and significance are still unknown. The thickening of 
the pia mater is a purely secondary phenomenon, which is always most marked 
on the posterior surface of the periphery of the cord, corresponding to the atrophy 
of the posterior columns. 

Clinical History. — A disease which has as its basis so definite and strictly lim- 
ited an anatomical change as is the case with tabes dorsalis would also be ex- 



TABES DOKSALIS 



965 



pected to give a very characteristic clinical picture. This supposition is entirely 
correct, and there are few diseases which can be diagnosticated, even in their 
earliest stages, with as much certainty as tabes. This fact is explained only by 
regarding tabes as a systemic disease, in which certain systems of fibers are always 
affected, while others are as constantly spared by the disease. The difference 
between individual cases of tabes lies, therefore, less in the symptoms themselves 
than in their intensity, their duration, and the order of their occurrence. In this 
regard, however, the differences in the clinical pictures are extremely varied, so 
that, even with a comparatively great personal experience, we often see new com- 
binations of symptoms and also peculiarities in their course. 

For the majority of cases we may sketch the following general description of 
the disease, in which it is better to divide the whole course into several stages; 
but, of course, this division can have only a schematic value. 

Tabes dorsalis begins, as a rule, with a stage of initial symptoms, which de- 
velop very gradually and insidiously, and which may be of very varying dura- 
tion. The most characteristic symptoms of this stage are those of sensory irrita- 
tion, most frequently in the form of the so-called lightning-like, " lancinating " 
pains in the lower extremities. They are sometimes very severe, but at other 
times only of slight intensity, and are comparatively little noticed by the patient, 
who regards them as " rheumatism." Many patients have a feeling of numbness 
and tingling in the tips of the fingers, especially of the ring and little fingers, and 
there is often a pronounced girdle sensation in the trunk. In some cases, too, 
neuralgic and migraine-like pains in the head may appear in the early stages. 

Besides these symptoms of sensory irritation, which may often be for years 
the only symptoms of which the patient complains, two objective symptoms ap- 
pear very early, which are of the greatest importance in the diagnosis of incipient 
tabes : the disappearance of the patellar reflex and the reflex immobility of the 
pupils. The absence of the patellar reflex is the most constant of all the known 
symptoms of tabes. It is, as a rule, to be found so early that we can hardly ever 
decide with exactness upon the time of its occurrence. The reflex immobility of 
the pupil — that is, the failure of the pupil to contract to light, while the changes 
on accommodation may be perfectly retained — is, indeed, not so constant as the 
failure of the patellar reflex, but it is present in almost all cases. If all three 
symptoms — lancinating pains, absence of patellar reflex, and immobility of the 
pupils — are present at the same time, the diagnosis of tabes is absolutely certain, 
even if all other symptoms are wanting, because this peculiar combination of 
three such apparently heterogeneous symptoms is seen in this disease alone. If 
only two of these symptoms are present, but if the reflex immobility of the pupils 
be one, the diagnosis is also practically certain ; but if this symptom be absent we 
should be very cautious in admitting that the affection is genuine tabes. 

Among the rarer initial symptoms we shall also learn to recognize diplopia, 
caused by paralysis of certain ocular muscles, and loss of vision, from optic atro- 
phy. In many other cases certain disturbances of cutaneous sensibility (a girdle 
feeling, paresthesia, a furry feeling) announce the approach of the disease. 
Sometimes disturbances in micturition appear quite early, while in other cases 
gastric crises (vide infra) or some joint affection are the first symptoms which 
the patient notices. 

After this first stage of the disease has lasted for a very varying period, from 
a few months to two or five or even twenty years, the second stage begins ; this 
we usually term the ataxic stage of tabes. 

The beginning of this stage is recognized by the appearance of disturbances of 
gait. The gait becomes more difficult and more uncertain, and there are certain 
peculiarities which we will describe more fully later. Careful examination shows 
that the disturbance in gait is due not to a paresis of the muscles but to a disturb- 



966 



DISEASES OE THE NERVOUS SYSTEM 



ance of co-ordination, ataxia of the lower extremities. This symptom usually 
increases very slowly, until it reaches a degree where the patient can walk only 
with assistance, and finally can not walk at all. There is often later, but almost 
always not for years, ataxia of the upper extremities. 

Besides the persisting symptoms of the first stage, there are often now more 
marked disturbances of sensibility, as well as ataxia. The patient has a feeling as 
if he were walking on wool, felt, or similar substances. If he closes his eyes there 
is great swaying of the whole body — " Romberg's symptom." Physical examina- 
tion of the sensibility almost always shows considerable disturbance of the cuta- 
neous sensibility, especially of sensibility to pain, or even of other forms of sen- 
sibility. A loss of muscular sense is very common. The disturbances of micturi- 
tion, such as incontinence, gradually become more marked, and very often cystitis 
gradually develops. This stage also may last for years. Sometimes the disease 
seems to stand still, frequently even manifest improvement is seen, but then the 
condition becomes worse again. 

The third stage, the terminal stage of the disease, develops if the patient has 
not previously succumbed to an intercurrent disease. The symptoms are the 
same as in most of the other chronic diseases of the spinal cord. The patient 
gradually becomes more and more wretched and helpless, and finally is confined 
almost wholly to his bed. The ataxia reaches an extreme degree, and finally there 
is sometimes an actual motor weakness or complete paralysis of the legs. In 
these cases, which are by no means frequent, we are correct in calling the third 
stage of tabes the " paralytic stage." A severe pyelo-cystitis usually develops, 
bed-sores appear, and death finally frees the patient from his lamentable con- 
dition. 

We must now complete this briefly sketched picture of the disease by a more 
careful description of the single symptoms. 

1. Disturbances of Motility in the Extremities. — The typical motor symp- 
tom of developed tabes dorsalis is the disturbance of co-ordination, the ataxia 
(see page 837). This is almost always seen in the lower extremities first. To 
test the ataxia it is most convenient to ask the patient to touch the knee-pan of 
one leg with the heel of the other foot (" knee-heel test "). We see then that the 
leg moved is often carried beyond the point designated several times before 
it reaches it. The ataxia is often noticeable, even in crossing one leg over 
the other, as the leg raised makes much too great and too " throwing " a 
movement. 

The alteration of the gait is very characteristic — the ataxic gait, from which 
we can often perceive the patient's disease at the first glance. If the patient sits 
down and tries to get up again to walk, there is difficulty in rising. He separates 
his legs to find a firm point of support, he takes a stick to help himself if he 
can, and he often gets the proper balance to keep himself erect only after several 
attempts. The gait itself is straddling, and the legs are raised abnormally high 
and set down with a stamp. The direction of the gait, however, is as a rule 
well preserved, and the trunk (vide infra) is often but little involved in the 
swaying. This is the distinction between the ataxic gait of, tabes (due to ataxia 
of the legs) and the staggering, wavering gait in cerebellar disease (" cerebellar 
ataxia " with ataxia of the legs and trunk), in multiple sclerosis, etc. If we have 
the patient turn rapidly or make a proper military " about face," the uncertainty 
of movement is still more marked, as it also is if the patient rises suddenly and 
begins to walk or makes a sudden halt when walking. These methods of testing 
are therefore especially suitable for ascertaining the first beginnings of ataxia. 
Very often the first uncertainty in the gait is noticed in going down-stairs, be- 
cause the patient can not put his foot securely on the next step below. Going 
up-stairs is at first far less affected because the perpendicular rise of the stairs 



TABES DOESALIS 



967 



prevents any excessive movement. If the ataxia reaches a higher degree, most 
tabid patients always walk with a stick and control the movements of their legs 
by keeping their eyes fixed on the floor as they walk. This control is particularly 
necessary when the sensibility of the legs, especially the muscular sensibility, is 
diminished at the same time. 

In more advanced cases the ataxia becomes apparent even on standing with 
the feet close together (static ataxia). We see continually in the muscles and 
tendons of the legs slight contractions which are necessary to maintain the con- 
stantly shifting equilibrium. These contractions become much more marked as 
soon as the patient stands with his eyes shut. There is then usually an evident 
swaying of the body, which is sometimes so great that the patient is in danger of 
falling. This phenomenon (Romberg-'s symptom) is due chiefly to the defective 
control of the muscular movements, which are necessary to preserve the equilibri- 
um, as a result of the impaired sensibility of the skin of the soles of the feet and 
that of the joints and the muscles themselves. If this control be supplied by the 
eyes, the swaying is insignificant, but it at once becomes more marked if the con- 
trol by the eyes is lost. From a like reason it is much harder for most ataxic 
patients to walk in the dark than by daylight. 

In many cases of tabes, especially when the disease is far advanced, the co- 
ordination of the maintenance of the position of the trunk is evidently dis- 
turbed. Such patients finally can not sit up, since the trunk sways so much. The 
gait of tabid patients with great ataxia of the trunk is still more uncertain and 
also plainly staggering. 

If ataxia of the upper extremities occur in the course of the disease, it is 
easily recognized if the patient tries to take hold of some definite object, such 
as his ear, or if he brings the tips of his two forefingers together from a certain 
distance, or if he tries to touch exactly with the tip of his finger the finger of the 
physician when held before him. The ataxia is of course also apparent in all fine 
complicated movements (eating, sewing, writing, tying a knot, drawing straight 
lines, etc.). The movements are irregular and uncertain, and the excursions are 
marked. If there be at the same time any sensory disturbance in the arms, the 
•anomaly in their movements is still greater with the eyes shut. 

There has been much written and much argued as to the cause of the ataxia in 
tabes dorsalis. The main reason why it is at present impossible to give an in- 
controvertible explanation of the occurrence of ataxia lies in the fact that we 
are not yet in a condition to know and to analyze with sufficient accuracy the 
process of normal co-ordination of motion (page 837) ; for manifestly every theory 
as to the causes of ataxia must begin with the processes involved in the co-ordina- 
tion of normal movements. If we try to get a clear idea of this, the most 
essential point to bear in mind is that co-ordination of motion is not a con- 
genital function, but a power of our organs of motion acquired by practice. The 
movements of little children who are learning to walk are ataxic, and even in 
later life it often happens that we have to learn how to perform certain compli- 
cated and difficult movements (so-called manual dexterity, exercises of skill). We 
can get no other idea of this " learning how to co-ordinate " than that it takes 
place by the aid of the constant action of controlling and correcting impressions 
coming from the periphery — that is, centripetal — but we must bear in mind that 
these actions are mainly unconscious. The surer we become in the execution of 
the movements, the more the regulatory influence of the centripetal irritations 
falls into the background, without ever wholly disappearing. In these cases we 
must not consider, by any means, merely the irritations which are brought to the 
central organs from the skin of the parts moved ; but we should consider, just as 
much or even more, those irritations which are due to the varying tension and 
position of the deeper parts, the muscles, the fasciae, the ligaments, and the articu- 



968 



DISEASES OE THE NERVOUS SYSTEM 



lar surfaces. Even the special organs of sense, particularly the eye, under some 
circumstances, assist materially in regulating motion. 

A disturbance of co-ordination must accordingly take place when this con- 
stant regulation of our movements by centripetal irritations ceases. Since the 
anatomical lesion in tabes, as we have seen, consists almost exclusively of a degen- 
eration of centripetal systems of fibers passing through the posterior roots, there 
can scarcely be a doubt in our opinion that tabetic ataxia is due to the degenera- 
tion of centripetal fibers regulating movements; but we must emphasize the fact 
that these centripetal co-ordinating fibers must not be identified without further 
proof with the centripetal fibers serving for conscious sensibility, for we can by 
no means establish a parallelism between the degree of ataxia and the severity of 
the sensory disturbances (in the skin and in the muscles), although of course 
disturbances of co-ordination and disturbances of sensibility very often co-exist 
in this disease. There are, however, undoubtedly cases of tabes with marked 
ataxia of the legs in which we can find on examination only slight disturbances 
of the cutaneous and muscular sensibility. This is still more frequently the case- 
in other diseases attended with ataxia. 

We may therefore very well imagine that ataxia is the consequence of a 
degeneration of those collaterals which go from the centripetal neurones to the 
motor ganglion-cells, and there provide for the regulation of the strength of 
motor innervation, although there are still enough conducting paths to conduct 
sensory impressions to the centers of consciousness. We do not as yet know, 
however, in what part of the motor tract the regulatory influence of centripetal 
irritations takes place; whether in the cells of the anterior horns of the cord,, 
which is the simplest explanation of the theory of tabetic ataxia, or higher up in 
the motor cortex or in part in the cerebellum, etc. This can be made perfectly 
clear only by further investigation. 

Ataxia is the chief motor disturbance in tabes. The crude strength of the- 
muscles may be perfectly normal, and it is chiefly a service of Duchenne's to have 
made clear for the first time the principal distinction between ataxia and paraly- 
sis. He showed that ataxics, who can no longer walk a step alone, can never- 
theless exert the greatest strength with their legs. We have ourselves treated a 
teacher of gymnastics who, in spite of the most marked ataxia of the arms, had 
still so much strength in them that he could support himself in bed on his 
arms and keep his whole body, with his legs extended, in the air. It sometimes 
happens, however, that the crude strength also disappears in tabes, and that 
the muscles become paretic. There may be a simulation of a certain " pseudo- 
paresis," since the patient with severe ataxia loses the ability to concentrate his 
muscular strength in the necessary direction. There is also in tabes occasionally, 
as we have said, an actual paralysis of the legs ultimately. We have stated 
above that even a complete paraplegia may finally develop in the course of the 
disease. In these cases we find, on anatomical examination, that the process is no 
longer confined to the posterior columns, but that there is also a systemic de- 
generation of the lateral pyramidal motor tracts in the lumbar cord. In some 
cases paraplegia has been observed to come on quite suddenly even in the early 
stages of the disease, and usually to disappear again in the course of a few 
weeks. Its origin has not yet been explained. The rare paralyses of certain motor 
nerves have another significance. They have usually been noted at the begin- 
ning of the disease, and affect the radial, peroneal, accessory, etc. They are 
probably due to changes in the affected peripheral nerves, but as a rule they are 
transitory, and, in our opinion, so far as they are not accidental complications 
(such as pressure paralyses), they are to be put in the same category with tabetic 
oculo-motor paralyses (vide infra). 

We may add, finally, that slight symptoms of motor irritation, slight twitch- 



TABES DOBSALIS 



969 



ings in the muscles, especially in the fingers, are not uncommon, but they are 
noticed only when the attention is especially directed to them. It is not certainly 
known how they arise ; perhaps they are of reflex origin, or perhaps they are con- 
nected with the ataxia and loss of muscle sense. 

The condition of the muscles on passive motion is very characteristic. We 
notice in most cases a very striking flaccidity of the limbs, so that there is hardly 
any muscular resistance to be felt. In bedridden tabid patients we can often, for 
example, flex the leg with ease at the hip far enough to touch the head. There 
is evidently a diminution of muscular tonus, a so-called hypotonia of the muscles. 
Since there are many reasons for believing that the normal muscular tonus is of 
reflex origin, we are led to think of a connection between the absence of muscular 
tonus and the loss of centripetal irritations. The diminution of the muscular 
tonus in tabes is evidently in close relation to the absence of the tendon reflexes. 

The electrical excitability of the nerves and muscles remains perfectly normal 
in uncomplicated tabes. 

2. Disturbances of the Cutaneous and Muscular Sensibility. — As we have 
already said, tabes begins, in the great majority of cases, with symptoms of sen- 
sory irritation, which usually persist in the later course of the disease. Be- 
sides the simple paresthesia — the feeling of tingling and numbness in the legs, 
and sometimes, too, a similar feeling which appears quite early in the upper ex- 
tremities (especially often, as we have said, in the ulnar region) — the tabetic 
pains are remarkably characteristic of the disease. 

The intensity of the pains differs very much in different cases; but we very 
rarely see a complete absence of them. The patient's attention is often 
first called to his slight and infrequent pains by direct questioning; but in 
some cases the severe pains are a constant distress to him. The pains most 
characteristic of tabes are the lightning-like, " lancinating " pains, which shoot 
like neuralgic pains for some distance along the course of the nerves. They often 
come on in very severe paroxysms (" pain crises," sometimes associated with con- 
siderable disturbance of the general condition, loss of appetite, etc.), last one or 
more days, and then disappear for a shorter or longer time. There are also boring, 
stabbing pains, which are fixed at one point and have their seat especially in the 
vicinity of the joints; and finally " constricting pains," which are felt most fre- 
quently in the back and loins. The well-known " girdle feeling " of tabid patients 
— that is, the sensation of a band tightly encircling the trunk, or a tight, " drawn- 
together " pressure on the lateral portions of the trunk — is a similar symptom of 
sensory irritation. The girdle feeling is manifestly due to irritative processes 
in the region of the lower dorsal or upper lumbar nerves. Since it is compara- 
tively frequent, and often appears quite early, it also has a certain diagnostic 
significance. 

The tabetic pains almost always show themselves first in the legs, but pares- 
thesia also occurs, and often very early, in the intercostal region (girdle sen- 
sation). In the ulnar region quite analogous pains sometimes appear, and in 
very advanced cases we have also observed pains in the region of the occipital 
nerves and of the trigeminus. On .the other hand, neuralgic pains in the face, 
especially in the region of the frontal nerve, or in the occiput, or even migraine- 
like attacks, also occur, even in the initial stage of tabes, as we have ourselves 
observed. In some cases the lancinating pains in tabes may be accompanied by 
the appearance of herpes zoster. 

Usually much later than the pains appears also a diminution of sensibility 
which can be made out objectively. As a rule, it may be stated that in most, but 
not in all, cases of tabes the sensibility does not remain normal; although well- 
marked anaesthesia never appears until the more advanced stages of the disease. 

The form of the disturbances of sensibility varies extremely, and no disease 



970 



DISEASES OF THE NERVOUS SYSTEM 



furnishes so many opportunities for the study of interesting details in the region 
of anomalies of sensation as tabes dorsalis. Our knowledge of the occurrence of 
partial paralyses of sensation especially is very largely based on the examination 
of tabid patients. In order to form a correct opinion upon the condition of the 
cutaneous sensibility it is therefore absolutely necessary to test carefully all the 
different qualities of sensation. Beginning with the examination of simple 
sensibility to contact (tactile sense), we often find this very well preserved even 
in advanced cases. There is often, of course, a certain blunting of sensibility. 
A slight touch with a camel's-hair brush is often, even in the early stages, no 
longer felt, or felt only very indistinctly, on the lower legs and feet, or on certain 
zones on the trunk {vide infra). The disturbance of the sensibility to pain is 
more marked. A blunting of the sensibility to pain on the legs is one of the 
most constant and early symptoms of tabes, but, in order to determine it, it is 
absolutely necessary to test at first only by brief pricks. We then find, as a rule, 
that such pricks can not be positively distinguished from a touch with the 
head of the pin or with the finger, because the specific sensation of pain from the 
pin-prick is lost. The case is quite different if we keep up a continuous pin-prick. 
In that case the patient at first usually feels only a painless touch, but after a 
short time (sometimes only some seconds later) there ensues often considerable 
pain accompanied by a reflex twitch in the leg pricked. This symptom was for- 
merly explained by !N"aunyn, E. Remak, and others as " double sensation," due to 
" delayed conduction of the sensibility to pain," but, in our opinion, it is depend- 
ent merely upon the slow summation of pain irritation which requires a longer 
time {vide page 793), but there is also perhaps a delay in conduction.* Only 
in far-advanced cases can the analgesia, especially in certain parts of the skin, 
reach so great a degree that even continuous painful irritants can no longer excite 
a sensation of pain. The patient may be nearly or wholly insensible to deep 
pin-pricks or strong f aradic currents. 

The after-sensations of tabid patients are another peculiar symptom. It may 
happen that a patient after a single prick may have five, six, or more painful 
after-sensations at varying intervals. 

Disturbances of the sense of pressure, and still more that of temperature, are 
also quite frequently found, especially as partial paralyses of sensation, when the 
sensibility is otherwise well preserved. We should note particularly the occur- 
rence of partial anaesthesia of the sensibility to heat or cold. On the other hand, 
the sensibility to temperature may sometimes be very keen, while in other re- 
spects there is quite a high degree of anaesthesia. Fischer has termed a peculiar 
disturbance of sensibility occurring in tabes, polyaesthesia ; the patient asserts, 
when examined with an aesthesiometer, that he feels several (four or five) points, 
although he was touched with but one. 

The considerable anomalies of the muscular sense, which are often to be made 
out in more advanced cases, have a special interest (see page 794). If the patient 
shuts his eyes, he is often entirely unaware of the situation and position of his 
limbs. He makes an indefinite or wholly false report as to the direction and 
extent of passive motions.f If the muscular sense in the arms be disturbed, and 
we put the arms into any unusual position, the patient has considerable trouble 
in bringing the hands together with his eyes shut. He gropes about in the air 
with his arms until he accidentally touches one arm with the other hand, and 

* If, while the patient's eyes are shut, we prick the leg and the arm or neck as nearly as possible 
at the same time, the prick on the leg would necessarily be felt much later than that on the arm, if 
there is a delayed conduction of sensory impressions from the leg ; but we have never as yet been 
able to make out this condition with certainty. 

+ We can describe different letters and figures in the air with the patient's extremities, and try 
whether they can be correctly recognized with the eyes shut. 



TABES DOKSALIS 



971 



then he feels down this to the hand. The action of ataxia and innscular anaes- 
thesia are accordingly combined in these cases. Pitres has lately described pe- 
culiar attacks of muscular rigidity, and attacks of a decided feeling of fatigue in 
the muscles, apparently coming on spontaneously in incipient tabes (" crises de 
courbature musculaire "). 

The limitation of the anaesthetic or hypoaesthesic cutaneous territories is of 
much interest, if we consider them with regard to the territories of distribution 
of the different spinal ganglia (page 924 et seq.). We would mention in par- 
ticular that in the very early stages of the disease we can often find one or more 
girdling zones of hyperesthesia [or hypoalgesia] on the trunk, especially in the 
region of the upper and middle dorsal nerves (Hitzig and Lahr and others). In 
the legs very anaesthetic and more sensitive regions sometimes alternate. 

Only in rare and far-advanced cases is there finally a complete anaesthesia of 
the lower, and exceptionally of the upper extremities. We then see also at times 
disturbances of sensibility in the region of the trigeminus, in the skin of the face. 
We must also mention the fact that the peripheral nerve-trunks, especially the 
ulnar nerve at the elbow, are often insensitive to direct pressure (ulnar phe- 
nomenon [Biernacki's symptom]). 

That the cause of all these disturbances of sensation is to be looked for in 
the disease of the peripheral sensory neurones needs no further argument. It is a 
question only what share the peripheral nerves and what share the spinal fibers 
and cells have in the causation, and how far in general such a localization of the 
symptom is justified. In general we regard it as most probable that the tabetic 
pains and paraesthesiae are due to irritation in the processes of the spinal ganglia 
leading to the periphery — that is, in the sensory peripheral nerves. Anaesthesia 
must of course arise from any degenerative destruction of sensory fibers. If there 
is marked anaesthesia, and especially analgesia and thermoanaesthesia, we may 
always assume an atrophy of the root-fibers entering the posterior horns. With 
sensory disturbances in the region of the trigeminus, we may look for anatomical 
disturbances in the neurones of this nerve. 

3. Disturbances of the Keflexes. — The cutaneous reflexes show no constant 
changes in tabes. They are usually approximately normal, but sometimes they 
are diminished, especially if there be at the same time a marked disturbance of 
sensibility. In many respects their condition corresponds to the condition of the 
sensibility to pain. The abdominal and cremaster reflexes are often preserved for 
a very long time. 

The absence of the tendon reflexes, especially of the patellar and Achilles 
tendon reflexes, is, however, an almost constant sign of tabes, and is a sign of the 
highest diagnostic value. As we have already said, the disappearance of the 
patellar reflex is one of the earliest symptoms of the disease, and is therefore of 
the greatest significance in the diagnosis of initial tabes. Since this symptom 
was first discovered by Westphal it is not infrequently called " Westphal's sign." 
There are certainly cases of tabes in which the patellar reflex may persist for a 
long time, in spite of the development of many other morbid symptoms. These, 
however, are only very rare exceptions, which do not disprove the rule, and do 
not at all contradict our general views as to tabes. In individual cases those 
fibers which serve to set free the reflex may be spared for a long time, just as 
any other characteristic symptom of the disease may under some circumstances 
occasionally be absent. Concerning the precise anatomical cause of the dis- 
appearance of the patellar reflex, it can be due only to a degeneration in the 
centripetal portion of the affected reflex arc — that is, only in the fibers which 
belong to the territory of the posterior roots. It is in accordance with this that 
disease of the middle portion of the posterior columns in the lumbar cord (that is, 
the root-zones, see Fig. 132) always seems to be accompanied by a failure of the 



972 



DISEASES OE THE NERVOUS SYSTEM 



patellar reflex. The direct mechanical irritability of the muscles, especially of the 
quadriceps, is almost always retained in tabes. 

4. Disturbances in the Eye and the Other Organs of Special Sense.— The 
justification for regarding tabes as a combined systemic disease lies in the fre- 
quency with which certain cerebral symptoms, as well as the spinal, are found 
in it. 

The symptoms in the eyes deserve the first attention. We find, of course not 
in all cases, but still in the great majority of them, that the pupils show no 



symptom, so that it also has a very great diagnostic importance, the more so 
that it is rarely found except in genuine tabes and the allied general paralysis. 
In regard to the average size of the pupils, they are often about normal, but we 
very often find both pupils unusually contracted (spinal myosis) or more rarely 
dilated. Quite frequently we find in tabes inequality of the pupils and, as a 
rare symptom, a striking change in the size of the pupils, so that first one and 
then the other pupil is the larger ("springing pupil")- We may also add 
that the dilatation of the pupil which is normally produced by painful irritation 
of the skin of the cheek is often absent in tabes (Erb). 

The paralyses of the ocular muscles in tabes are also very interesting (see Eig. 
133). They are usually unilateral, but sometimes bilateral, and often appear 
even at the beginning of the disease, so that diplopia may be the first subjective 
symptom of which the patient complains. In every sudden oculo-motor or abdu- 
cens paralysis, coming on without any other cause, we must think of the possibil- 
ity of an incipient tabes. It is remarkable that these paralyses in many cases 
disappear permanently and entirely after some time, but it is always possible that 
they may recur later. We once saw a case of tabes with pronounced periodical 



Fig. 133.— Paralysis of the left oculo-motor nerve in tabes. 
(Erlangen Medical Clinique.) 




trace of contraction to light, 
although the well - known 
changes in the pupils are, as 
a rule, yet not invariably, 
very manifest upon any varia- 
tion of the accommodation — 
dilatation of the pupils on 
looking at distant objects with 
approximately parallel axes of 
vision and contraction of the 
pupils on fixing a near object 
with the greatest possible con- 
vergence of the eyeballs. We 
give this phenomenon, first 
described by Argyll Robert- 
son, but the precise anatom- 
ical cause of which is not yet 
known, the name of reflex im- 
mobility of the pupils with re- 
tained mobility on accommo- 
dation [reflex iridoplegia]. 
It is a very characteristic 
feature that the immobile pu- 
pils are often not perfectly 
round, but on careful inspec- 
tion seem rather irregular or 
polygonal. As we have al- 
ready said, the immobility of 
the pupils is often a very early 



TABES DOESALIS 973 

oculo-motor paralysis (vide page 857). The oculomotor paralysis, however, when 
it has once appeared, may be permanent, as we have repeatedly seen, especially 
in a case with bilateral abducens and unilateral oculo-motor paralysis, and also in 
a case with almost complete bilateral oculo-motor paralysis. In the autopsies on 
such cases we find the trunks of the affected nerves and their nuclei markedly 
atrophic, but it is very probable that the temporary ocular paralyses in tabetic 
patients depend upon changes in the peripheral nerves of the ocular muscles. 

The third complication in the eyes in tabes is optic atrophy. It occurs in 
about ten or fifteen per cent, of all cases, and is usually an initial symptom, at 
a time when the absence of the tendon reflexes, which may usually also be no- 
ticed, is the only thing, except this, to render the diagnosis of the disease pos- 
sible. The patient complains of diminution of vision; and the power to distin- 
guish colors, especially green, disappears quite early. On objective examination, 
we find, besides this anomaly in the color sense, usually a limitation of the field of 
vision, and the beginning gray degeneration of the optic nerve can easily be made 
out on ophthalmoscopic examination. The affection sometimes makes little halts 
and slight apparent improvements, but it usually ends with complete blindness. 
The optic atrophy more rarely may not appear until the later stages of the dis- 
ease, when all the other symptoms are already fully developed. 

Auditory disturbances are much rarer than those of sight, but they also occur. 
The cause, in at least a part of the cases, is an atrophy of the acoustic nerve. 
We had a patient with tabes under treatment for a long time who was finally 
entirely blind in both eyes, entirely deaf in both ears, and almost entirely anaes- 
thetic up to the forehead. The only possible way of communication was by writ- 
ing the different letters of each word on his forehead with the finger ! Symp- 
toms are also frequently seen which resemble those of Meniere's disease — tin- 
nitus, vertigo, and deafness. 

Changes in the senses of taste and smell have been observed only in a few 
cases. 

5. Disturbances in the Bladder, the Bectum, and the Sexual Organs. — Diffi- 
culty in emptying the bladder is an almost constant symptom in the later stages 
of tabes. It sometimes, indeed, appears very early. The patient feels the desire 
to urinate more frequently than normal, there is often a slight involuntary mic- 
turition or dribbling of urine, and at other times there is retention of urine, 
sometimes coming on quite suddenly; in advanced stages there is frequently 
complete incontinence. A cystitis very often develops as a result of all these 
disturbances, which may be the starting-point of severe pyelo-cystitis and pyelo- 
nephritis, and thus be the cause of death. 

Persistent constipation is also a very frequent symptom of tabes, the reason 
for which is perhaps to be sought in the defective reflex excitation of intestinal 
peristalsis. The constipation may in many cases give rise to very painful sensa- 
tions in the loins and abdomen. The coccygodynia, which sometimes occurs in 
tabes, has already been mentioned (see page 820). Incontinence of faeces occurs 
quite rarely in the last stages of the disease. 

A diminution in sexual power is found almost constantly in advanced cases; 
and it is also often one of the initial symptoms. 

6. Symptoms in the Internal Organs. — We see, not very infrequently, in tabes 
certain nervous symptoms in the internal organs which are in part very charac- 
teristic. The most important and the most frequent are the so-called " gastric 
crises." These almost always come on suddenly and paroxysmally, and consist 
of an extremely severe cardialgic pain, which is accompanied by violent vomiting. 
The vomitus usually consists of fluid slimy masses stained with bile, and usually 
contains so much hydrochloric acid that we can call it an actual hypersecretion 
(vide page 459). In these attacks the patient feels very wretched, and there is 



974 



DISEASES OE THE NERVOUS SYSTEM 



often at the same time palpitation, acceleration of the pulse, vertigo, etc. The 
attacks last about two or three days. In many patients they are repeated every 
few months. As we have said, the gastric crises may appear very early. We 
ourselves know cases where, in consequence of severe gastric crises, a serious gas- 
tric affection has been falsely diagnosticated, in the beginning of the disease. 
Attacks of diarrhoea, " intestinal crises," usually not associated with pain, have 
also been repeatedly observed. 

We term attacks of severe dyspnoea " laryngeal crises." These depend per- 
haps upon a (reflex?) spasm of the glottis, and may attain a very alarming degree. 
They are also associated with a severe spasmodic nervous cough like an attack 
of whooping-cough. These laryngeal crises may come on so suddenly that the 
patient may sink to the floor with symptoms of the most extreme suffocation. 
Paralysis of the laryngeal muscles (posterior crico-arytsenoids) has also been 
observed, and it is analogous to the other tabetic paralyses (ocular muscles, etc.). 
We may assume changes in the vagus-accessory nucleus, or in the vagus or recur- 
rent itself (Oppenheim), as the anatomical cause of all these symptoms. 

In a few cases " renal crises " (" crises nephritiques ") have also been de- 
scribed. They consist of severe attacks of pain, like renal colic. French authors 
also describe " urethral crises " and " crises cliioridiennes" the paroxysmal ap- 
pearance of voluptuous feelings with a vaginal secretion in women, in the begin- 
ning of the disease. 

We may mention, finally, that we sometimes see in tabetic patients a constant 
and very great frequency of the pulse, 100 to 120 a minute. We also frequently 

see the combination of tabes with aortic in- 
sufficiency which has been mentioned by 
some authors. The essential connection be- 
tween the two affections lies probably in the 
previous syphilis. 

7. Trophic Disturbances. — Although 
trophic disturbances are wholly absent in 
many cases of tabes, they may, on the other 
hand, occur so frequently and in such mani- 
fold forms as actually to be classed among 
the most interesting although least under- 
stood symptoms of tabes. We must first 
mention that the general nutrition of many 
patients with tabes, although of course not 
of all, gradually suffers in a marked fash- 
ion. The patients grow thin and have a 
peculiar suffering, faded look. We can not 
wholly deny a possible connection between 
this symptom and the primary disease. The 
trophic disturbances in the different tissues 
are still more striking. We have already 
spoken of the occasional appearance of 
herpes zoster. In some cases a marked ex- 
foliation of the epidermis has been seen, 
and also a falling out of the hair, nails, and teeth. Peculiar pargesthesise 
and hyposesthesia of the mucous membrane of the jaws and gums often pre- 
cede the loosening and falling out of the teeth. Sometimes there are small 
haemorrhages, apparently spontaneous, into the skin or into the visible mu- 
cous membranes, especially into the conjunctiva, as we have seen in several 
cases. The so-called mal perforant du pied is the worst trophic disturbance of 
the skin; this is a round, deep ulceration, situated on the ball of the foot or on 




Fig. 134.— Tabetic arthropathy of the right 
knee and left ankle. (Personal observation.) 



TABES DOESALIS 



975 




/ 



the heel, which is very hard and slow to cure in spite of the most careful treat- 
ment. 

The most interesting- trophic disturbances in tabes, however, are sometimes 
found in the bones and joints. These are the tabetic osteopathies and arthropa- 
thies, first accurately described by Charcot (Fig. 134). In the bones there 
sometimes develops a peculiar brittleness, which may lead to a sudden fracture, 
which apparently occurs quite spontaneously or on the slightest occasion, even 
in bed. The painlessness of these fractures, which is due to the tabetic analgesia, 
is very striking; the bones get out of place without the patient's noticing it, and 
thus the fracture often heals with 
displacement and an unusual callus 
formation. The tabetic joint affec- 
tions are found most frequently in 
the knee and hip, more rarely in the 
foot, shoulder, or even in one thumb. 
They often seem to begin very acute- 
ly, a very great serous effusion some- 
times taking place into the cavity of 
the joint. Besides this effusion there 
gradually develop the manifold pro- 
cesses of a chronic arthritis defor- 
mans: on the one hand, atrophy of 
the articular ends of the bones; on 
the other, thickening of the cap- 
sule, the formation of osteophytes, 
etc. In connection with the arthrop- 
athy there is often permanent dislo- 
cation of the joint. Thus we often 
see, following a tabetic affection of 
the knee, a genu recurvation (Fig. 
135). Arthropathia muscular atro- 
phy is often seen, and is worthy of 
note (atrophy of the quadriceps in 
disease of the knee-joint, etc.). Ta- 
betic arthropathy may thus finally 
lead to monstrous changes in the 
joints such as can scarcely be found 
under other circumstances. Corre- 
sponding changes are also seen in the 
vertebral column. They may give 
rise to fracture of the vertebras, 
spinal curvature, etc. The develop- 
ment of the so-called "pied tabe- 
tique " (Charcot) is also an osteo- 
pathic process; this consists chiefly 
of a considerable thickening and pro- 
trusion of the dorsum of the foot 
with a marked flattening of the sole. 

We are not yet able to explain fully the occurrence of all these changes. It is 
hard to avoid entirely the assumption of trophic nervous disturbances. It has 
been claimed that degenerative changes have been found in cases of tabetic os- 
teopathy and arthropathy in the nerves leading to the bones and joints; but it is 
also possible, on the other hand, that many of the so-called tabetic arthropathies 
may be of syphilitic origin. It is an important fact that conditions may exist in 



\Vp 




Fig. 135. 



-Genu recurvatum in tabes dorsalis. 
(Personal observation.) 



976 



DISEASES OF THE NERVOUS SYSTEM 



tabes, which must have a very unfavorable influence upon any existing bone or 
joint affection. The most important of these is analgesia. That is the reason why 
patients, in spite of a beginning arthropathy, do not spare the affected joint but 
continue to irritate it still more. We saw a patient, for example, where an affec- 
tion of the knee-joint developed in a comparatively very early stage of tabes, 
which up to that time had not been diagnosticated at all. As the patient felt no 
pain whatever in his knee, he hunted most vigorously through a whole autumn, 
until finally an extremely severe swelling of the knee-joint and an actual subluxa- 
tion of the leg ensued. It is also possible that pronounced ataxic movements may 
frequently aid in irritating the articular surfaces. 

The muscles preserve in general their normal state of nutrition, except as they 
take part in some joint affection or in a general emaciation. Charcot described 
a case of a combination of tabes with genuine progressive muscular atrophy, in 
which the autopsy showed a degeneration of the anterior gray cornua in the spinal 
cord besides the atrophy of the posterior columns. The first report upon a unilat- 
eral atrophy of the tongue, which sometimes develops quite early in tabes, is due 
to the same observer. These and similar atrophies sometimes seen in other mus- 
cular territories are due to degeneration of the corresponding motor nuclei (hypo- 
glossal nucleus, etc.) ; but peripheral neuritis may also lead to muscular atrophy 
in tabes. Joffroy described a special form of tabetic club-foot (" pied hot ta- 
betique "), which seems to be due to an atrophy of the calf muscles. 

Some observations of apparently spontaneous rupture of the tendons (Achilles 
tendon, ligamentum patellae) show that peculiar trophic disturbances may also 
develop in them. 

8. Cerebral Symptoms. — Besides the frequent important disturbances on the 
part of certain cerebral nerves, such as the optic and oculo-motor, which have 
already been discussed, we must mention here the relation between tabes and 
progressive general paralysis (q. v.). On the one hand, the symptoms of tabes 
are often present in the course of general paralysis, so that the autopsy shows a 
typical degeneration of the posterior columns (Westphal) ; and, on the other 
hand, it also happens that the whole process begins with tabes, which may exist 
alone for years without any mental symptoms, and then only at the close do the 
symptoms of paralytic dementia (mental weakness, disturbances of speech, para- 
lytic attacks, delusions of grandeur, etc.) appear. This combination of the two 
diseases is nothing strange, since general paralysis is also a post-syphilitic nerv- 
ous disease, and is to be regarded as almost wholly analogous to tabes. Paralytic 
dementia has been called, not without reason, " tabes of the brain." 

The complication of tabes with hemiplegia repeatedly occurs. The latter de- 
pends upon a cerebral haemorrhage or an embolic or thrombotic softening, so that 
the two diseases are probably connected only so far as they are both perhaps re- 
lated to previous syphilis. It seems to us worthy of note that in two such cases 
we saw scarcely any contracture develop in the paralyzed limbs. 

Course and Prognosis. — Although most of the characteristic symptoms of 
tabes develop in almost all cases, still the order and the intensity of their onset 
vary greatly. We have already briefly described the general type of the disease 
which most frequently comes under observation, and many other peculiarities in 
its course have been mentioned from time to time. 

We have stated that the initial period is usually characterized — apart from 
the symptoms that can be made out only objectively, such as absence of the patel- 
lar reflex and reflex immobility of the pupils — by the lancinating pains ; that these 
may differ very much in intensity ; and that the duration of this first stage may 
vary between a few months and ten or twenty years. The optic atrophy, the 
ocular paralyses, gastric crises, vesical disturbances, etc., were mentioned as 
rarer initial symptoms. The passage from the first stage to the second — the stage 



TABES DOESALIS 



977 



of ataxia — is sometimes very gradual, but in other cases very rapid and sudden. 
We have repeatedly seen such transitions. Frequently they come on clearly 
after some special exciting cause, as after some injury, some physical over-exer- 
tion, etc. If the previous symptoms were slight, the patient dates his disease 
from this point,, and says that he was quite suddenly broken down by some cause, 
and that since then he has not been able to walk at all, or else only with diffi- 
culty. Even in such cases there is often slow improvement following the sud- 
den change for the worse, but the gain, of course, is not permanent. In other 
cases, however, the ataxia develops only very slowly and never reaches a very 
marked degree. Experience teaches, in particular, that tabid patients with early 
atrophy of the optic nerves or with unusually severe attacks of pain are often 
without more than a trace of ataxia for a very long time — many years ! 

Xo rules of general value can be given as to the further advance of the disease, 
the invasion of the arms by the ataxia, or the occurrence of the rarer symptoms, 
such as the joint affections, etc. Almost every individual case affords its idiosyn- 
crasies, since one group of symptoms is often especially prominent, while another 
is entirely absent or developed only to a slight degree. On the whole, however, we 
can almost always make out a gradual, even if a very slow, advance in the disease. 
Xew symptoms appear, the old ones increase, the general condition becomes worse, 
until finally the last stage of the disease comes on. 

Recovery from tabes in the sense that all the existing symptoms (immobile 
pupils, absence of patellar reflex, etc.) wholly disappear, have never yet been 
observed with certainty, and a priori such a thing is hardly conceivable; but it 
is not so very rare for the tabetic process to be arrested for at least a year. We 
have become acquainted with such cases only since we have been able to recognize 
with certainty the initial stages of the disease. We have ourselves known for 
many years a number of mild cases of tabes in whom it is scarcely possible to 
detect any recognizable progress in the disease and who regard themselves as 
almost perfectly well. They go to their business and have little or no trouble 
from their disease. Of course we must be prepared for an ultimate change for the 
worse even in such cases. In more advanced tabes, treatment may at most cause 
some improvement, delay the course of the disease, and alleviate certain symp- 
toms ; many patients, especially under favorable external conditions, may even in 
this stage lead a tolerable existence for years. 

Diagnosis. — There is scarcely any other disease of the spinal cord whose diag- 
nosis can in most cases be made with so great certainty and such comparative 
ease. Since tabes is a combined systemic disease, it affords a definite combina- 
tion of symptoms such as can occur under no other conditions. The diagnosis, 
therefore, is never to be made from any one single symptom, but only from the 
combination of all and from the whole course of the disease. 

The diagnosis of initial tabes is especially important. In every case of obsti- 
nate " rheumatic " pains, or similar pains in the lower extremities, we should 
think of the possibility of tabes, and examine the tendon reflexes and the pupils. 
The combination of characteristic pains, absence of the patellar reflex on the two 
sides, and reflex immobility of the pupils, usually makes the diagnosis almost 
absolutely certain, as was said above; two of these symptoms, especially if the 
reflex immobility of the pupils be one, make it at least very probable. Ocular 
paralyses, temporary ptosis, or temporary diplopia, may be very important for the 
diagnosis. We should also remember that the disease may begin with optic atro- 
phy, and that early gastric crises may simulate a gastric affection, early disturb- 
ance in micturition a vesical trouble, or swelling of the joints, a joint disease, 
until careful examination of the other symptoms explains the true nature of the 
disease. The essential point is to think at once in every such case of the possi- 
bility of tabes, and look for the distinctive objective symptoms. Among the latter 
62 



978 



DISEASES OE THE NERVOUS SYSTEM 



we would call especial attention here, besides the symptoms generally recognized 
(absence of tendon reflexes, immobile pupils, slight vesical weakness), to the 
limited girdle-like disturbance of sensation on the trunk, since in doubtful cases 
this is often of decided significance in diagnosis. 

In the fully developed ataxic stage of tabes the diagnosis is almost always 
easy, and it often can be made at the first glance. The history, the characteristic 
ataxic gait, the swaying with the eyes shut, the absence of the reflexes, etc., ex- 
clude every doubt. The diagnosis may be more difficult if we happen to see the- 
patient for the first time in the final stage, when actual paralysis has set in, when 
a complicating hemiplegia has arisen, etc. In such eases we must lay stress on 
the development of the disease and find out what characteristic tabetic symptoms 
— pupillary symptoms, absence of patellar reflex, vestiges of ataxia, or pains — can 
now be discovered. With proper attention and knowledge of the case, the diag- 
nosis can even then almost always be made correctly. 

Vertebral affections are to be mentioned first of the diseases which may be 
confused with tabes. These also cause, under some circumstances, lancinating 
pains and an absence of the patellar reflex, as a result of compression of the spinal 
i-oots; but in these cases the later course of the disease is entirely different, 
apart from the changes in the vertebral column and the absence of other charac- 
teristic symptoms of tabes, especially the immobile pupils. The same holds true 
of certain deep-seated tumors in the vicinity of the spinal cord. We have already 
said that in rare cases a multiple sclerosis may offer symptoms similar to 
those of tabes. In these cases the chief stress in regard to diagnosis is to be 
laid on the condition of the tendon reflexes, the pupils, the disturbances of sen- 
sation, and the bladder. It is of greater practical importance that certain toxic 
nervous diseases may have a great similarity to tabes. Chronic alcoholic neuritis 
has already been spoken of in this connection — the so-called pseudo-tabes of alco- 
holic subjects. In these cases, however, the reflex immobility of the pupils and the 
disturbances of the bladder are usually absent, while atrophic paralysis may 
develop at the same time, which hardly ever happens in tabes. The serological 
factors (alcoholism) are also, of course, to be taken into account. In adults post- 
diphtheritic ataxia may be mistaken for tabes. In such cases a consideration 
of the aetiology, and especially the condition of the pupils and of the vesical dis- 
turbances, will usually make the correct diagnosis easy. " Diabetic tabes " (page- 
758) can scarcely, with proper attention, be mistaken for true tabes. The dif- 
ferential diagnosis between tabes and Friedreich's hereditary ataxia will be de- 
scribed in the next chapter. 

Finally, it may be mentioned here that we have twice seen a group of nerv- 
ous symptoms in men who have worked many years in tobacco factories, which 
resembled tabes in so many points that we might term it " nicotine tabes." The 
morbid symptoms, which resemble tabes, consist of painful sensations, absence of 
the patellar reflex, contracted pupils with reflex immobility, and uncertainty of 
gait; but the whole type of the disease is distinguished from tabes by a peculiar 
tremor, by a marked increase of the cutaneous reflexes, especially in the lower 
extremities, etc. , 

Treatment. — The tedious course of tabes demands that the physician have at 
hand a number of remedies and methods of treatment which he can vary according 
to the predominating circumstances, either to obtain a certain amount of improve- 
ment by a new way of attacking the disease, or at least constantly to kindle the 
patient's hope and courage anew. 

The first question which is usually raised at present in regard to the treat- 
ment of tabes is in regard to the efficacy of a specific antisyphilitic treatment. 
In our opinion, the ability to answer this question correctly depends not merely 
on recognizing the fact of the connection between tabes and syphilis, but also on 



TABES DORSALIS 



979 



forming a clear conception of the nature of this connection. There can then be 
no doubt that in tabes there is not even a remote question of such efficacy of mer- 
cury or iodide as we see almost as a rule in true tertiary, gummatous syphilitic 
diseases. We very often see in tabes no benefit at all from an inunction cure 
or from the internal use of iodide of potassium, and in some cases the con- 
dition seems even to grow worse under such treatment. Such observations were 
for a long time cited as the chief evidence against the connection between the 
two diseases. If, however, we adopt the position which we have advanced that 
tabes is a post-syphilitic degenerative nervous disease, just as ataxia may some- 
times be a post-diphtheritic disease, we can easily understand the inefficacy 
of a specific remedy, which acts only on syphilitic new formation of tissue. 
Nevertheless we may not wholly exclude antisyphilitic methods of treatment from 
the therapy of tabes; for, in the first place, it is always possible (and it seems to 
us to be confirmed by many trials) that an antisyphilitic treatment (inunction, 
iodide of potassium) may influence in a way beneficial to the patient the con- 
ditions which cause tabes to advance. It has, furthermore, been fully attested by 
repeated observations that, besides the tabetic changes in the cord, there may also 
be at the same time actual syphilitic gummatous processes, which of course may 
contribute their part to the symptoms of the disease. That these morbid processes 
require thorough specific treatment is certain, and therefore we regard it as justi- 
fiable and even desirable to make a trial of inunction in beginning tabes, and 
under some circumstances even in advanced tabes, especially if any anomalies in 
the type of the disease suggest the possibility of co-existing gummatous changes. 
Very experienced observers, especially Erb, have gained the impression that a 
careful inunction treatment sometimes visibly benefits the patient. We can not, 
of course, report much that is favorable from our own experience, but we often 
employ specific treatment, especially iodine preparations, in cases that seem 
suitable. Every inunction treatment prescribed in tabes must be carefully 
watched, that no injury be done to the patient by this potent remedy. In many 
advanced cases of tabes, especially where the patient's general condition is feeble, 
we must abstain wholly from mercurial treatment. 

If the antisyphilitic treatment be not indicated, or if it has been unsuccessful, 
electricity and balneo-therapeutics or hydro-therapeutics deserve relatively the 
most confidence, although of course we must beware of exciting too sanguine 
hopes. 

The electrical treatment consists chiefly of the passage of the ascending con- 
stant current through the spinal cord. The current must not be too strong, and 
the sittings should take place daily, or every other day. Erb recommends placing 
the medium-sized cathode in the vicinity of the sympathetic, and the large anode 
close to the spinous processes on the other side of the vertebral column, moving it 
at intervals from above downward. This procedure lasts about four or five min- 
utes for each side. We also obtain good results symptomatically when there are 
severe pains, vesical weakness, etc., by peripheral galvanization. If we find pain- 
ful points on the vertebral column, as is rarely the case, they should be especially 
treated with the stabile anode. The treatment recommended by Rumpf with the 
faradic brush has also been used at times with good results. This consists in 
brushing the skin of the back and the extremities with a strong current for five 
or ten minutes. Every form of electrical treatment, in order to obtain results, 
must be kept up for months. 

Hydro-therapeutics, used rationally, have often resulted in considerable im- 
provement in tabes, although they may cause much mischief. Hot baths, espe- 
cially vapor-baths, are often followed by a rapid change for the worse — a fact 
which, unfortunately, we can often observe where vapor-baths have been pre- 
scribed for patients at the beginning of their disease " for rheumatism." Con- 



980 



DISEASES OF THE KEKVOITS SYSTEM 



tinuous wet packs and severe rubbings are also often accompanied by unfavorable 
results. Tepid half or full baths, however, of 75° to 86° at most (20° -24° K.), 
associated with gentle rubbing of the skin, or brief cold sponging, etc., often do 
good service. Wet compresses, applied around the abdomen or the legs at night, 
often have a favorable influence on the pains. In general, it is a good plan to 
send well-to-do patients in summer to a water-cure establishment which is con- 
ducted by an experienced director and well equipped, but the necessary procedures 
may also be undertaken at home. 

Of the baths whose use is recommended in tabes, Oeynhausen has the greatest 
reputation. The baths in Nauheim have a composition and action very similar to 
those at Oeynhausen. We have also seen very good results from the baths at 
Kissingen. Many physicians praise mud-baths and iron-baths (Pyrmont, Dri- 
burg, Cudowa, Elster, Eranzensbad, etc.), while the indifferent thermal baths 
(Teplitz, Wildbad, Ragatz, etc.), formerly much in favor, are at present rarely 
used in tabes. For the preparation of artificial carbonic-acid salt baths see 
pages 952, 953. 

Besides the methods of treatment thus far mentioned, there are still a number 
of internal remedies, the use of which seems sometimes to be of advantage. The 
chief ones to be mentioned are nitrate of silver, first recommended by Wunderlich, 
one-sixth-of-a-grain pills (gramme 0.01), at first three, gradually increasing to 
six a day, before meals; and ergotine,* one-grain pills (gramme 0.05), three to 
six a day; we may also try iodide of potassium, phosphorus, arsenic, etc. All 
these remedies, especially the two first named, may be used for a long time, and, 
with interruptions, even for years. 

In consequence of a somewhat too sanguine indorsement by Langenbuch, 
nerve-stretching (usually the operative stretching of both sciatics) was for some 
time practiced on many tabid patients, but since experience has taught us that 
nerve-stretching, in spite of some apparent successes, scarcely ever exerts a perma- 
nent favorable action, and is also not wholly without danger, the operation has 
been almost entirely given up in tabes. It may still be tried in those cases where 
we have unusually severe attacks of pain in the region of definite nerves. In 
such cases we should first try bloodless stretching (page 820). The "suspension 
treatment " of tabes has also had only a brief vogue. This consisted in hang- 
ing up the patient for a short time by an apparatus fastened under the chin 
[and arms], thus stretching the spinal cord and the nerve-roots by the weight of 
the body. The successes at first reported are of very doubtful significance, while 
there were certainly some very unfortunate consequences. We ourselves can 
not advise the use of this method. The treatment of tabes by firmly fitting 
corsets is also much praised and recommended. If we listen to the patients who 
have just left the sanitarium of some eminent orthopaedic surgeon, they know 
no end to their praise. If we see them again in a year and a day, we find them 
ataxic as before, and the corsets — in some corner ! Temporary symptomatic bene- 
fit should not be denied, but of course the corset treatment can not affect the 
tabetic process itself. 

Symptomatically, the same remedies are to be considered as were mentioned 
in the treatment of chronic myelitis. We try to alleviate the pains by narcotic 
embrocations and bandaging the legs. Of internal remedies, sodic salicylate and 
antipyrine, and also antifebrine, phenacetine, or a mixture of these remedies, 
sometimes undoubtedly alleviate and shorten the pains. [Chloride of aluminium, 

* There is only an apparent contradiction in the fact that, in spite of the occurrence of an " ergo- 
tine tabes 1 ' (vide supra), ergotine is also used as a remedy against tabes. It may very well be that 
the same remedy, which in large doses causes certain systems of fibers to atrophy, may in smaller 
doses have some favorable (stimulating) action on the same system of fibers ; but we must always be 
cautious in the use of ergotine. 



HEKEDITAEY (JUVENILE) ATAXIA 



981 



in doses of two to four grains (gramme 0.1-0.25) three times a day, occasionally 
relieves the pain. — K.] Some observers praise the action of the so-called points de 
feu (circumscribed burning of the skin with the thermo-cautery) along the spine 
at the points of exit of the affected nerve-roots. In bad cases morphine is indis- 
pensable. We try to remove the constipation by prescriptions as to diet, or by mild 
cathartics, such as the bitter waters, tamarinds, and rhubarb, by enemata, or by 
electrical treatment and massage of the abdomen. Galvanic treatment often 
acts very favorably on the bladder symptoms. For these symptoms Charcot 
praises the action of ergot, and other physicians recommend strychnine. Mor- 
phine is the best remedy in the gastric crises. We may also try warm poultices, 
washing out the stomach, belladonna, chloral, cocaine, etc. Severe laryngeal 
crises also require morphine injections as a rule. Optic atrophy unfortunately 
defies any treatment. We usually try strychnine injections to encourage the 
patient. 

One method for the symptomatic treatment of tabes deserves special mention, 
and that is the treatment of ataxia by methodical exercises (G. Frenkel). If 
ataxic patients are systematically admonished to execute all the movements of 
the several joints slowly and as regularly as possible several times each day for a 
definite time, and also to perform certain other movements (touching a definite 
point with the fingers or toes, walking a chalk mark, walking between the rungs 
of a ladder, seizing swinging balls, putting stoppers into definite holes, etc.), 
we may often recognize that the practice actually has an influence upon the 
certainty of the movements and leads to an improvement in the ataxia. Certain 
sanitaria carry out this method of treatment by the use of complicated apparatus. 
The benefit, however, should not be overvalued. 

It is also of the greatest importance that the physician should regulate and 
supervise the patient's mode of life in its general hygienic and dietetic aspect. 
We must warn him especially against any physical or mental over-exertion, 
prescribe a prudent but strengthening diet, withdrawing all large amounts of 
alcoholic drinks, and enjoin good air, a country residence in summer, or a medium 
mountain climate, and in winter at times southern resorts. How effective this 
general dietetic treatment of tabes is, may be seen in hospitals, where tabid pa- 
tients of the lower classes are sometimes much benefited by simple rest and good 
care. The earlier we get the patient under treatment, the more persevering and 
careful should we be in our treatment, because then we can still hope for a cer- 
tain success. In old and far-advanced cases we must confine ourselves to a purely 
symptomatic treatment. 



CHAPTER VIII 
HEREDITARY (JUVENILE) ATAXIA (FRIEDREICH'S DISEASE) 

etiology and Pathological Anatomy.— In 1861 Friedreich first described a 
peculiar disease observed by him in several members of the same family. He at 
first regarded the disease as a special form of tabes on account of the marked 
ataxia attending it, but later investigations have shown that this "Friedreich's 
disease" has nothing in common with true tabes except a certain similarity of 
symptoms (especially ataxia), which is due to the fact that the anatomical 
changes in the cord agree in part in the two affections. While tabes represents 
an acquired degeneration of different neurone systems, Friedreich's disease is 
undoubtedly due to a congenital morbid predisposition of certain neurone sys- 
tems, as a consequence of which these neurone systems have not developed their 



982 



DISEASES OF THE NERVOUS SYSTEM 



full and permanent functions and therefore atrophy slowly and prematurely. 
This congenital origin of the disease is most evident from the fact that the disease 
is not infrequently seen in several (two to five) brothers and sisters, and in some 
cases in members of two or more generations of the same family. Of course 
sporadic cases of Friedreich's disease are seen with comparative frequency, but 
in such cases the youthful age at which the first symptoms of the disease are no- 
ticed indicates the congenital abnormal tendency. The first symptoms sometimes 
appear at the age of seven to ten years, but frequently not until puberty, and in 
some cases even somewhat later (eighteen to twenty years). It is usually hard to 
determine accurately the period of onset, because the disease begins very gradual- 
ly, and therefore its onset may certainly remain unnoticed for a long time. The 
disease is about equally common in the two sexes, perhaps a little commoner in 
the male. The first symptoms sometimes seem to follow some acute disease 
(scarlet fever, measles, influenza), injury, etc., but these are exciting causes 
which make the existing morbid tendency manifest. 

Clinical History. — The first symptom invariably to be noticed, which is by far 
the most important later, is ataxia. It shows itself at first as a slowly increasing 
uncertainty of gait; almost at the same time or only a little later the ataxia 
is noticed in the upper extremities. When the disease is fully developed the gait 
is unusually characteristic. In regard to the ataxic movements of the legs the 
gait resembles that of tabes, but it usually differs from it in the much greater 
swaying of the trunk. In this respect the gait is more like that of the so-called 
cerebellar ataxia. The fact that in Friedreich's disease the muscles of the trunk 
and pelvis are also affected by the ataxic disturbance, and even to a greater de- 
gree, is the reason why the patient usually manifests more of the so-called static 
ataxia than is the case in tabes — that is, that he continually sways very much 
when standing quietly (vide Fig. 136). The patient therefore always stands and 
walks with the legs wide apart to give the body a better support. If we make 
him stand still with the legs as close together as possible, we notice the constant 
muscular contractions necessary to maintain the equilibrium. "With the removal 
of the visual control by closing the eyes, the uncertainty and swaying of the 
body increases. The ataxia is also very well marked in the legs, as is most readily 
shown by the well-known "knee-heel test," and also in the arms, as tested by 
bringing the finger-tips together, by reaching for an object held before one, 
writing, etc. The disturbance of speech, which is often noticed in the later 
stages, is due to an ataxia of the muscles requisite for speech, and consists of 
an indistinct articulation and a slow, scanning, badly modulated manner of 
speaking. Nystagmus of the eyes, especially on looking far to one side, some- 
times occurs as a further ataxic symptom, just as in multiple sclerosis, but it is 
by no means invariable, or at least it may not appear until late in the disease. 

Besides the ataxia, which finally becomes very pronounced, for a long period 
we can usually detect only one other important symptom, which is probably 
always of very early occurrence — the complete absence of the patellar reflex. All 
other nervous functions may remain wholly unaffected for a long time. The 
motor strength of the muscles is very well retained. We know a patient who, in 
spite of the most marked ataxia, has traveled several miles a day by the aid 
of a cane. The muscles are usually not remarkably well developed, but they show 
no striking atrophy, apart from rare complications. Many patients show a 
peculiar choreic muscular unrest. The sensibility of the skin and deeper parts 
(joints, muscular sense) may for a long time remain perfectly normal, a condi- 
tion which has been justly brought forward, especially by Friedreich, as an argu- 
ment against the dependence of ataxia upon sensory disturbances. Of course this 
preservation of sensibility must not be too much emphasized, since many other 
observers and we ourselves have repeatedly found slight disturbances of sen- 



HEREDITARY (JUVENILE) ATAXIA 



983 



sibility (especially on the feet, toes, and lower legs) on careful testing: for ex- 
ample, a slight diminution of the tactile sense, the pressure sense, sometimes the 
muscular sense, etc. The sensibility to pain seems almost always to remain un- 
affected. Paraesthesise and spontaneous pains are also entirely absent. The 
cutaneous reflexes show no material disturbance and the pupil reflexes are always 
preserved. Disturbances of the bladder are also absent. In some cases, however, 
there may be atrophy of the optic nerves, just as in tabes. We niay also note that 
the toes, especially the great toes, 
have a very striking tendency to 
assume a position of extreme dor- 
sal extension, and we sometimes 
see a tendency for the foot to as- 
sume the equinus position. The 
vertebral column often shows an 
evident scoliosis. 

The course of the disease is 
very chronic and it may last for 
years and years. The ataxia 
finally becomes so great that the 
patient is bedridden. In such 
cases there is finally actual paraly- 
sis, greater disturbance of sensa- 
tion, disturbances of intelligence, 
etc. Death often ensues from 
some intercurrent disease. 

Pathological Anatomy.— He- 
reditary ataxia was the first form 
of disease in which a combined 
systemic lesion of the spinal cord 
was discovered by careful anatom- 
ical investigation by Kahler and 
Pick. Later observers (F. 
Schultze, Riitimeyer, and others) 
have confirmed these discoveries. 
We find the posterior roots and 
the posterior columns most dis- 
eased, and chiefly the zone of the 
entering root-fibres. Lissauer's 
areas are usually exempt, in con- 
trast to the degeneration of tabes. 
The cerebellar lateral tract (in- 
cluding probably the cells of 
Clarke's columns) is also regular- 
ly affected, and also Gowers' tract 
(see the chapter on secondary de- 
generations in the cord) and the 
neighborhood of the pyramidal lat- 
eral tract, although in lesser degree. The histological process, as in all systemic 
diseases, consists of a degenerative atrophy of the nervous elements and a con- 
siderable secondary increase of the neuroglia. 

It would be very interesting to make a careful comparison between the ana- 
tomical lesions and the symptoms in Friedreich's disease, on the one hand, and 
in tabes on the other; but we are still greatly in want of a sufficient number of 
careful observations. The absence of marked sensory disturbances and of lan- 




Fig. 136.— Attitude of a patient with hereditary ataxia. 
(Personal observation.) 



984 



DISEASES OE THE NEKVOUS SYSTEM 



cinating pains in hereditary ataxia is striking. The absence of pain is explained 
perhaps by the integrity of the peripheral nerves, or perhaps by the different 
nature of the disease : in tabes we have the action of irritating toxines, in hered- 
itary ataxia simple endogenous atrophy. 

Diagnosis. — The diagnosis of Friedreich's disease is easy, if we are acquainted 
with the disease, and it is usually perfectly definite. The marked ataxia, espe- 
cially the tottering, uncertain gait, besides the youth of the patient, and at times 
the hereditary conditions, as a rule soon render a correct decision possible. The 
absence of immobility of the pupils, of marked sensory disturbances, of symptoms 
of sensory irritation, of vesical disturbances, etc., distinguish the disease from or- 
dinary tabes. It is easier to mistake it for multiple sclerosis, since this also comes 
on in youth; but Friedreich's disease often begins in childhood, which is only 
exceptionally the case with multiple sclerosis. The examination of the patellar 
reflex is most distinctive ; this is entirely absent in hereditary ataxia and increased 
in multiple sclerosis. The condition of the patellar reflex also distinguishes 
Friedreich's disease from hereditary cerebellar ataxia, soon to be described (vide 
infra) . The distinction from post-diphtheritic and similar forms of ataxia should 
also give rise to no difficulty. 

Treatment. — Although there are some variations in the course of the disease, 
it seems in general always to advance and to be' incurable. We can therefore 
merely try to obtain temporary improvement and an arrest of the disease by in- 
telligent care of the patient and by all the methods employed in chronic nervous 
diseases (see the previous chapter). 



APPENDIX 

HEREDITARY CEREBELLAR ATAXIA 

(Heredo-ataxie Cerebellevse) 

As an appendix to Friedreich's ataxia we must here mention still another 
remarkable hereditary and family disease, the chief symptom of which is also 
ataxia, while the most essential anatomical change consists of an atrophy of the 
cerebellum (JSTonne, P. Marie, Londe, and others). 

The disease occurs in brothers and sisters and members of different generations 
of the same family, but there are probably sporadic cases besides. The two sexes 
are about equally affected; the male sex seems to predominate somewhat. The 
first symptoms of the disease usually appear between the twentieth and the thir- 
tieth year, sometimes earlier, rarely later. They consist of the slow onset of 
ataxia of the extremities and particularly of a staggering, reeling gait. Stand- 
ing is also insecure, but on the whole it is only slightly altered by closing the 
eyes. In the arms the ataxia may become so great as to render all the finer 
occupations (writing, etc.) almost impossible. The ataxia of the facial muscles 
causes mimetic movements of expression which are often extremely peculiar and 
bizarre; the speech is usually considerably disturbed. The muscular strength is 
not diminished, although the patient often complains of feeling fatigued. The 
sensibility is perfectly retained and, in particular, we find the muscular sense 
wholly unaffected. The cutaneous reflexes are normal or somewhat diminished, 
but the tendon reflexes are almost invariably increased, although marked spastic 
symptoms are absent. The innervation of the bladder undergoes no change. The 
pupils usually retain their normal reaction, but atrophy of the optic nerves with 
the corresponding disturbance of vision has been repeatedly observed. Pro- 
nounced mental disturbances, such as weakness of memory, abnormal irritability, 
etc., may also develop. 



PEIMAEY DEGE^ T EEATIONS OF THE MOTOE TEACT 985 



Tlie disease has a very tedious course and usually lasts many years. The 
prognosis is absolutely unfavorable. Death ensues from some intercurrent dis- 
ease or as a result of the ultimate general weakness. Anatomical examination, as 
has been said, shows as the most striking change an atrophy of the cerebellum, 
which is diminished about one half in size. The spinal cord is sometimes poorly 
developed on the whole, but it shows no columnar degeneration. 

The disease is distinguished very essentially from Friedreich's hereditary 
ataxia, which otherwise is very similar to it, by this anatomical condition, which 
is, however, still in urgent need of thorough study. Clinically the two diseases 
are to be distinguished particularly by the condition of the tendon reflexes and 
the fact that cerebellar ataxia usually comes on somewhat later in life. The 
differential diagnosis between cerebellar ataxia and multiple sclerosis is often 
very difficult. The generic (family) occurrence is the chief distinction. 

The treatment can be merely symptomatic, and it has little prospect of success. 



CHAPTEE IX 

THE PRIMARY DEGENERATIONS OF THE MOTOR TRACT, INCLUDING 

THE MUSCLES 

1. Preliminary Eemarks 

In the two preceding chapters we have become acquainted with two diseases 
whose anatomical basis is a primary degeneration of a number of systems of 
fibers whose conduction was chiefly centripetal. In tabes we found the cause of 
the degeneration to be exogenous, acquired noxious influences, coming from with- 
out and probably of chemical nature ; in hereditary ataxia, on the contrary, the 
cause was endogenous anomalies — that is, anomalies in the embryonic predisposi- 
tion, and therefore congenital, which caused a premature atrophy of nerve-fibers 
which had from birth an abnormally weak power of resistance. In this chapter 
we shall become acquainted with a number of diseases, which are due chiefly to 
primary degeneration of the great centrifugal motor conducting tract, especially 
the pyramidal tract. We will see that, just as with hereditary ataxia, the basis 
of the disease is chiefly an endogenous, congenital weakness of this portion of the 
nervous system, so that it is therefore very often a family, generic disease; 
although in some cases exogenous noxious influences are probably also to be con- 
sidered. 

In order to obtain a preliminary review of the whole group of diseases here 
under consideration, we may picture to ourselves, as in the accompanying dia- 
gram ((Fig. 137), the course of the long conducting tract leading from the 
central convolutions to the muscles, as has been fully described on page 829. 
In the first place we will consider a form of disease in which ultimately the 
whole cortico-muscular conducting tract, from the cortical cell, C, up to and 
including the muscle, M, is found degenerated. This is amyotrophic lateral 
sclerosis. We will next describe a form of disease in which only the second 
portion (the so-called second neurone) of the whole tract — namely, the portion 
from the ganglion-cell in the anterior horn of the cord (F) up to and including 
the muscle — is affected. This is spinal muscular atrophy, and the completely 
analogous progressive bulbar paralysis. In the third place we shall see that the 
first main portion of the tract, PyS, may be alone affected up to the cell of the 
anterior horn, but without involving it. We then have the true primary pyramidal 



986 



DISEASES OF THE NERVOUS SYSTEM 



lateral sclerosis, with the clinical picture of pure spastic spinal paralysis. In the 
fourth place the disease may involve only the peripheral motor nerve, ra, with 
its corresponding muscles (neurotic muscular atrophy), and finally we may also 
place here by far the commonest form of disease, the progressive muscular dys- 
trophy — that is, that disease in which only the terminal apparatus of the whole 
tract, the muscle itself, undergoes a progressive atrophy. 

The forms of disease just mentioned are probably, so far as they are endoge- 
nous diseases, all closely allied, but it is still necessary for a time to keep them 

separate, at least so far as they show 
very definite marks of distinction, 
both clinically and anatomically. 
Only with a more advanced knowl- 
edge of the special nature of all these 
morbid conditions can we make a 
strict serological division of them. 
At present we must remember that 
we can not consider the different clin- 
ical and anatomical forms as different 
diseases, strictly separate from one 
another. The more our knowledge 
increases, the more prominent seem 
to be transitions and connecting links 
between the different forms. 

2. Amyotrophic Lateral Sclerosis 

iEtiology and Pathological Anat- 
omy. — For the first accurate knowl- 
edge of amyotrophic lateral sclerosis 
we must thank Charcot, who pub- 
lished in 1869, in company with 
JofTroy, his first observations upon 
such cases, and who in 1874 was able 
to give quite a complete description 
of the disease; but an exact knowl- 
edge of amyotrophic lateral sclerosis 
was first made possible by Flechsig's 
investigations upon the course of the 
conducting tracts in the spinal cord. 
From these we can now say that the 
disease is manifested anatomically 
essentially as a primary systemic de- 
generation of the whole cortico-mus- 
cular conducting tract, and not only of the spinal portion thereof belonging 
to the extremities, but also of the bulbar portion belonging to the muscles of the 
face, tongue, soft palate, etc. These two parallel portions 'must be regarded as 
completely equivalent parts of one great motor system — a point to which we shall 
frequently return later. The motor-nerve nuclei in the medulla and pons (for the 
hypoglossus, facial, motor, trigeminus, etc.), and also the nuclei for the oculo- 
motor nerves, are to be regarded as precisely analogous to the ganglion-cell groups 
in the anterior horns of the cord for the muscles of the extremities. 

In amyotrophic lateral sclerosis a large part of this motor conducting tract 
undergoes degeneration, and sometimes, as it seems, throughout almost its whole 
extent. If we examine the nervous system in such a case we find in the spinal 
cord that the large ganglion-cells of the anterior horns in the cervical and lumbar 




Fig. 137.— Diagram of the motor tract. C. Motor gan- 
glion-cell in the cortex. PyS. Pyramidal lateral 
tract. V. Ganglion-cell of the anterior horn. m. 
Motor nerve. M. Muscular fiber. 



PEIMAEY DEGENERATIONS OF THE MOTOR TRACT 987 



cord, or in the cervical cord only, are atrophied and in part wholly absorbed 
(Fig. 138). We find the pyramidal tracts greatly degenerated in both lateral 
columns, and, of course, in one or both anterior columns when there is an anterior 
pyramidal tract. In the anterior horns also the number of medullated fibers, 
part of which are cer- 

pyramidariaSral^ tract 2 " 

(PyS) * fibers, is dimin- 
ished. Farther upward, 
as was first discovered by 

Charcot and Marie, we * 
can follow the degenera- ' Z'Sk 

tion of the pyramidal "- ~- _ - : . '~ .-/ 

tract, not in all, but cer- .. ' 

tainly in many cases, . ' ' 

through the pyramids of 
the medulla, the pons, 

the Crura, and the inter- Fl(J 138i _ Section of the cer vical cord in amyotrophic lateral sclerosis, 
nal capsule to the central Degeneration of the pyramidal tracts, in part of the other antero- 

-, ,. . , lateral tracts, pronounced atrophy of the anterior horns. (Person- 

COnvolutlonS, m whose al observation.) 

ganglion-cells we can also 

find atrophy. The bulbar motor nuclei, especially the hypoglossus nucleus and the 
vagus-accessory nucleus, more rarely the facial nucleus, etc., are also atrophied 
as a rule, just like the anterior horns of the cord. From all these bulbar and 
spinal ganglion-cells a further (secondary?) degeneration also extends toward the 
periphery into the corresponding nerve-roots (hypoglossus, etc., spinal anterior 
roots) and nerve-trunks. It is difficult to make out atrophied fibers in the periph- 
eral nerves, and up to tne present time they have not always been looked for with 
sufficient care, but it can scarcely be doubted that the affected motor fibers, which 
are processes of the atrophied ganglion-cells, are likewise to be found in a condi- 
tion of degeneration. Finally, the muscles show a considerable atrophy, as is 
plainly manifest even during the life-time of the patient. Their volume is much 
diminished; many muscles (for details vide infra) finally almost wholly disap- 
pear, so that in their place there is little left but connective tissue and fat. In 
the other muscles we find, besides a number of normal fibers still preserved, many 
very small fibers, showing various degrees of atrophy, with their transverse stria- 
tion usually preserved, but more rarely indistinct. The nuclei of the sarcolemma 
are much increased, and the interstitial fat tissue is often, but not always, abun- 
dantly developed. 

Although we may undoubtedly designate amyotrophic lateral sclerosis as, in 
the main, a primary degeneration of the pyramidal tract, yet in many cases the 
disease is not limited absolutely to this one system. It has long been noticed 
that the diseased area in the lateral columns extended farther forward and inward 
than the actual pyramidal lateral tract, PyS, and that, accordingly, bundles of 
fibers in the anterior portion of the lateral columns and in the so-called lateral 
limiting layer were involved in the disease. Indeed, it often seems as if the 
whole region of the anterior and lateral columns were poorer in fibers than the 
area of the posterior columns. Only toward the lateral cerebellar tract, KIS, is 
the degeneration almost always very sharply limited — that is, the lateral cere- 
bellar tract remains as a rule perfectly normal, but disease has repeatedly been 

* Abbreviations' infrequent use in whatjfollows : PyS = pyramidal lateral tract (Pyramiden-Seit- 
enstrangbahn) ; Py V = anterior pyramidal tract (Pyramiden-Vorderstrangbahu) ; KIS = lateral cere- 
bral tract (Kleinhirn-Seitenstrangbahn. , i 



988 



DISEASES OF THE NEEVOUS SYSTEM 



found in Goll's columns. All these degenerations, last mentioned, have no known 
clinical significance. They show only how other bundles of fibers may sometimes 
suffer under the same noxious influence as well as the pyramidal tract. 

Our knowledge in regard to the questions as to where the degeneration begins,, 
in what way it progresses, and what is primary and what secondary atrophy, is 
most uncertain. The anatomical examination gives only the result of the destruc- 
tion, but it shows very few details of its course. Much may be inferred from 
clinical observation, but much work is still needed to attain perfectly clear knowl- 
edge. Perhaps different possibilities should be considered, which would explain 
many variations in the clinical course. At any rate, the different portions of the 
system may be affected in varying sequence, and the disease may also extend with 
varying rapidity, but the destruction of the nerve-fibers is always the primary 
process ; the increase of the interstitial connective tissue and the slight changes 
in the vessels are a secondary, accidental process. 

We know as yet hardly anything definite as to the causes of amyotrophic 
lateral sclerosis. Eor one class of cases we believe we may assume a congenital 
weakness of the motor system. The disease usually begins at the period between 
thirty-five and fifty, but not infrequently later. No special external causes of the 
disease have thus far been found. The male sex seems to be affected somewhat 
more frequently than the female. 

Clinical History. — In all typical cases the clinical symptoms give a perfectly 
characteristic type of disease, limited strictly to the motor sphere, corresponding 
to the perfectly systemic anatomical lesions just described. 

The first signs of the disease almost always begin in the arm. The patient 
notices a difficulty in working, and becomes easily tired. The weakness of the 
arm gradually increases, and finally, usually some months later, involves the 
other arm. A wasting of certain muscles, which gradually increases and becomes 
more extensive, is now often noticed by the patient. About six months or a 
year later, symptoms appear in the lower extremities. The gait becomes stiff 
and uncertain, the patient gets tired more easily, and quite a marked tremor of 
the legs often comes on, apparently spontaneously. 

If we now examine the patient carefully, the type of the disease is usually 
perfectly plain. We notice, first in the upper extremities, a very pronounced 
and more or less extensive muscular atrophy. This is usually most marked 
where it begins — namely, in the thenar and hypothenar eminences. The inter- 
ossei are also plainly atrophied, and the muscles on the extensor side of the 
forearms, but the flexors of the hand and of the terminal phalanges of the fingers 
remain intact longer. In the upper arm the triceps and the deltoid are usually 
the most atrophied, and later, and to a less degree, the biceps and the muscles of 
the shoulder. We find a functional disturbance of the muscles — a paresis — corre- 
sponding to the degree of atrophy. The functional capacity depends upon how 
much muscle is left, and only with a complete disappearance of the muscle is 
there a complete loss of the corresponding motion, but a marked paresis can 
sometimes be noticed in muscles which are not yet much atrophied. Fibrillary 
muscular contractions are almost always to be detected in the affected muscles 
on careful observation. The electrical excitability of the muscular fibers still 
preserved is normal. The strength of contraction of the muscle irritated by the 
faradic current is therefore proportional to the amount of muscular substance 
still present. In the much atrophied muscles the effects of irritation are finally 
very slight, and then we can always detect a distinct reaction of degeneration in 
the muscular fibers that are still left, especially in the ball of the thumb. We 
can scarcely ever make out with certainty a loss of excitability in the nerve-trunk, 
probably because here a greater number of normal fibers are always present. 

The examination of the tendon reflexes is very important. They are invariably 



PRIMARY DEGENERATIONS OF THE MOTOR TRACT 989 



much increased, even from the early stages of the disease. We obtain vigorous 
reflex contractions from a gentle blow on the tendons of the biceps and the triceps, 
and on the lower ends of the bones of the forearm. This increase of the tendon 
reflexes is extremely important in diagnosis, because it never occurs in this way 
in ordinary " progressive muscular atrophy " — that is, in that disease in which the 
degeneration extends merely from the muscles to the motor ganglion-cells in the 
anterior cornua, while the lateral motor tracts remain free (vide infra). In the 
later stages of the disease marked contractures in the arms and hands sometimes, 
but not always, develop. The sensibility of the skin and deeper parts, however, 
remains absolutely normal. 

The first morbid symptoms usually develop in the lower extremities some 
months later than in the arms. The pure spastic symptoms are here remarkably 
prominent, while the muscular atrophy is late in its development, and is but slight. 
The legs become stiff, and oppose considerable muscular resistance to attempts 
at passive motion, but the crude strength of the muscles is decidedly below the 
normal. There is an obvious paresis, although there is, as it seems, hardly ever 
a complete paralysis of the legs ; and the disturbance of motion, at any rate, is 
considerably increased by the spastic symptoms (vide infra, spastic spinal paraly- 
sis). The spastic symptoms are connected with the hypertonicity of the muscles 
(the increased muscle tonus) and the increased tendon reflexes. These symptoms 
depend mainly upon the great increase of the tendon reflexes. The patellar reflex 
is very vigorous, and we often find a marked and persistent ankle clonus. The 
patient can still walk quite a distance, but the gait is, of course, difficult and 
laborious. The patient walks with short, slow, dragging steps — the spastic-paretic 
gait. Only in a few cases does a marked atrophy of the muscles appear in the 
early stages in the legs as well as in the arms. The sensibility of the skin and 
deeper parts is also perfectly preserved in the legs in amyotrophic lateral sclero- 
sis. The cutaneous reflexes from the soles of the feet show no striking changes. 
[There may be dorsal extension of the great toe on testing the plantar reflex — 
Babinski's reflex. — K.] Disturbances in micturition are also entirely absent. 
The bowels may be somewhat costive, but they are otherwise normal. 

After the condition has lasted for some time (a year or two) in this form — 
muscular atrophy and increased tendon reflexes in the upper extremities and 
spastic paresis in the lower — and has slowly grown worse, bulbar symptoms come 
on in the third and last stage of the disease. The speech gradually becomes more 
indistinct, and there is difficulty in swallowing. If we examine closely we find 
the lips atrophied, so that puckering the mouth, whistling, etc., are difficult. We 
also notice a decided atrophy of the tongue. Its surface is uneven, and we notice 
more or less marked fibrillary twitchings of single muscular bundles. The sensi- 
bility is also normal here. We sometimes find a vigorous masseter reflex (jaw- 
jerk) on striking the lower jaw, analogous to the increased tendon reflexes in the 
extremities. The other muscles of the face, the muscles of mastication and the 
ocular muscles, usually remain unaffected. The patient's intelligence is un- 
changed. The ready onset of marked mimetic emotional movements is sometimes 
striking. Many patients with amyotrophic lateral sclerosis break out into spas- 
modic laughter or weeping and wailing upon the slightest provocation (" impul- 
sive laughing and crying"). This remarkable symptom, which also occurs in 
multiple sclerosis (page 957), is probably due to the disappearance of certain 
fibers which inhibit affective movements. The face is sometimes peculiarly dis- 
torted and broadened by a persistent tonic contraction of the facial muscles (see 
Eig. 156, page 1010). In one case under our observation there were frequent' 
attacks of severe spasm of the glottis with danger of suffocation. 

If the patient have trouble in taking food, from difficulty in swallowing, the 
state of the general nutrition soon becomes worse. Respiratory disturbances are 



990 



DISEASES OF THE NEKVOTJS SYSTEM 



usually the final immediate cause of death, if an intercurrent disease, such as in- 
halation pneumonia, etc., does not previously put an end to the patient's melan- 
choly condition. 

Variations from this typical picture of the disease sometimes occur, but only 
as the sequence may vary in which the different symptoms come on or the differ- 
ent muscular regions are affected. If the anatomical lesion begins exclusively in 
the central motor neurones, there are at first purely spastic symptoms, either 
spastic rigidity of the lower extremities only or rigidity of the trunk and arms as 
well, and a distorted facial expression; and only later, when the second motor 
neurones are affected, is added atrophy of the muscles, at first usually either in 
the forearms and hands or in the bulbar region (tongue, lips, etc.). In other cases 
how T ever, the type of progressive muscular atrophy is from the first more 
prominent, and the spastic symptoms, if marked anywhere, appear only in the 
legs. In these cases the disease of the peripheral motor neurones is at first evi- 
dently greater than that of the central motor neurones ; but even here the in- 
creased tendon reflexes point from the outset to an implication of the central 
motor neurones. Increased tendon reflexes, however, can of course occur only in 
those muscles whose ganglion-cells in the anterior horns are not yet completely 
destroyed. The bulbar symptoms are wholly analogous to the other muscular 
atrophies; they are due to the degeneration of the nerve-nuclei in the medulla. 
We shall become more fully acquainted with them later (vide infra, progressive 
bulbar paralysis). 

The diagnosis of the disease is rarely difficult. Its usually typical course, the 
muscular atrophy co-existing with increased tendon reflexes, the rigidity in other 
muscles, especially in the legs, the complete absence of sensory or vesical disturb- 
ances, and the final appearance of bulbar symptoms, are chiefly to be considered 
in diagnosis. Mistakes may arise from the fact that tumors or myelitis may for 
a long time have a similar localization, as in the gray matter of the cervical cord, 
and therefore provoke analogous symptoms. It is probable that in the past there 
was often confusion with syringomyelia (q. v.), but such mistakes may easily be 
avoided if we remember the sensory disturbances in the arms which are so very 
characteristic of this disease. The distinction between amyotrophic lateral scle- 
rosis and the other primary diseases of the motor system will be self-evident from 
the description of these diseases which follows. 

The prognosis of amyotrophic lateral sclerosis must be regarded as absolutely 
unfavorable. The disease advances slowly but unceasingly, and usually leads to 
death in a few years. Only in a few cases, occurring in early youth (Seelig- 
miiller), does the disease seem to come to a standstill. 

We can therefore expect but slight results from treatment. At most we can 
perhaps check the advance of the disease by an electrical or gymnastic treatment, 
kept up with very great patience and perseverance. 

3. Spinal Progressive Muscular Atrophy 
Preliminary Remarks and Pathological Anatomy. — Few diseases of the 
spinal cord have been the subject of such different conceptions and inter- 
pretations as progressive muscular atrophy. The reason for this lies chiefly in 
the fact that its main symptom, the progressive atrophy of the voluntary muscles, 
may be found in many totally distinct diseases, and hence this has given rise to 
constant confusion and mistakes. If, at the present time, we read the older and 
even a part of the newer literature on this subject, we find everywhere a mixture 
of different cases, not at all of the same disease, and only the latest accurate clin- 
ical and anatomical methods of investigation have enabled us to bring at least 
some order out of this chaos. 

Except for a few earlier observations, Duchenne and Aran, in 1849 and 1850, 



PRIMARY DEGENERATIONS OE THE MOTOR TRACT 991 



gave the first good description of progressive muscular atrophy. The French 
observers, therefore, at present speak of the disease, in distinction from other 
similar affections, as " atropine musculaire progressive, type Duchenne-AranP 
A short time after, in 1855, Cruveilhier, on the ground of a positive lesion on 
autopsy, first pronounced the opinion that a disease of the gray matter in the 
spinal cord was to be regarded as the special anatomical cause of the disease. 
Since then a tedious dispute has been carried on, and even in part kept up to the 
present time, as to whether, in fact, the disease has its seat in the spinal cord, or 
in the muscles themselves — a dispute which was necessarily without results for 
a long time ; the more because the actual pathological data were very scanty, and 
because the results of examinations often contradicted one another, owing to the 
confusion between different morbid processes which did not belong together at all. 

At present we know that the great majority of progressive muscular atrophies 
certainly have their starting-point in the muscles themselves (vide infra, pro- 
gressive muscular dystrophy), but that there is also a rare but definitely estab- 
lished spinal form of progressive muscular atrophy. This is closely allied to amy- 
otrophic lateral sclerosis, which we have just described, but although in amyo- 
trophic lateral sclerosis the whole pyramidal motor tract may be degenerated, and 
the lateral pyramidal tracts in the cord are in particular always affected, in 
" spinal progressive muscular atrophy " the degeneration, as we have said, is con- 
fined to the peripheral motor neurone — that is, to that portion of the motor con- 
ducting tract which extends from the ganglion-cells of the anterior cornua to the 
muscular fibers themselves. The second central motor neurone — that is, the lat- 
eral pyramidal tract — remains perfectly normal. It is very improbable that this 
difference in the extent of the anatomical localization causes a fundamental dis- 
tinction between the two diseases mentioned. The clinical distinctions due to 
the different anatomical localization are, however, of sufficiently marked promi- 
nence to justify, at least provisionally, a special limitation of amyotrophic lateral 
sclerosis on the one side and spinal progressive muscular atrophy on the other, 
as two different clinical forms of the same morbid process. 

The precise anatomical lesion in progressive (spinal) muscular atrophy is as 
follows : 

In the spinal cord, particularly in the cervical cord, we find the ante- 
rior gray cornua very small; the ganglion-cells have wholly or largely disap- 
peared, and those remaining are atrophied ; and the neuroglia is changed to a fine 
fibrous tissue, sometimes studded with spider-cells ; but the lateral columns, espe- 
cially the pyramidal tracts — that is, the portion of the motor conducting tract 
central to the ganglion-cells of the anterior cornua — are perfectly normal ; the an- 
terior roots and the affected motor fibers in the peripheral nerves, however, are 
atrophied, although in the nerve-trunks the discovery of degenerated fibers mixed 
with many other normal fibers is not perfectly easy. In the muscles the atrophy 
is, of course, still more noticeable on a post-mortem examination than on exami- 
nation during life. The muscles most affected are reduced to small, pale, and 
flabby bundles, in which fat and connective tissue outweigh the proper muscular 
tissue. On histological examination, we find, besides some muscular fibers which 
are still of normal diameter or even hypertrophied, ail degrees of diminution and 
atrophy in the other fibers, so that finally all that seems to be left of many fibers 
is merely the empty sheaths of sarcolemma ; but most of the diminished fibers 
retain their transverse striation to the last, and only occasionally do we see signs 
of granular (fatty?) and waxy degeneration of the muscular fibers, a splitting 
longitudinally and transversely, etc. The interstitial connective tissue is always 
hyperplastic, the muscular nuclei are considerably increased in number, and we 
often find an abundant deposit of fat between the fibers which are still preserved. 

So far the actual lesion. In comprehending it, the only difficulties arise 



'992 



DISEASES OF THE NERVOUS SYSTEM 




Fig. 139. 



from the questions as to the mode of development, and as to the reciprocal 
dependence of the different disturbances. Is the atrophy of the anterior cor- 

n u a to be regarded as primary, 
and the atrophy of the nerves and 
muscles as a secondary descend- 
ing degeneration; or does the 
process begin in the muscles or 
nerve-endings, and extend up- 
ward from them to the spinal 
^jfc^- 7 jffl? \ jT cord ; or, finally, do we have to do 

^^IfJ f jJr with an approximately simultane- 

ous degeneration of the whole 
motor portion affected? These 
are questions to which at present 
no definite answer can be given. 
Many reasons seem to us to favor 
the belief that the degenerative 
process begins in the last ter- 
minal branches of the motor 
nerves, and from these ascends 
gradually to the spinal cord. 
This, however, is not yet proved, 
and possibly the starting-point of 
the disease and its further prog- 
ress may differ in different cases. 

^Etiology and Clinical His- 
tory. — Progressive muscular atro- 
phy is an extremely slow and 
chronic disease from the begin- 
ning. The special causes are as 
little known as those of amyotro- 
phic lateral sclerosis. Here, too, 
we shall probably have ultimately 
to fall back upon the hypothesis of 
conditions of congenital weakness 
in the affected systems of fibers. 
Hereditary and generic influences 
are often not to be detected, but 
they are sometimes undoubtedly 
present. We ourselves and other 
observers have repeatedly seen 
spinal muscular atrophy occur in 
several members of the same fam- 
ily. The disease sometimes be- 
gins in childhood and sometimes 
in youth, but often in more ad- 
vanced age (from forty to fifty). 
Although, as we have said, a con- 
genital weakness of the motor 
system is probably always to be 
regarded as the special cause of 
the disease, in some cases certain 
external conditions, especially persistent over-exertion of the muscles in hard 
work, seem to favor its outbreak. 




Figs. 139-141.— Atrophy of the small muscles of the hand, 
especially of the thenar and hypothenar muscles, in spi- 
nal progressive muscular atrophy, a. Hand of a healthy 
man. b. Atrophied hand. (Erlangen Medical Clinique.) 



PEIMAKY DEGENERATIONS OF THE MOTOR TRACT 993 



The disease begins, by far the most frequently, in the upper extremities, and 
-especially, as it seems, in the right arm, but sometimes in the left, or in both arms 
at once. As a rule, it begins with an atrophy of the short muscles of the thumb 
and of the hypothenar eminence, which is accompanied by a corresponding dis- 
turbance of functions (see the accompanying figures, 139 to 141). Other 
symptoms — disturbances of sensibility, paresthesia, or pain — are usually en- 
tirely absent. The atrophy usually affects the 
abductor pollicis brevis and the opponens first, 
and then the flexor brevis and the adductor. 
We notice very early the characteristic sinking 
in and flattening of the ball of the thumb, and 
the abnormal position of the thumb, which is 
persistently approximated to the second meta- 
carpal bone — the " ape hand." It becomes con- 
stantly harder and finally impossible to oppose 
the thumb to the other fingers (performed by 
the flexor brevis for the index and middle fingers 
and by the abductor brevis and opponens for 
the ring and little fingers). At the same time, 
■or a little earlier or later, the interossei begin 




to atrophy, as is recognized by the sinking in 
of the interosseous spaces and the increasing 
incomplete extension of the terminal phalanges 
of the fingers. The atrophy of the lumbricales 
causes a visible flattening of the hollow of the 
hand. If the disturbance in the function of 
the interossei has reached a certain degree, the 
same claw-like position of the fingers appears, 
as we have already learned to recognize in 
ulnar paralysis (see Fig. 142), due to the con- 
tracture of the antagonist of the interossei, the 
extensor communis digitorum. 

In the further progress of the disease the 
atrophy either extends to the muscles of the 
forearm, or, what is not at all rare, it jumps 
over these and attacks the muscles of the shoul- 
der, usually the deltoid first. In the forearm 
it is usually the muscles on the extensor side 
which are first attacked, the abductor and ex- 
tensor longus pollicis, the extensors of the 
wrist and fingers, and only later the supinators, 
flexors, etc. In the upper arm the deltoid al- 
most always atrophies first, and then the biceps, 
while the triceps may remain intact somewhat 
longer. There are also cases in which the atro- 
phy begins in the deltoid and the muscles of the 

upper arm, while the small muscles of the hands and fingers are not affected until 
later. The muscles of the trunk are usually added to the list quite late : the mus- 
cles that extend the head and keep it erect, so that the head sinks forward, the 
trapezii, the infra-spinati and supra-spinati, the rhomboidei, the latissimi dorsi, 
the pectorals, etc. (see Figs. 143 and 144). The disturbance of function caused 
by the atrophy of all these muscles is readily apparent from what was said in 
ihe chapter on the different form of paralysis. In advanced cases the arms hang 
down laxly by the sides of the trunk. Only with the greatest difficulty, if at 
63 



Fig. 142.— Atropr _ 

of the hand and the muscles on the 
extensor side of the forearm in spinal 
progressive muscular atrophy. The 
last three fingers can no longer be ex- 
tended. (Personal observation.) 



991 



DISEASES OF THE NERVOUS SYSTEM 



all, can the patient do anything with them — as to dress or undress himself ; but he 
sometimes learns to help himself, at least in some degree, by " throwing " move- 
ments, by motions of the trunk, by using his mouth in taking hold of things, 
etc. Quite rarely the atrophy finally attacks the muscles of the neck. The 
severest respiratory disturbances, and finally a fatal termination, may be brought 
about by an implication of the diaphragm and the other muscles of respiration. 

The time which elapses before the gradual appearance of the more marked 
disturbances of function is almost always very long. Years may elapse before 

the atrophy extends from 
the little muscles of the 
hand to the other mus- 
cles of the arm. In the 
muscles of the legs the 
first signs of atrophy al- 
most always develop very 
late if at all. The arms 
are often perfectly use- 
less when the patient 
can still walk for hours. 
Of course there are some 
exceptions to this rule, 
and then the muscles of 
the lower leg (peronei) 
especially seem to be first 
affected. 

Besides the atrophy, 
and the loss of function 
that runs parallel to it, we 
must mention some other 
changes in the muscles. 
The fibrillary muscular 
twitchings are often very 
striking. A constant 
tremor and wave of the 
muscle may be provoked 
by them. In some cases 
they are weak and they 
can be detected only by 
special attention. They 
usually become vigorous 
if one irritates the mus- 
cle mechanically by a blow. The electrical excitability of the diseased muscles 
varies, inasmuch as it depends entirely upon the number of normal fibers still pre- 
served in the muscle. Since the atrophy affects only one fiber after another, the 
faradic and galvanic excitability decrease gradually, and are lost completely only 
when the greatest part of the muscle is destroyed. On careful testing, we can 
then, however, almost always make out a decided galvanic reaction of degeneration 
in single muscles that are much diseased, especially in the form of the so-called 
partial reaction of degeneration : the excitability of the nerves is retained, but the 
contractions in the muscles themselves seem very slow, and the anodic closure 
contractions (AnSZ) predominate (see page 851). 

In many cases there is an increase of the fatty tissue (which is always of mod- 
erate degree) at the same time with the atrophy of the muscular substance, and 
this often makes it ver3~ hard to judge of the atrophy; but the loss of function in 




Fig. 143. 



Fig. 144. 



Figs. 143 and 144. — Spinal progressive muscular atrophy. 
(Personal observation.) 



PRIMARY DEGENERATIONS OF THE MOTOR TRACT 995 



the muscles, the diminished electrical excitability, and the peculiar soft feeling 
which atrophied muscles have when covered with fat, reveal the true condition of 
things. There are no trophic disturbances in the skin. Almost all the former 
statements in regard to this refer probably to the confusion between progressive 
muscular atrophy and similar forms of disease, especially syringonryelia. The 
coldness and cyanosis sometimes seen in the hands is due to the fact that the 
arms constantly hang down and to the lack of any muscular movement. 

The examination of the tendon reflexes is of great diagnostic importance. 
While they are invariably decidedly increased in the upper extremities in amyo- 
trophic lateral sclerosis, they are only feebly manifest or entirely absent in genu- 
ine progressive muscular atrophy, a condition which is easily explained by the 
atrophy of the motor ganglion-cells belonging to the reflex arc, or by the atrophy 
of the centrifugal motor fibers. Since no degeneration of the lateral pyramidal 
tract precedes this atrophy, it goes without saying that the muscular rigidity, 
associated with paresis and increase of the tendon reflexes, so characteristic of 
amyotrophic lateral sclerosis, is also absent. Muscular weakness and muscular 
atrophy are completely parallel in spinal progressive muscular atrophy. In the 
lower extremities the patellar reflex is retained as long as the disease spares the 
legs, but it is not increased. If the atrophy involve the legs, the patellar reflex 
is usually lost. 

In distinction from all these manifest disturbances in the motor region, the 
sensibility of the skin and deeper parts remains perfectly preserved. A careful 
test of the sensibility is therefore indispensable to avoid mistaking it for similar 
morbid conditions, such as syringomyelia. There are also never any morbid symp- 
toms on the part of the bladder or rectum. 

In many cases the affection finally invades the muscular region innervated 
from the medulla; the symptoms of "progressive bulbar paralysis" (vide infra) are 
added to those of progressive muscular atrophy. This combination of spinal and 
bulbar disease, as we have previously shown, is a usual occurrence in amyotrophic 
lateral sclerosis, even when the disease has lasted a comparatively short time. 
In genuine progressive muscular atrophy, however, the bulbar symptoms usually 
develop, if at all, only after the disease has gone on for years. Then the speech 
begins to become indistinct from the atrophy of the tongue, swallowing is diffi- 
cult, and the patient finally succumbs to increasing inanition or to respiratory 
disturbances. In their principal characteristics the muscular atrophy of the ex- 
tremities and the bulbar symptoms, as we have said, are precisely analogous phe- 
nomena, inasmuch as the nerve nuclei in the medulla have precisely the same sig- 
nificance for the muscles of the tongue, the pharynx, and the face, as the anterior 
gray cornua of the cord have for the muscles of the trunk and the extremities. In 
many cases, however, bulbar symptoms do not develop at all, since the patients die 
early of some intercurrent disease, or the fibers of the bulbar region are 
not involved in the morbid process ; but the whole process may begin, as we shall 
see later, in the region of the bulbar nerves as "bulbar paralysis," while the 
spinal muscular atrophy does not come on in the arms until afterward. 

Diagnosis. — The diagnosis of spinal progressive muscular atrophy can easily 
be made if we confine ourselves strictly to the definition of the disease, and do not 
confuse it with other affections in which the muscular atrophy is only one symp- 
tom which may have an entirely different origin — muscular atrophies in extensive 
diffuse myelitis, in tumors, in the formation of cavities in the cord, in multi- 
ple neuritis, as a result of articular affections and injury, etc. We should con- 
sider especially the typical course of the affection in most cases of genuine 
progressive muscular atrophy, its beginning in the upper extremities, the small 
muscles of the hand, or more rarely the muscles of the shoulder and upper 
arm, its slow advance, the peculiar " individualization " of the atrophy — 



996 



DISEASES OE THE NERVOUS SYSTEM 



that is, the affection of some muscles while other neighboring muscles remain 
completely normal ; the special form of atrophy recognizable by fibrillary contrac- 
tions and electrical reaction of degeneration ; and, finally, the absence of all dis- 
turbances of sensibility or of the sphincters. Progressive muscular atrophy is 
doubtless nearly allied to amyotrophic lateral sclerosis, but the latter is distin- 
guished by its more rapid course, and especially by the increase of the tendon 
reflexes due to the affection of the lateral columns, and the corresponding appear- 
ance of spastic symptoms. The differential diagnosis between the spinal and the 
myopathic (juvenile) muscular atrophy (muscular dystrophy), which is also per- 
fectly certain at present in most cases, will be described later. 

The prognosis of progressive muscular atrophy is to be regarded as absolutely 
unfavorable. The disease appears comparatively benign only from the fact that 
it is apt to advance very slowly, since it may last for ten or fifteen years, or even 
longer. As we have already said, the fatal termination at last appears from some 
intercurrent disease, or as a result of the final appearance of dangerous bulbar 
symptoms, paralysis of deglutition and respiration. 

The results of treatment are accordingly very slight. An electrical treatment, 
continued for months and years with very great persistence, can alone produce 
a little improvement or check the advance of the atrophy somewhat. Temporary 
improvement may also sometimes be attained by methodical massage of the 
muscles and a rationally conducted gymnastic treatment. In other respects, the 
treatment must be symptomatic. [Gowers claims that daily subcutaneous injec- 
tions of strychnine, grains y-^o to jV (gramme 0.0005-0.002), often arrest the 
disease. — K.] 

4. Neurotic Muscular Atrophy 

( Type Charcot- Marie. Peroneal- Forearm Type of Progressive Muscular Atrophy) 

This name is given to a form of progressive muscular atrophy which has be- 
come known through many recent observations (Charcot and Marie, Tooth, J. 
Hoffmann, and others), and which is manifested by several very characteristic 
clinical features. The disease is often a pronounced hereditary and family affec- 
tion, which can sometimes be traced through four or five generations, but, on the 
other hand, it also occurs in members of the same generation without being pres- 
ent in the antecedents, and individual cases have also repeatedly been observed in 
which there was apparently no hereditary predisposition. The first symptoms 
of the disease usually appear in childhood, but some cases have also been ob- 
served in later life. There is no essential difference between the two sexes. 

Next to the conditions mentioned (beginning in childhood, generic occur- 
rence), the most noticeable feature is the very regular localization of the muscu- 
lar atrophy (see Fig. 145). The atrophy almost always begins symmetrically in 
the portions of the extremities most distant from the trunk — that is, in the hands 
and forearms and the feet and lower legs. The lower extremities are often af- 
fected for a longer or shorter time (even for years) before the upper, but the con- 
trary sequence may also occur. Since the atrophy of the small muscles of the 
feet causes symptoms that attract little attention (a claw-like position of the 
toes), the disease may often remain unnoticed until the peronei, the tibiales an- 
tici, and the long extensors of the great toe are involved. The gait then becomes 
impaired from the dropping of the toes and shows all the characteristic peculiar- 
ities of bilateral peroneal paralysis (q. v.). In older cases there often develops 
on both sides a complete talipes equinus or varo-equinus. As the atrophy 
progresses, the muscles of the calves gradually become affected, and finally the 
muscles of the thigh as well. Atrophy and paresis of the muscles go always hand 
in hand. The same is seen in the upper extremities. Here the small muscles of 
the hand, the interossei and thenar and hypothenar muscles, atrophy first, just 



PKIMAEY DEGENERATIONS OF THE MOTOR TRACT 997 



as in spinal muscular atrophy and amyotrophic lateral sclerosis. The fingers 
therefore assume the claw position; the movements of the thumb become more 
and more impaired, so that it lies adducted against the hand. The atrophy then 
extends to the forearms, where the extensors are earlier and more markedly 
affected than the flexors. Later in the course of the disease, when the forearms 
and hands are already greatly emaciated, we can usually discover the beginning 
of atrophy in the muscles of 
the shoulder and upper arm. 
The muscles belonging to 
the trunk resist the morbid 
process the longest. The 
facial muscles also are usu- 
ally spared, although mani- 
fest changes may finally oc- 
cur even in them, but no 
disturbances have thus far 
been observed in the domain 
of the bulbar nerves. Final- 
ly we may mention the ob- 
servations reported by Hanel 
where the disease was traced 
in many members of one 
family through four genera- 
tions and was always con- 
fined to the upper extrem- 
ities. 

It is of the greatest im- 
portance for our compre- 
hension of the whole disease 
that the atrophying muscles 
show fibrillary contractions, 
usually slight but sometimes 
lively, and that we can 
invariably find the most 
marked changes in the elec- 
trical excitability of the 
muscles and their corre- 
sponding nerves. The nerves 
soon show a marked diminu- 
tion or even a total loss of 
galvanic and faradic excita- 
bility. In the muscles we 
find either the same condi- 
tions or a pronounced galvanic reaction of degeneration. It is a very interesting 
fact that, on electrical examination, we can often detect manifest changes in 
excitability, just as in lead paralysis, in muscles which apparently show no 
atrophy or paralysis at all. 

The mechanical excitability of the muscles is also diminished. The tendon 
reflexes of the affected muscles are wholly absent or much diminished. They are 
never increased. The sensibility is never much affected, but it is often not per- 
fectly normal. Paresthesia and painful sensations in particular are often pres- 
ent, and there is sometimes a manifest but slight blunting of the cutaneous sensi- 
bility. The functions of the bladder and rectum remain normal. 

From the clinical facts just described the conclusion may be drawn that the 




Fig. 145.— Neurotic muscular atrophy. The disease cauie on in 
almost the same fashion in three members of one family. 
(Personal observation). 



998 



DISEASES OF THE NEKVOUS SYSTEM 




a 




form of muscular atrophy under discussion must have a neurotic or a spinal ori- 
gin. The assumption of a neurotic origin is favored not only by the results of the 
electrical examination and the occurrence of pain and slight sensory disturbances, 
but also by the results of the anatomical investigations thus far reported, al- 
though they are of course still few 
in number. According to these, 
the disease seems to be confined 
mainly to the muscles and the 
peripheral motor nerves, while the 
anterior roots and the ganglion- 
cells in the anterior horns show 
no perceptible alteration, but a 
moderate loss of fibers is some- 
times found in the region of the 
columns of Goll. 

Further observations and in- 
vestigations must teach us whether, 
as is probable, we shall find closer 
relations and transition forms be- 
tween neurotic and spinal atrophy ; 
but meanwhile the disease just de- 
scribed is a form of progressive 
muscular atrophy so well charac- 
terized and so readily recognizable 
in its clinical aspect that a sepa- 
rate description of it is undoubt- 
edly warranted. 

5. Progressive Muscular 
Dystrophy 

( The Myopathic Juvenile Forms of Pro- 
"'\ - ' f gressive Muscular Atrophy) 

The so-called purely myopathic 

Fig. 146.— Peroneal muscular atrophy. Legs of the brother * J J Jr 

of the patient shown in Fig. 145. muscular atrophies are much com- 

moner than the forms of muscular 
atrophy thus far described, in which, besides the wasting of the muscular 
fiber, there is a more or less extensive atrophy of the motor nervous sys- 
tem. Myopathic muscular atrophy is the name given to all those forms in 
which anatomical investigation has thus far found atrophic processes, not in 
the cord or in the peripheral nerves, but exclusively in the muscles themselves. 
The old, long contest whether the " seat " of progressive muscular atrophy was 
to be looked for in the spinal cord or in the muscles themselves, has thus at last 
been decided : that each of these hypotheses was correct for certain cases. Thanks 
to persistent clinical and anatomical investigations, we are /now in a position to 
distinguish, easily and positively for the most part, the spinal (and neurotic) 
from the myopathic cases even during the patient's life. Of course many facts 
even now seem to indicate that there is no very strict division, and that even 
here transition forms may occur which can be fully understood only by a still 
more accurate insight into the nature of the morbid process in question. 

In spite of many common peculiarities, the individual cases of myopathic 
muscular atrophy differ in many respects from one another. These differences 
relate either to the localization of the muscles chiefly or at least first affected, or 
to the special variety of change in the muscles (simple atrophy or atrophy 




PRIMARY DEGENERATIONS OF THE MOTOR TRACT 999 



with a large interstitial development of fat). These differences were the reason 
why it was .formerly believed that several forms of disease could be recognized, 
whereas in reality we are dealing only with different types of the same disease. 
These varieties, of course, have so much individuality and so constantly recur 
in the same way that we are perfectly justified in differentiating them, 
from a clinical standpoint; but, on the other hand, there are so many transitions 
between the different types that their intimate relationship is undoubted. Erb 
has therefore been perfectly correct in proposing to group together all these differ- 
ent types under one common name — progressive muscular dystrophy — in order to 
attest their kinship. We can then distinguish the different sub-types by spe- 
cial terms. 

Before we proceed in what follows to describe these different sub-types in 
greater detail, we would first mention the most important points which are 
common to all forms of myopathic muscular atrophy — that is, of so-called mus- 
cular dystrophy. They are as follows : 1. All forms of dystrophy occur gener- 
ically or hereditarily. We therefore see the disease most frequently in brothers 
and sisters, or more rarely in members of the same family in different genera- 
tions. On the other hand, sporadic cases are of course not uncommon. If the 
disease occurs in members of the same family it usually assumes the same form in 
each of them; but different forms may exceptionally occur in one family — a cir- 
cumstance strongly suggesting an intimate relation between the different types. 
2. The first symptoms of the disease almost always appear in youth, sometimes in 
childhood, sometimes not until puberty. Only in rare cases does the disease 
begin between thirty and forty or even later. It is worthy of note that certain 
forms usually begin in childhood (" infantile " form with implication of the 
facial muscles, pseudo-hypertrophy), and other forms only at puberty (" juvenile " 
form with implication of the shoulder and upper-arm muscles). 3. The localiza- 
tion of the muscular atrophy is extremely irregular. The different forms or types 
are of course distinguished by their special localization; but as the disease ad- 
vances, or in the frequent transition cases, it often happens that other muscular 
regions besides those chiefly affected are also involved to a lesser degree. It thus 
appears that in all forms it is finally the same muscular regions which are chiefly 
affected with atrophy, while, on the other hand, in all forms certain muscular re- 
gions with scarcely an exception remain intact. The groups of muscles most 
exposed to the disease are : (a) Facial muscles, as far as they are innervated by 
the facial nerve, especially the orbicularis palpebrarum and orbicularis oris. 
(&) Muscles of the shoulder-girdle: pectoralis, latissimus dorsi, serratus anticus 
major, rhomboidei, trapezius, (c) Muscles of the upper arm: biceps, brachialis 
anticus, supinator longus, triceps, (d) Long extensors of the back (erectores 
spinse). (e) Pelvic muscles (glutsei) and muscles of the thigh. Other muscles, 
however, are almost always spared in muscular dystrophy: (a) Deltoids, supra- 
spinal, and infra-spinati. (b) Forearm muscles, and especially the small mus- 
cles of the hand and fingers, (c) Lower leg muscles, especially the gastrocnemius 
and the small muscles of the foot, (d) Tongue and muscles of deglutition. All 
these statements are not absolutely without exception, but they show the usual 
Tule, which must depend upon the essential nature of the disease. 4. The ana- 
tomical changes in the muscles are essentially the same in all the different forms 
of dystrophy. They consist first of the most varied changes in volume of the indi- 
vidual muscular fibers. Many fibers show an atrophy which progresses finally to 
complete disappearance, while, on the other hand, so-called hypertrophic (hypervo- 
luminous) fibers are also almost always to be found. Erb suspects that the hyper- 
trophy is the first stage of the disease of the fiber, and that the atrophy follows 
this later. Besides these changes in volume, we see regularly an evident increase 
in the muscle nuclei and a considerable increase in the interstitial connective 



1000 



DISEASES OE THE NERVOUS SYSTEM 



tissue. If there is pronounced pseudo-hypertrophy the interstitial tissue is per- 
meated with an abundant accumulation of fat-cells. In the muscular fibers them- 
selves the transverse striation is almost always preserved to the last, and we 
never find granular or fatty, so-called degenerative destruction in any great 
degree. The peripheral motor nerves and the motor ganglion-cells in the anterior 
horns — that is, the peripheral motor neurones — remain perfectly normal. Two 
clinical facts, which are very important in diagnosis, are associated with this cir- 
cumstance : (a) In all forms of dystrophy the fibrillary contractions in the dis- 
eased muscles, which are so common in spinal atrophies, are almost invariably 
absent, (b) Distinct electrical reaction of degeneration is almost never found in 
dystrophy (in contrast to the spinal atrophies). Since the disease is also a 
motor system disease, like all the other forms of progressive muscular atrophy. 




3 4 
Fig. 147.— Positions of a child with hereditary (pseudohypertrophic) muscular atrophy, on rising to an 

erect attitude. (From Gowers.) 

it is self-evident that in dystrophy the sensibility, the functions of the bladder, 
etc., remain perfectly normal. 

Since we have mentioned the most important features common to all forms of 
dystrophy, we will pass to the description of the chief individual clinical types. 
We would emphasize the fact once more that transition forms between these 
types are by no means rare. 

1. Pseudo-hypertrophy of the Muscles {Lipomatosis luxurians muscularis 
progressiva of Heller; Atrophia musculorum lipomatosa of Seidel). — Pseudo- 
hypertrophy is the rarest form of muscular dystrophy, but it was the first to be- 
come accurately known, on account of its striking aspect. It was quite fully de- 
scribed in Germany by Griesinger (1864), while in France Duchenne gave 
in 1868 a very complete clinical description of it. In 1866 !M. Eulenburg and 
Cohnheim had already shown, by the careful anatomical examination of a case, 
that the nervous system remained perfectly normal, a statement which was con- 
firmed by all subsequent investigations (Charcot, F. Schultze. and others). 

Pseudo-hypertrophy develops almost invariably in childhood, somewhere be- 
tween the ages of five and eight years. It is a pronounced family or even hered- 
itary disease. The male sex is decidedly more disposed to the disease than the 
female [but the disease seems to be transmitted through the female in the 



PEIMAEY DEGENEEATIONS OF THE MOTOE TEACT 1001 



hereditary cases. — K.] Sometimes, but not always, we also find in the affected 
families some disposition to a nervous taint, such as hysteria, epilepsy, feeble- 
mindedness, anomalies of the skull, etc. 

The disease begins gradually and almost always without a special exciting 
cause. The parents notice that the child, who had been previously perfectly 
well and strong, becomes insecure on his legs, so that he can no longer jump or 
go up-stairs as well as he used to do. This points to the first characteristic pecul- 
iarity wherein pseudo-hypertrophy differs from spinal progressive muscular 
atrophy. It begins, with rare exceptions, in the muscles of the trunk, especially 
in the muscles of the back and pelvic muscles (glutasi), and in the muscles of the 
lower extremities, especially in those of the thigh. While 
the arms and hands are still perfectly normal, walking 
constantly grows more and more difficult, and the gait 
very soon assumes so characteristic a type that from this 
alone the diagnosis can often be made at the first glance. 
The gait becomes waddling (chiefly on account of the 
weakness of the glutsei medii), the belly appears very 
prominent, the vertebral column is arched forward in 
the lumbar region in marked lordosis, and the whole 
upper part of the body is balanced on the legs. The legs 
are raised slowly and with difficulty, and the toes usually 
droop from paresis of the dorsal extensors. The child's 
movements, when he tries to raise himself from the floor 
or pick up any object, are very characteristic, and are alike 
in almost all cases, as a result of paresis of the extensors 
of the thigh and leg (glutaei and extensores cruris). Since 
it is impossible to raise the trunk, the child usually first 
gets on all fours, and then gradually straightens himself 
up [" climbs up his thighs "] by leaning his arms on his 
knees (see Fig. 147). Later on disturbances of rnotion 
appear in the upper extremities also, and in general they 
are very similar to those to be described more fully in the 
next type. 

If we inspect the patient more closely we shall usually 
find at the first glance an extraordinary increase in the 
volume of single muscles (see Fig. 148). The calves are 
disproportionately thick, and sometimes the thighs also; 
the arms are affected later, especially the deltoids, the 
triceps, etc. This increase of volume is caused by an ab- 
normal interstitial development of fat, " pseudo-hyper- 
trophy." Hence the muscles do not feel firm, but soft 
and spongy. It is by no means rare, however, that, be- 
sides the pseudo-hypertrophy in some muscles, a genuine atrophy develops in 
others, with a pronounced loss of substance and without any co-existing de- 
velopment of fat. This is seen especially in the upper extremities in the 
groups of muscles previously mentioned. Finally, there seems to be in addi- 
tion even a genuine muscular hypertrophy. In several cases we have seen a 
marked increase in volume in the muscles of the calves, which were capable 
of quite an extraordinary display of strength. In such cases, however, there is, 
probably, in our opinion, a sort of compensatory hypertrophy, since the muscles 
that are still able to work are exerted excessively. 

Fibrillary twitchings of the muscles are scarcely ever seen. Electrical exami- 
nation shows a diminution of excitability corresponding to the atrophy and to 
the increased deposit of fat, but never reaction of degeneration. The sensibility 




Fig. 148. — Pseudo-hyper- 
trophy of the muscles. 
(From Duchenne.) 



1002 



DISEASES OF THE NERVOUS SYSTEM 




remains perfectly normal, and also micturition and defecation. The patellar reflex 
is sometimes absent, because the quadriceps is involved. It is noticeable that 
the skin, especially in the legs, very often shows a peculiar bluish marbled color- 
ing. Bulbar symptoms ap- 
parently never occur. The 
intelligence in most cases 
is perfectly normal, but 
exceptionally children with 
hereditary muscular atro- 
phy also show manifest 
signs of mental or even of 
moral weakness. 

The disease advances 
very slowly but without 
remissions. Finally the 
patient can not walk at 
all; he is confined to the 
bed, and becomes more and 
more helpless. Death usu- 
ally ensues from some in- 
tercurrent disease, but 
sometimes from insuffi- 
ciency of the respiratory 
muscles. 

2. The Infantile Atro- 
phic Form of Muscular 
Dystrophy usually with 
Implication of the Facial 
Muscles. — Simple atrophic 
forms of progressive mus- 
cular wasting develop far 
more frequently in early 
childhood than pseudo-hy- 
pertrophy. They may be 
combined with pseudo-hy- 
pertrophy, as we have said above, especially in the form where there is lipoma- 
tosis in the lower extremities and simple atrophy in the shoulders and arms; 
but what gives the simple atrophic infantile form a special stamp is the com- 
paratively frequent implication of the facial muscles. These muscles may not 
be involved, and, on the other hand, they may be affected in rare instances in 
the juvenile form as well, but marked atrophy of the facial muscles is a peculiarity 
chiefly of the infantile atrophic form. 

Duchenne had already observed that in children there is a form of muscular 
atrophy which begins in the muscles of the face ; but his statements were almost 
forgotten until, a few years ago, Landouzy and Dejerine called attention anew 
to this subject, and demonstrated, contrary to previous belief, that implication of 
the facial muscles is by no means an unusual symptom. If the atrophy is already 
plainly pronounced, characteristic symptoms ensue: the eyes can no longer be 
completely closed, and the movements of the mouth in whistling, laughing, and 
talking become impaired. From the sinking in of the cheeks, the drooping of the 
under lip, etc., there develops a very characteristic type of countenance (" fades 
myopathique"), by which the practiced eye can recognize the affection almost 
at once (Fig. 149). There may finally ensue complete rigidity and immobility of 
the face. At the same time or somewhat later, as a rule, other muscular regions 



Fig. 149.— Juvenile myopathic muscular atrophy in a ten-year-old 
child, with marked implication of the facial muscles. Inabili- 
ty to close the eyes or move the lips. Atrophy of the pecto- 
rals, etc. (From the Erlangen Medical Clinique.) 



PEIMAKY DEGENEKATIONS OF THE MOTOE TRACT 1003 



may be affected, and again, as in other forms, chiefly the shoulder muscles, the 
muscles of the upper arms, the extensors of the spine, and the muscles of the 
pelvis and thigh. The child's gait becomes as waddling as that of children with 
pseudo-hypertophy, which we have just described. The spine has a lordotic curva- 
ture, the child rises from the floor by the aid of the arms (Fig. 147), etc. The 
sequence in which the different muscles are attacked by the atrophy is not always 
the same. The facial muscles, for example, may often be attacked later than the 
muscles of the shoulder, upper arm, and trunk. In order to detect the slighter 
degrees of implication of the face, it is advisable to have the patient close his 
eyes when the head is bent backward; we can then readily detect the fissure 




Fig. 150.— Two brothers with juvenile muscular atrophy. (Personal observation from the Erlangen 

Medical Clinique.) 

left between the eyelids (insufficiency of the orbicularis palpebrarum). We 
can also notice in the early stages that the patient can not protrude the lips 
to whistle. 

The muscles of mastication, the internal ocular muscles, and the muscles of 
the forearm and hand almost always remain normal. A slight persistent con- 
tracture of the biceps is sometimes present and is characteristic. Fibrillary con- 
tractions and reaction of degeneration are almost always absent. 

3. The Juvenile Form of Dystrophy. — The peculiarities of this form were 
first carefully studied by Erb. It usually does not begin until after actual child- 
hood, in the years of puberty or sometimes later (between twenty and forty). 
It occurs sporadically occasionally, but it is also frequently hereditary or generic 
(that is, occurring in families), and the girls of the family are often attacked 



1004 



DISEASES OE THE NERVOUS SYSTEM 



by this form, while the infantile form is seen especially in boys. The disease 
is also, like pseudo-hypertrophy, sometimes seen to begin in the pelvic muscles 
and the legs, but more often the shoulders and upper extremities are first at- 
tacked. There is also a remarkable regularity in the choice of the muscles 
attacked, as has been mentioned above. According to Erb, the following muscles 
are almost constantly diseased in the trunk and the upper extremities: the 
pectoralis major and minor, the trapezius, the latissimus dorsi, the serratus 
anticus major, the rhomboidei, the sacro-lumbalis and longissimus dorsi, and 
later the triceps. The following, however, almost always remain normal; the 
sterno-mastoid, the levator anguli scapulas, the coraco-brachialis, the teres major 
and minor, the deltoid, the supra-spinatus and infra-spinatus, and, as must 
be mentioned especially in distinction from spinal musciilar atrophy, the small 

muscles of the hand. The 
muscles of the forearm, 
too, except the supinator 
longus, remain intact for 
a long time, if not per- 
manently; but exceptions 
also occur : for example, 
the accompanying illus- 
tration (Fig. 150) shows 
two brothers with juvenile 
muscular atrophy which 
in other respects is char- 
acteristic, but the muscles 
on the extensor side of 
the forearm are also com- 
pletely atrophied. In the 
lower extremities the 
atrophy attacks chiefs 
the glutsei and the quadri- 
ceps, more rarely the per- 
onei and the tibialis an- 
ticus, while the sartorius 
and the muscles of the 
calf are usually wholly 
exempt. Fibrillary 
twitchings in the affected 
muscles are generally ab- 
sent, and there is hardly 
ever any reaction of de- 
generation. 

The disturbances of 

function due to this condition are self-evident, so that a full description of them 
may be omitted. The arms usually suffer first, as we have said. The marked 
projection of the scapulas, from the paralysis of the serratus, is especially char- 
acteristic (Fig. 152). If we try to take the patient under the shoulders and lift 
him, the shoulders are perfectly limp. They are therefore immediately raised so 
high that the head comes between the shoulders ("loose shoulders ")• The most 
striking features in the anterior wall of the chest are the flattening in the region 
of the pectoralis and the peculiar folds of skin on the anterior edges of the axilla?. 
If the patient walks we can often recognize the disease at a distance at the 
first glance by the peculiar gait. The upper part of the body is carried back- 
ward (lordosis of the lumbar vertebras), and the gait is waddling, since the pelvis 




Fig. 151. — Juvenile muscular dystrophy.? Prominence of the scapulae 
when the arms are raised in consequence of atrophy of the ser- 
ratus and rhomboidei. (Personal observation from the Erlangen 
Medical Clinique.) 



PRIMARY DEGENERATIONS OF THE MOTOR TRACT 1005 




Fig. 152.— Muscular dystrophy. Prominence 
of the scapulae when the arms are hanging 
down. ( Erlangen 3Iedical Clinique.) 



been seen to begin at a more ad- 
vanced age — from forty to fifty — 
but in other respects these cases do 
not differ from the general type, al- 
though we have noticed that, in 
such cases as begin relatively late 
in life, the muscles of the pelvis 
and thighs were chiefly affected, so 
that the patient could not 
stand or walk while the arms 
still performed their functions I 
tolerably well (Fig. 154). 

Diagnosis of Myopathic 
Muscular Atrophy (Muscular . " 
Dystrophy ) .—Xow that the 
type of myopathic muscular 
dystrophy has been established 



can no longer be held properly by the weak 
glutsei. On stooping and rising, the same 
symptoms are seen as have previously been 
described (Fig. 147). As a rule, in the 
juvenile form the face is not involved, but 
we can sometimes detect slight disturb- 
ances of the facial muscles, especially defec- 
tive closure of the lids and inability to 
whistle (Fig. 153). "We once made the 
interesting observation that the adult 
brother of a young girl suffering from 
juvenile dystrophy showed these (congeni- 
tal^) anomalies in the face from earliest 
childhood, without showing any further in- 
dications of dystrophy. Bulbar symptoms 
are as rare as in the other forms. It is of 
significance that the intercostal muscles 
and the diaphragm may finally atrophy, and 
the consequent respiratory disturbance may 
be the cause of death. 

The course of juvenile dystrophy is very 
chronic, like that of all the other forms. 
The disease progresses very slowly and 
often seems almost to stand still for a long- 
time. Many cases have been under ob- 
servation for twenty or thirty years. 

We may mention in conclusion that in 
some cases of dystrophy the trouble has 




J 



Fig. 153. — Juvenile muscular dystrophy. Insufficient closure of 
the eyes. Myopathic faeies. (Personal observation.) 



1006 



DISEASES OF THE NEKVOUS SYSTEM 



in all its details by numerous observations, the diagnosis is usually no longer 
difficult. The generic occurrence of the disease, its development usually in child- 
hood or youth, the remarkable regularity in the selection of muscles affected, the 
absence of fibrillary contractions and also of electrical reaction of degeneration in 
the affected muscles, are the chief points upon which the diagnosis is to be based 
in the individual case. If we bear in mind these peculiarities, the distinction from 
the spinal and neurotic amyotrophies or from other similar types of disease (syr- 
ingomyelia) is usu- 
ally easy. Only a few 
cases, which clinic- 
ally seem to present 
transition forms, re- 
main for a time un- 
certain in their ana- 
tomical determina- 
tion. We must, how- 
ever, indicate one 
condition which may 
sometimes give rise to 
mistakes in diagnosis 
— namely, congenital 
muscular defects. In 
some persons we find 
that certain muscles 
or parts of muscles 
are absent from birth, 
and it is remarkable 
that it is most fre- 
quently the same 
muscles which are 
most often affected 
in muscular dystro- 
phy, especially the 
pectoralis major, or 
at least its sternal 
portion, the serrati, 
the rhomboidei, the 
trapezii, etc. Such 
congenital muscular 
defects naturally pre- 
sent at the first glance 

a very similar picture to that of a patient with dystrophy; but we can usu- 
ally decide correctly as to the condition by careful inquiry, since in case of 
congenital muscular defects the abnormalities have always been present, and 
they also show no noticeable increase in the course of years. 

Treatment. — The treatment of myopathic muscular dystrophy is seldom suc- 
cessful. We may sometimes obtain a certain improvement by persistent treat- 
ment by electricity or massage; but at present any considerable alteration in 
the coure of the disease is beyond the domain of possibility. [Persistent and 
systematic gymnastic exercises sometimes have a decidedly beneficial effect. — K.] 




Fig. 154. — Progressive myopathic muscular atrophy of the pectorals, upper 
arms, and muscles of the pelvis and thigh. Ordinary position of the 
patient in sitting ; he can neither stand nor walk. (Personal observa- 
tion.) 



PEIMAKY DEGEKEEATIONS OF THE MOTOE TEACT 1007 



6. Primary Degeneration of the Pyramidal Tracts 

(Primary Lateral Heterosis. Spastic Spinal Paralysis. Motor Tabes. Spasmodic Tabes Dorsalis) 

While in all the forms of primary disease of the motor system thus far de- 
scribed the muscles are involved primarily or secondarily, and muscular atrophy 
therefore plays a leading part in the clinical picture of all the diseases described 
above, in rare cases the degeneration may be limited to the central neurone 
(PyS of Fig. T37, page 986) of the motor tract. In such cases a type of disease 
develops, in which indeed the disturbances are exclusively motor, but in which 
muscular atrophy is completely absent — a type of disease to which has been given 
the name of "spastic spinal paralysis" (Erb, Charcot). There is no doubt that 
such primary, isolated degeneration of the pyramidal tract may occur, without 
involving the peripheral motor neurone (cell of the anterior horn with its process, 
the peripheral motor nerve) ; but we must add that primary degeneration of the 
pyramidal tract is especially apt to be associated with degeneration of other sys- 
tems of neurones (lateral cerebellar tract, fibers of the posterior columns), so that 
the anatomical picture of the disease is not a simple one, but corresponds to a 
" combined system disease" 

Type of Spastic Spinal Paralysis. — Three symptoms predominate in the pic- 
ture of spastic spinal paralysis : motor paresis, hypertonicity of the muscles (mus- 
cular rigidity), and the increase of the tendon reflexes — the patellar reflex, and 
ankle clonus. The loss of motor power — we are speaking at present only of the 
spastic paralysis of the legs, which is by far the most frequent and the most 
clearly marked — is found in various degrees, from a simple weakness of move- 
ment to a complete and more or less extensive paralysis. The other two symp- 
toms, however — the hypertonicity (rigidity) of the muscles, and the increase of 
the tendon reflexes — give the disturbance of motion its characteristic " spastic " 
feature. Both symptoms, indeed, are to be regarded as in part identical, for the 
rigidity of the muscles is also of reflex origin. If the tendon reflexes be much in- 
creased, the reflex tension of the muscles comes on even upon the stretching and 
pulling of the tendons, which are excited by the weight of the limbs, or by any 
active or passive movements. The reflex muscular tension opposes any attempt 
at motion. The muscles feel rigid and firm, and the legs are often found in 
almost permanent contracture and extended, with the feet in plantar flexion. If 
we try to flex the leg passively at the knee, or if we try to extend the foot dorsally, 
we find it almost impossible to do so. The more rapidly and suddenly we try to 
produce the motion, the more marked is the muscular resistance, which can 
scarcely be overcome. If, however, we go to work very slowly and cautiously, and 
avoid any sudden tension of the tendons, we can almost always flex the leg with- 
out special trouble. If we put the patient on the edge of the bed, the legs do not 
hang down laxly, but they usually fall at once into a vigorous extensor tetanus, 
since the weight of the leg puts the quadriceps into contraction by the tension on 
the ligamentum patellae. A convulsive, reflex tremor of the whole leg often comes 
on at once, similar to ankle clonus. If we examine the patient while in the bath 
we find the spasms decidedly less, because in the water the influence of the weight 
of the limb is diminished. It must still remain undecided whether the existence 
of muscular rigidity in spastic paralysis is to be explained exclusively by the 
increase in the tendon reflexes. In some muscles there is sometimes so persistent 
a condition of tonic irritation that we are led to think of processes of direct, 
abnormal motor irritation. Thus the adductors of the thigh, in particular, 
and often the dorsal extensors of the great and other toes, etc., show a constant 
rigidity and tension, the reflex origin of which can not be established, at least 
with any certainty. 



1008 



DISEASES OF THE NERVOUS SYSTEM 



Active motion, as is easily explained, must also be impaired from the inhibi- 
tory action of the tonic and reflex spasms. The degree of disturbance of motion 
is thus increased, and the paresis often seems greater than is really the case. The 
influence of the muscular tension is especially manifest in the gait of the patient. 
As long as walking is still possible, we notice very plainly that it is rendered diffi- 
cult, not only by the muscular paresis, but also by the stiffness of the legs. The 
patient walks with short and difficult steps, the legs are scarcely flexed at the 
knee, and the feet are scarcely raised at all. The feet " stick to the floor " and 
are slowly slid forward, and there is a marked tendency to walk on the toes, from 
the contraction in the muscles of the calves. The weight of the body alone presses 
the feet downward. We term this very characteristic form of gait the spastic- 
paretic gait. It is also characteristic of spastic paralysis of the legs that the 
patient is unable to execute certain isolated movements. Thus the patient, like 
a hemiplegic (vide infra), often can not dorsally extend the foot by itself; but if 
he flexes the whole leg and draws it up to the trunk, there always follows a marked 
dorsal extension of the foot with great tension of the tendon of the tibialis anti- 
cus muscle. 

The increase in the tendon reflexes may also exist without the presence of any 
special motor paresis of the muscles at the same time; but since the motion 
is not a little influenced in such a case by the constant spasms, a disturbance of 
motility may be produced, which we have called " spastic pseudo-paralysis," or, 
more properly, pseudo-paresis. In these cases the muscular strength is almost 
normal, and the patient can walk for quite a long time. Nevertheless, all his 
movements are stiff and difficult, and the gait shows all the peculiarities of the 
pure spastic gait. The steps are not very short and they follow one another quite 
rapidly, but the legs remain perfectly stiff and are scarcely raised from the 
ground, and the patient walks almost entirely on his toes. In the house the 
patient walks with a noisy shuffle, and in soft sand we can see the furrows drawn 
by the feet as they slide along the ground. Since the Achilles tendon is made 
tense at each step, and since a reflex contraction of the muscles of the calf re- 
sponds to this tension, each step is often followed by a short lifting of the whole 
body ("teetering" spastic gait). 

Although the symptoms mentioned are the characteristic positive features of 
" spastic spinal paralysis," yet, in the original sense of the word, the affection is 
also characterized by the fact that certain other spinal symptoms, especially dis- 
turbances of sensibility, disturbances in micturition and defecation, muscular 
atrophy, and other trophic symptoms, are entirely absent. Only when such was 
the case have Erb and Charcot claimed that a special anatomical cause must lie 
at the bottom of the peculiar group of symptoms, which they suspected to be a 
primary disease of the lateral columns — that is, of the pyramidal tracts particu- 
larly. This suspicion was entirely warranted, since the picture of pure spastic 
spinal paralysis could be explained by no other anatomical theory. A degenera- 
tion in the lateral columns explains the motor paresis, explains the increase of 
the tendon reflexes by the loss of reflex inhibitory influences, and finally it also 
explains any direct tonic contraction of the muscles by the hypothesis of processes 
of motor irritation. Actual evidence of the occurrence of primary systemic de- 
generation in the lateral columns could of course be furnished only by anatom- 
ical observation. This has now actually taken place, so that at present there can 
no longer be any doubt of the occurrence of a " spastic spinal paralysis " in the 
original sense of Charcot and Erb. If we observe the same morbid picture not 
only in primary degeneration of the pyramidal tract, but also in other cases, it is 
due to the fact that, under certain circumstances, other diseases may, at least for 
a time, involve the lateral columns almost exclusively, and especially the pyrami- 
dal tracts. 



PRIMARY DEGENERATIONS OF THE MOTOR TRACT 1009 




I 



So far as our present knowledge extends, the affection comes on in two some- 
what distinct clinical forms. The first may be brought into the closest relation 
with amyotrophic lateral sclerosis. As we have seen above (page 989), we often 
find in typical amyotrophic lateral sclerosis a pure spastic paresis in the legs 
without any trace of muscular atrophy, 
while in the arms and the bulbar region 
there is a more or less marked muscu- 
lar atrophy besides the spastic symptoms. 
There are also cases of disease — they oc- 
cur usually in somewhat advanced life 
and sporadically, that is, not generically 
as a family disease — where spastic rigid- 
ity and paresis develop not only in the 
legs, but also in the trunk, the arms, 
and the face, without a trace of muscu- 
lar atrophy. In the course of a few years 
the patient finally becomes almost com- 
pletely stiff (Fig. 155), without being 
entirely paralyzed. The stiffness is due 
solely to the muscular rigidity. The 
arms also show pronounced hypertonicity 
on passive movement. Impulsive laugh- 
ing and crying also occur, just as in 
-amyotrophic lateral sclerosis (Fig. 156). 
If we have the rare opportunity to make 
an autopsy on such a case, we find a 
marked systemic degeneration in both 
lateral columns, chiefly in the region of 
the pyramidal tract, PyS, but usually in- 
volving other bundles of fibers in the lat- 
eral columns as well. The degeneration of 
the pyramidal tract, PyS, may be traced 
upward through the pyramids, the pons, 
and the crus to the internal capsule. The 
ganglion-cells in the anterior horns of the 
spinal cord are entirely normal or they 
show only insignificant changes. The close 
relationship between this form of "pure 
lateral sclerosis " and amyotrophic lateral 
sclerosis is shown by the fact that the one 
disease may develop into the other. After 
the typical affection of lateral sclerosis has 
continued in its pure form for some years, 
atrophy may sometimes finally develop in 
the small muscles of the hand, the tongue, 
etc. — in short, there is clinical evidence 
that the peripheral motor neurone has be- 
gun to degenerate; but the atrophy, as a rule, remains comparatively slight, 
although different degrees of transition forms probably occur. 

A second well-characterized form of primary degeneration of the pyramidal 
tract is the hereditary or family spastic spinal paralysis which has been described 
by us. This shows itself in several members of the same family, especially in 
brothers and sisters ; in this form there very gradually develops, in the course of 
years and years, a constantly increasing rigidity of the legs with increased tendon 
64 




Fig. 155 



Spastic spinal paralysis. Enormous 
muscular rigidity of the trunk, arms, and 
legs. When supported from behind, the pa- 
tient can stand as stiff as a post. (Erlangen 
Medical Clinique.) 



1010 



DISEASES OE THE NEKVOUS SYSTEM 



reflexes and all the motor disturbances dependent thereon. The gait is pro- 
nouncedly spastic, the feet cling- to the floor, the legs are pressed firmly together 
from the contracture of the adductors, and on walking, one foot can pass the other 
only with difficulty. The patient treads only on the anterior part of the foot ; the 
whole body is projected stiffly forward, so that the patient has to hold a cane in 
front of himself to keep from falling forward (Fig. 157). Eor a long time the 
purely spastic symptoms outweigh the paretic (spastic pseudo-paralysis), and 
only very gradually does the spastic gait become spastic-paretic, and an actual 
loss of muscular strength ensue. The general condition, the sensibility, the 

bladder and the mus- 
cular nutrition may re- 
main unaffected for a 
long time or until the 
end. The disease usu- 
ally begins somewhere 
between twenty and 
thirty, but some cases 
apparently occur in 
children also. There 
can hardly be any doubt 
that the disease is due 
to a congenital morbid 
predisposition of the 
pyramidal tract, and 
that thus it is closely 
connected, serological- 
ly, with the other forms 
of hereditary systemic- 
disease, especially with 
hereditary muscular- 
atrophy; but the ana- 
tomical examination of 
the spinal cord, which 
has been possible thus 
far in only a few cases,, 
has shown disease in the^ 
lateral cerebellar tract 
(KIS) and the columns 
of Goll, besides degen- 
eration in the pyramidal lateral tract (PyS) — that is, in the territory of the* 
neurones of the lumbar spinal ganglia. Anatomically, therefore, hereditary- 
spastic spinal paralysis must also be termed a combined systemic disease. 

Besides the two forms of primary degeneration of the pyramidal lateral tracts- 
(PyS) already mentioned, which in our opinion are perfectly well established 
clinically and anatomically, there are in reality several other forms of disease 
whose clinical symptoms are in the main those of spastic spinal paralysis, while 
the anatomical changes consist of a primary, more or less strictly systemic dis- 
ease of the lateral columns alone, or of the lateral and posterior columns. In the 
latter case ataxia, bladder disturb inces, slight disturbances of sensation, etc., 
may at times be added to the spastic symptoms; but since we have very little 
definite knowledge of these rare forms of disease, we can not at present give any 
suitable description of them. Many of these diseases seem to be exogenous in 
origin and to be especially connected with previous syphilis. Other cases are- 
related serologically to severe general constitutional diseases, especially perni- 




Fig. 156. — Spastic spinal paralysis. Impulsive laughing. The same pa- 
tient as Fig. 155. Symptoms of amyotrophic lateral sclerosis came 
on later. (Erlangen Medical Clinique.) 



PRIMARY DEGENERATIONS OF THE MOTOR TRACT 1011 



cious anaemia (page 723). We may also mention that a pure type of spastic 
spinal paralysis may be produced by chronic poisoning- with lathyrus seeds 
(lathyrus sativus and lathyrus cicera, the so-called vetches, which are used to 
make bread in southern countries). Systemic degenerations of the spinal cord 
also occur in pellagra, which is common in northern Italy from the continued use 
of diseased or fermented maize. This sometimes causes especially marked spastic 
symptoms, besides, of course, many other spinal and mental symptoms (Tuczek). 

[Gowers has given the name of ataxic paraplegia to a class of cases of com- 
bined degeneration of 
the lateral and posterior 
columns, which are by 
no means rare. The 
disease comes on grad- 
ually in middle life, 
usually without any 
definite cause. Men 
are much more fre- 
quently affected than 
women. The early symp- 
toms resemble those of 
spastic paraplegia, with 
the addition of atax- 
ic unsteadiness, which 
may be at first the 
most prominent symp- 
tom. There are very 
rarely any lightning 
pains, but there is at 
times a dull pain in the 
legs or the sacrum. 
There is rarely any im- 
pairment of sensation. 
The tendon reflexes are 
usually much exagger- 
ated. Sexual power 
may be lost early, and 
the bladder and rectum 
are often affected. Re- 
flex immobility of the 
pupils and optic atro- 
phy are rare, but nys- 
tagmus is occasionally 
noticed. The arms are 
usually involved later. 

Mental symptoms are rare. The disease is slowly progressive, but it rarely 
proves fatal, death being usually due to some intercurrent disease. The extent 
of the degeneration in the cord varies, but it is never so well marked in the pos- 
terior columns as it is in true tabes. Putnam has also described a type of degen- 
eration occurring also in adult life, but much more frequent in women. In his 
cases the trouble seemed to be not infrequently associated with profound anaemia 
or other forms of malnutrition. Parsesthesia is a very prominent symptom of 
the earlier stages of the disease, and it may come on suddenly or rapidly 
increase. Its appearance in an anaemic person of middle age is therefore 
suggestive of the onset of this form of disease. Disturbances of micturition 




Fig. 157.— Family spastic spinal paralysis. 
(Erlangen* Medical Clinique.) 



1012 



DISEASES OE THE NERVOUS SYSTEM 



are also very common in the early stages. Inco-ordination and muscular weak- 
ness develop later, and the weakness may increase to complete paraplegia. The 
reflexes are usually exaggerated, but they may be absent. The disease is apt 
to terminate fatally within four or five years. The pathological changes are 
of a degenerative nature, and are most marked in the posterior and lateral 
columns, but they are quite diffuse, so that this type of disease is more closely 
allied to diffuse chronic myelitis than to a systemic degeneration. In some 
cases systematic gymnastic exercises, by ErankeFs method, prove of de- 
cided benefit. The treatment otherwise is the same as that of chronic mye- 
litis.— K] 

Diagnosis. — Since the symptom-complex of spastic spinal paralysis must al- 
ways arise if the pyramidal tracts are affected by any disease in any part of 
the two lateral columns of the spinal cord or even higher up, it is easily seen 
that it may often be very difficult or even quite impossible to decide in a given 
case whether we have to do with a primary systemic degeneration or with some 
other circumscribed disease of the pyramidal tracts. The chief weight in 
diagnosis should always be laid on the general development of the morbid condi- 
tion, the serological conditions (several in a family affected), and the strict 
limitation of the symptomatic picture (absence of any sensory or bladder disturb- 
ances, etc.). 

The morbid conditions chiefly to be considered in differential diagnosis are 
the following: 1. Multiple sclerosis. As previously stated (page 956), this may 
for some time resemble very closely the type of pure spastic spinal paralysis. 
2. Syphilitic disease of the upper dorsal cord, the so-called syphilitic spastic spinal 
paralysis. We will consider this important disease more fully in a subsequent 
chapter on syphilis of the spinal cord. 3. Chronic hydrocephalus (vide infra, 
the section on diseases of the brain). 4. Subacute and chronic myelitis following 
other acute diseases (typhoid fever, influenza, etc.). This can, as a rule, be 
easily distinguished from genuine spastic spinal paralysis by the mode of ori- 
gin, and also by the clinical symptoms. 5. Slight compression of the spinal 
cord, from vertebral caries, tumors, traumatic affections of the vertebrse, etc., 
may for some time give rise to typical symptoms of spastic spinal paralysis, 
but with careful attention and longer observation there will only rarely be any 
mistake. 

Prognosis and Treatment. — The prognosis of genuine spastic spinal paralysis 
is naturally as unfavorable as that of any other systemic disease. The treat- 
ment can therefore be merely symptomatic. The spastic symptoms, which are 
often very troublesome, are most readily alleviated by the use of long-continued 
warm baths. In other respects the treatment follows the rules that obtain in all 
chronic affections of the spinal cord. 



APPENDIX 

CONGENITAL SPASTIC PARAPLEGIA IN CHILDREN 

{Spastic Cerebral Paralysis. Infantile Spastic Diplegia. Little's Disease) 

In this place we would also speak briefly of a morbid condition, first described 
by J. Heine and the English physician Little, which is not very rarely observed 
in children. The symptoms in these cases are probably usually congenital, or at 
least they arise during birth (vide infra), but from reasons that are easy to 
understand they are not noticed until later. When the children come under 
medical observation they are usually from three to six years old, or even older. 



CONGENITAL SPASTIC PARAPLEGIA IN CHILDREN 1013 



The most striking- symptom is that the child can not walk at all, or he walks only 
with difficulty and with assistance. If we examine the legs carefully we usu- 
ally find that they are quite stiff. The thighs are usually somewhat flexed and 
firmly adducted, and also rotated inward. The knees are also slightly bent, while 
the feet are often in a position of equinus or equino-varus (Fig. 158). From the 
contracture of the thighs in adduction it readily happens that the legs cross each 
other when the child lies down, or especially when he tries to walk. Passive move- 
ments of the legs can be performed only by overcoming more or less muscular 
resistance. The tendon reflexes, especially the 
patellar reflex, are much increased, and there is 
often a persistent ankle clonus. The sensibility 
and micturition are normal. The arms, as a rule, 
are readily moved, but slighter spastic symptoms 
may also occur in them. Many of these children 
are mentally perfectly normal, learn to talk and 
write well, etc. ; but in other cases cerebral disturb- 
ances are also plainly manifested, feeble intelli- 
gence, defective speech, epileptic attacks, strabis- 
mus, etc. As the child's physical development pro- 
ceeds the symptoms often improve, but in general 
the condition is stationary and not progressive. 

Our knowledge is still very defective as to the 
causes of these congenital spastic paraplegias and 
the anatomical changes which underlie them. First 
of all we must make a fundamental division of 
the cases into two groups. In the one we have to 
do with children who are born with great difficulty 
and with artificial aid (forceps, etc.). In this 
group we can probably assume injuries of the brain 
in parturition from haemorrhage, etc., which result 
in permanent disturbances of function. In the 
other group, where the history affords no such evi- 
dence (except that often the children are born 
prematurely), we usually have to assume some con- 
genital defect (so-called porencephaly in the cere- 
brum, congenital aplasia of the motor centers or of the whole pyramidal tract). 
This congenital form of spastic paraplegia may also occur generically, but it is 
to be distinguished from the hereditary spastic paralysis above described, which 
develops slowly and only in later life and is progressive. 

In the way of treatment, we may expect most from regular gymnastic exer- 
cises. Surgical interference (tenotomy, transplantation of tendons) and ortho- 
paedic appliances may sometimes considerably improve the child's ability to 
walk. 




Fig 



. 158.— PositioD of the legs in 
congenital spastic cerebral pa- 
ralysis. (Sketch from personal 
observation.) 



1014 



DISEASES OF THE NERVOUS SYSTEM 



CHAPTER X 
ACUTE AND CHRONIC POLIOMYELITIS 

1. Spinal Paralysis of Children 

[Acute Poliomyelitis in Children) 

iEtiology and Pathological Anatomy. — In children there occurs quite fre- 
quently a definite and well-characterized form of paralysis, for the first accurate 
knowledge of which we must thank Jacob von Heine in 1840. Although Heine 
subsequently, in 1860, expressed the opinion that a disease of the spinal cord 
formed the basis of the paralysis, the first actual confirmation of this opinion was 
furnished by Prevost and Vulpian, Charcot and JofTroy, and others, so that at 
present we are justified in exchanging the old term " essential paralysis of chil- 
dren " for the name of " spinal paralysis of children." 

As the name indicates, the affection occurs chiefly, if not exclusively {vide 
infra), in children, and is most frequent in the earlier years, somewhere between 
one and four. An exciting cause, such as taking cold, has hardly ever been made 

out. The children are almost 




always perfectly healthy* pre- 
viously, and come of healthy 
families without any neuro- 
pathic predisposition. The 
whole course of the disease 
makes the hypothesis very 
probable that we have to do 
with an acute infectious dis- 
ease — with an infectious pro- 
cess, which often causes first 
a mild or severe general in- 
fection of the body, and then 
is localized chiefly in a cir- 
cumscribed portion of the 
spinal cord. It also, perhaps, 
bears some relation to this 
hypothesis that most of the 



cases occur in warm weather. 
The fact should also be mentioned that small and even extensive epidemics of 
spinal paralysis of children have been repeatedly observed. We have ourselves 
seen three children fall ill in a little village in a few days with acute poliomyelitis. 

With reference to its anatomy, the disease may be defined as an acute inflam- 
mation, which affects chiefly a definite portion of the anterior gray matter of the 
spinal cord, usually attacking only the anterior gray horn of one side ; yet it does 
not always limit itself strictly to this, but it may involve the white matter in the 
vicinity somewhat, although, of course, to a lesser extent than the gray matter. 
Although fresh cases have so far been examined in very scanty numbers, still we 
can sometimes make out clearly the signs of inflammation in the older centers 
of disease. The lesion which is most frequently found in old cases consists 
of a considerable atrophy of one anterior horn, which is cicatrized and shriv- 



* The paralyses arising after acute diseases — such as measles, scarlet fever, small-pox, etc. — are 
perhaps partly of spinal origin, but they can not be identified with the idiopathic spinal paralysis of 
children. 



ACUTE AND CHRONIC POLIOMYELITIS 



1015 



eled and changed to a dense sclerosed tissue, often pierced by dilated and thick- 
ened vessels, and containing scarcely a single normal ganglion-cell. If the 
paralysis affects one arm, the corresponding anterior horn in the cervical enlarge- 
ment is atrophied (see Fig. 159) ; if the leg be paralyzed, the process is seated 
in the lumbar enlargement. In bilateral paralysis we must think of an affec- 
tion of both anterior horns at the corresponding level of the cord. 

This inflammation of the anterior horn, the poliomyelitis, is to be regarded as 
the primary focus of disease, dependent upon the local action of the excitants of 
inflammation. From this point, as in every severe lesion of the motor ganglion- 
cells there situated, there develops a secondary degeneration, which, extending 
to the periphery, affects the corresponding anterior roots, and later their appro- 
priate motor nerves and the muscles supplied by them. In the paralyzed muscles 
and nerves we accordingly find a high degree of degeneration and atrophy, such 
as we have learned to recognize in severe peripheral paralyses. 

Although at present the spinal origin of the atrophic paralysis of children is 
regarded as sufficiently certain, we must mention that it is not improbable, at 
least in many cases, that the peripheral nerves are also primarily involved; the 
poliomyelitis may be combined with a multiple neuritis, produced by the same 
causes and thus co-ordinate. Under this heading should be classed those cases 
where there is at first great pain in the extremities, especially on pressure and 
passive movement. The rapid disappearance of many of the initial paralytic 
symptoms may perhaps be referred in part to the presence of co-existing neuritic 
processes. We shall also see later that there are perhaps serological relations be- 
tween spinal and cerebral infantile paralysis. 

Clinical History. — The disease almost always begins suddenly. A child who 
was previously perfectly well and lively is all at once attacked "with severe fever, 
often reaching 105° or 106° (40°-41° C), and quite severe general symptoms are 
also associated with the fever even from the beginning. The child complains of 
headache, and sometimes of pain in the loins and in the limbs (vide supra), and is 
decidedly stupid and somnolent. Very often still more marked cerebral symptoms 
develop: complete loss of consciousness, single twitchings in the face or the ex- 
tremities, or general convulsions. The eclamptic attacks, turning of the eyes, and 
clonic contractions in the face and extremities, sometimes appear even at the 
beginning of the disease. On the part of other organs we see most frequently 
gastro-intestinal symptoms, especially vomiting, more rarely diarrhoea. All the 
initial symptoms, whose intensity varies very much in the different cases, some- 
times last only a very short time — a day or two — although they often continue 
for a week or two. Indeed, we even know cases in which, as the mothers have 
assured us, the children are said to have " lain in spasms," almost uninterrupt- 
edly, even for four or five weeks before the beginning of the paralysis — that is, 
before it became noticeable. On the other hand, however, it may happen that the 
initial symptoms, especially the severe cerebral symptoms, are entirely absent or 
greatly modified. 

After the initial period of the disease just described has passed away, the 
parents usually notice that the child is attacked by a more or less extensive 
paralysis. If its development can be followed closely, we always find that it 
spreads rapidly, often in single spurts which quickly follow one another, so that 
it usually reaches a considerable extent in a short time. Either both legs, or the 
legs and one arm, or all the extremities, and even the muscles of the trunk, are 
affected. In some cases one oculo-motor or facial nerve has been observed to 
be affected at the beginning, a symptom which we would most readily refer to 
a neuritic process. The paralysis scarcely ever remains permanently as exten- 
sively distributed as at first; it diminishes rapidly, and soon is limited to 
a definite muscular region, which remains permanently paralyzed. In some 



1016 



DISEASES OE THE KEKVOITS SYSTEM 




cases the paralysis may entirely disappear, but as a rule a complete paralysis 
is left in one extremity, or at least in a portion of it; most frequently 
in one leg, especially in the peroneal muscles ; somewhat more rarely in the arm, 
chiefly in the deltoid ; sometimes in both legs ; or, very rarely in spinal paralysis,, 
in one arm and leg on the same side or on opposite sides. Meantime the child's 
general health has been completely restored. He is well and vigorous, has an ex- 
cellent appetite, never shows any permanent cerebral disturbance — only the pain- 
less, flaccid paralysis, the inability to use the affected extremity, is left behind. 
In the following weeks and months a further, slower improvement in the power 

of motion often becomes noticeable, but, 
as a rule, a permanent and more or less 
complete paralysis of certain muscles re- 
mains. 

In regard to the more intimate pecul- 
iarities of this remaining paralysis, it 
may invariably be characterized as a flac- 
cid atrophic paralysis. A marked atrophy 
of the paralyzed muscles shows itself a 
\ few weeks after the beginning of the pa- 

} ralysis. This atrophy gradually spreads, 

I and it may finally attain the highest de- 

gree. The atrophy is often, but not al- 
ways, partly concealed by a more abun- 
dant development of fat tissue. The 
changes in the electrical excitability of 
the paralyzed nerves and muscles come 
on still more rapidly than the visible atro- 
phy. Since we have to do with a com- 
plete degeneration of the nerves, as fol- 
lows from the anatomical basis of the dis- 
ease, a pronounced electrical reaction of 
degeneration must necessarily develop in 
the affected parts. Duchenne found that 
usually the faradic excitability of the 
nerves and muscles is completely lost after 
__JHtttftf JlL; ' a week or two. On galvanic examina- 

--^i^^^S^S Jill * tion, we can at first detect an increase of 

/ ^H il m aMiSp ' »'lfr'' - \ excitability in the muscles with a pre- 

^^SPP^ -fa JBBP dominance of slow anodic closure contra c- 

'- ■ (ions (AnSZ), while later, after two or 

three months, the galvanic excitability 
„ iC . . . . , _ . . . , also sinks very considerably; but the mus- 

Fig. 160.— Old spinal infantile paralysis, acquired . , . , . 

at the age of six. (Personal observation.) cular contractions preserve their qualita- 
tive peculiarities characteristic of reac- 
tion of degeneration (see page 847). Very often the whole affected extremity 
remains backward in its growth, so that later the bones may show a shortening 
of several centimetres (Fig. 160). The parallelism between the muscular atrophy 
and the stunted growth is not, however, present in all cases, as Volkmann, in 
particular, has stated. 

Passive motion of the paralyzed extremity is at first, on account of the 
absence or diminution of the muscular tonus, perfectly free, and so remains 
except for the contractures that finally set in (vide infra). Many joints are 
so flaccid that we can actually make flapping movements with the paralyzed limbs 
and give them the most extraordinary positions. The tendon reflexes are invaria- 




ACUTE AND CHRONIC POLIOMYELITIS 



1017 



bly completely absent in the paralyzed extremities, and so almost always are the 
cutaneous reflexes — a condition which is to be referred to the interruption of the 
reflex arc in the anterior horns, which may sometimes be of diagnostic signifi- 
cance. The skin often shows certain trophic disturbances (atrophy, anomalies in 
the growth of the hair and in the secretion of sweat) ; it almost always feels 
cool and has a cyanotic appearance. Its sensibility, however, is completely re- 
tained in all cases. Micturition is sometimes a little disturbed at the beginning 
of the disease, but in most cases this disturbance completely disappears later. 

After the paralysis has existed for a time, certain secondary contractures 
almost always develop in the paralyzed parts, some of which are of a very 
characteristic type. In the legs especially the "paralytic club-foot" (talipes 
varo-equinus) is a condition long known. It is due to the fact that, from the 
paralysis of the peronei muscles and of the tibialis anticus, the point of the foot 
constantly droops, and that a contracture is gradually developed in the antago- 
nistic unparalyzed muscles of the calf, whose points of insertion are permanently 
approximated. In paralysis of the muscles of the calf there arises, on the other 
hand, a moderate degree of calcaneus from the contracture of the antagonists. 
In the arms and in the vertebral column, in paralyses of the spinal muscles, the 
most manifold and sometimes very considerable contractures and deformities 
may also arise, which are in the main always to be referred to the contracture of 
unparalyzed antagonists and to external mechanical conditions, such as weight 
and pressure. 

In conclusion, if we simply compare the type of disease sketched with its ana- 
tomical cause, the general agreement of the two may at once be seen. The affec- 
tion of the anterior gray cornua must have as a result a paralysis with a subse- 
quent atrophy and reaction of degeneration, in which the reflexes must be lost by 
the destruction of the reflex arc, but the sensibility must remain perfectly normal 
from the persistence of the sensory conduction (the posterior columns and the 
posterior gray cornua), and the vesical functions must also remain normal. The 
subsequent paralysis is the result of the permanent destruction which the morbid 
process, in itself completely ended, has caused in the spinal cord. 

We must also mention the peculiar fact which has been observed in some cases, 
that progressive muscular atrophy may come on in later life in persons who long 
before have had spinal infantile paralysis. The cells of the anterior horns once 
injured by the acute disease seem never to have become equal to the functional 
demands made upon them, and therefore they succumb to a premature atrophy. 

Diagnosis. — The diagnosis of the spinal paralysis of children is almost always 
easy to make correctly, if we hold strictly to the definition and peculiarities of 
the disease, and do not reckon as spinal paralysis every paralysis appearing in a 
child. We should consider chiefly the acute beginning, the subsequent flaccid 
paralysis with atrophy and reaction of degeneration, with the loss of the reflexes, 
but with retained sensibility. If we observe these features, we are sufficiently 
protected against confusion with cerebral diseases and other diseases such as 
spondylitis, hereditary muscular atrophy, or spastic cerebral and spinal paralysis. 
We have already mentioned above that transitional forms between acute polio- 
myelitis and acute polyneuritis probably occur; but we would constantly empha- 
size one principal distinction between polyneuritis and genuine, circumscribed 
acute poliomyelitis — polyneuritis has a general, hematogenous, toxic or toxic-in- 
fectious origin, while acute poliomyelitis seems to be a true local inflammation, 
dependent upon the local presence of the (organized?) excitants of inflammation. 
In the clinical differential diagnosis we should consider chiefly the existence of 
any initial pains and any initial sensitiveness of the peripheral nerves and mus- 
cles. The further course of the disease may also be decisive, since the neuritic 
paralyses afford a much better prognosis than the paralyses of poliomyelitis. 



1018 DISEASES OF THE NERVOUS SYSTEM 



Prognosis. — It is not impossible, but it is not yet proved, that many of the 
cases where children die speedily with convulsions are to be regarded as the initial 
stage of acute poliomyelitis. If, however, the first stage of the disease be past, 
the prognosis as regards life is entirely favorable, since the rest of the child's 
physical development is no further affected in any way. The prognosis as regards 
the complete restoration of the disturbance of function is, however, much more 
unfavorable. Although we should not forget that the paralysis is at first much 
more extensive than it is later, nevertheless this lessening of the paralytic symp- 
toms occurs only in the first weeks or months. A limb which has not recovered 
in six to nine months usually remains paralyzed for life. Nevertheless, this 
should not restrain us from persevering in treatment, at least in the first years, 
since sometimes a very noticeable improvement in the functions of the paral- 
yzed parts is thus procured. 

Treatment.- — If we have an opportunity, even during the initial stage of the 
disease (when, of course, the diagnosis can not usually be made with certainty), 
to attack the disease by our treatment, we may prescribe cold compresses or an 
ice-bag to the head, and eventually, when there is high fever or great stupor, a 
tepid bath with cool affusions. We are but rarely led to try blood-letting by 
leeches behind the ears or on the temples, when there are signs of marked cere- 
bral hyperemia. Internally we usually prescribe a mild " intestinal derivative," 
such as half a grain or a grain (gramme 0.03-0.05) of powdered calomel every two 
or three hours, infusion of senna, etc. 

After paralysis appears, we may expect the most success from electrical treat- 
ment, kept up consecutively for months, and, with interruptions, for years. We 
put a large, broad electrode on the vertebral column at the spot which corresponds 
to the place of the lesion in the spinal cord — on the cervical vertebras in paralysis 
of the arm, and the lower dorsal in paralysis of the leg — while the other electrode 
serves for peripheral application to the paralyzed nerves and muscles. In this 
way we apply a moderately strong constant current, reversing it occasionally, for 
two or three minutes, partly stabile and partly labile, passing the cathode, or even- 
tually the anode, slowly over the paralyzed muscles and nerves. We may also 
employ occasional interruptions and reversals of the current. Duchenne has also 
found persistent treatment by the faradic current of advantage. The sittings 
should take place three or four times a week, and later even oftener, if possible. 

Besides electrical treatment, methodical gymnastic exercises of the muscles, 
that can still be moved to some degree actively, may also be of distinct advantage. 
Regular and persistent massage of the muscles is also to be recommended in the 
later stages. In practice we can not avoid prescribing certain embrocations, such 
as spirit of camphor, spirit of mustard, or spirit of formic acid. Passive mo- 
tion is very important to guard against contractures, and to improve the already 
existing deformities. 

The use of baths, of brine or ferruginous waters, is to be recommended, 
although, of course, they must not be overvalued. They may be given at home. 
If circumstances permit sending the child to a bath during the summer months, 
we should chiefly consider the brine baths at Reichenhall, Kreuznach, Kosen, and 
Colberg; the acid salines at Rehme, Nauheim, and Soden; and eventually, with 
weak and anaemic children, the use of the iron baths at Driburg, Pyrmont, or 
Schwalbach. Good results are sometimes obtained at the indifferent thermal 
baths at Teplitz, Wildbad, Ragatz, or Gastein, but these must be used only with 
caution. We also obtain good results, especially with older children, at the cold- 
water cures. 

Very little is to be expected from the use of internal remedies. Iodide of po- 
tassium and strychnine are recommended, the latter in the form of subcutaneous 
injections, to -VV grain (gramme 0.001-0.003) daily. 



ACUTE AND CHRONIC POLIOMYELITIS 



1019 



When the acute process is wholly past and we can no longer count on any fur- 
ther regenerative process, the mechanical surgical treatment of the patient may 
often be of material service. In the first place the power of movement may be 
improved by orthopaedic appliances, and troublesome contractures may also be 
relieved by tenotomy. The therapeutic attempts to join the tendons of muscles 
which can still contract to the tendons of the paralyzed muscles, in order to ren- 
der it once more possible to obtain the effect of movement of these muscles 
(Nicolodoni, Yulpius, and others), are of especial interest. The symptomatic 
benefit thus obtained is very considerable. Details as to all the orthopaedic and 
surgical methods of treatment are to be found in the special treatises. When we 
can no longer hope for any further improvement in the paralysis w T orth mention- 
ing, the treatment is limited to improving the patient's general condition and 
strengthening him as much as possible by proper food and good air. 

2. Acute Poliomyelitis of Adults 

{Acute Atrophic Spinal Paralysis of Adults) 

Although it had been believed for a long time that the form of acute atrophic 
spinal paralysis, just described, occurred only in children, later observations by 
Moritz Meyer, Ducherme, Erb, F. Schultze, F. Miiller, and others, have established 
the fact that precisely analogous cases of disease may also develop, although 
far less frequently, in adults, especially in young persons under thirty. There is 
no longer any doubt of this fact, especially if we consider an authentic ana- 
tomical lesion found by F. Schultze. We have, however, once before had to say 
that for a long time we have regarded the diagnosis of acute, and, as we shall soon 
see, of chronic poliomyelitis also, as too lightly made, and that certainly very 
many of the cases diagnosticated and published as poliomyelitis are to be classed 
as primary neuritis (see page 885). Since we know that primary degenerative 
processes may develop acutely and subacutely in the motor nerves, and may also 
lead to an atrophic paralysis, a greater part of the teaching on poliomyelitis needs 
new and careful revision in order to exclude what does not belong to it. 

The type of acute poliomyelitis of adults, so far as it has been established by 
definite observations, which at present are not numerous, is not materially differ- 
ent from the type of the spinal paralysis of children. 

We often can not make out any ^etiological conditions; sometimes exposure 
to cold, over-exertion, etc., seem to favor the development of the disease. Cases 
are seen more frequently in men than in women. 

The disease likewise begins with quite severe initial symptoms, fever, head- 
ache, somnolence, delirium, and vomiting, which may last from a few days to a 
week or two. The violent spontaneous pains which are very often reported in the 
extremities usually belong probably to those cases in which a primary neuritis, 
but not a poliomyelitis, is the chief anatomical lesion; but severe pain in the 
back may also occur in genuine poliomyelitis in the first acute stage of the dis- 
ease. After the end of this first stage the paralysis appears. This develops with 
varying distribution, usually in single spurts, but always rather rapidly. The 
paralyzed muscles are perfectly flaccid, the cutaneous and tendon reflexes are 
wholly absent, and very soon a pronounced atrophy and reaction of degeneration 
appear, while the sensibility and the vesical and sexual functions remain normal. 

The distribution of the paralysis shows certain peculiarities, which must be 
briefly described here, since they can be studied much better in adults than in 
children. The paralysis may be very extensive, it may affect all four extremities, 
or it may occur in the form of paraplegia, or even of monoplegia. In the ex- 
tremities we very often find certain groups of muscles paralyzed, to which E. 
Kemak first called attention. Since the muscles that are paralyzed at the same 



1020 



DISEASES OF THE NERVOUS SYSTEM 



time are not supplied by the same peripheral nerves, but usually are connected 
in their functions, we may suppose that the corresponding ganglion-cells in the 
anterior cornua of the spinal cord also lie together, without regard to the dis- 
tribution of their peripheral processes in the different motor nerves. Thus, for 
example, it is worthy of note that, in paralysis of the crural region, the sartorius 
often remains entirely free ; that in the leg the tibialis anticus, on the one hand, 
and the peronei and the extensor digitorum on the other, may be separately dis- 
eased; that in the forearm the supinator longus, supplied by the radial nerve, 
remains free, while all the other muscles on the extensor side of the forearm are 
paralyzed (" forearm type " of E. Remak) ; and that, on the other hand, the supi- 
nator may be paralyzed alone or together with the biceps, brachialis anticus, and 
deltoid ("upper-arm type" of E. Remak). From the group of muscles para- 
lyzed we can determine with some degree of accuracy the location of the disease 
in the cord according to the statements previously made in regard to the position 
of the spinal motor centers (page 921). 

In regard to diagnosis, especial attention must be paid to the distinction be- 
tween poliomyelitis and neuritis. The greatest stress is to be laid on the initial 
pains and any other slight disturbances of sensibility. In other respects, the 
course of the two diseases is so similar that we can indeed imagine that they are 
closely allied in their serological relations, and exhibit merely different forms of 
localization of the same (probably infectious) morbid agency. It always seems 
to us, however, as we have said above, that the principal distinction is that in 
genuine circumscribed poliomyelitis there is an actual local focus of inflamma- 
tion, but in polyneuritis there is a toxic (haematogenous) degeneration of the 
peripheral motor neurones. In the latter case, of course, the motor ganglion-cell 
itself may also be destroyed if the disease be severe, but this would always be a 
different process from the local poliomyelitic inflammation. 

The prognosis is not wholly unfavorable, as sometimes a complete recovery 
has been observed, although only after months. Of course, it is very possible that 
such cases are multiple neuritis. On the other hand, however, the same perma- 
nent paralyses as in spinal paralysis of children may be left, with atrophy and 
contractures. 

The treatment follows precisely the same rules that we have mentioned in the 
spinal paralysis of children. The internal or subcutaneous use of ergotine may 
be added on the recommendation of some physicians. F. Miiller recommends a 
solution of two and a half drachms of ergotine (grammes 10) with a third of a 
grain of sulphate of atropine (gramme 0.02) in five drachms of water (grammes 
20), of which he injects seven to fifteen minims twice a day. 

3. Subacute and Chronic Poliomyelitis 

(Subacute and Chronic Atrophic Spinal Paralysis. Paralysie generale spinale anterieure 

suoaigue [Duchenne]) 

While the anatomical basis of acute poliomyelitis in adults still leaves much 
to be desired, our anatomical knowledge of the occurrence of a subacute and 
chronic poliomyelitis, in the sense of the authors who have described it, is still 
more defective. Confusions with multiple neuritis are also undoubtedly very 
common here, and the diagnosis is not incontestable in all the cases published 
under the name of " subacute poliomyelitis " ; but there can be no doubt, from 
some recent and perfectly accurate observations (Oppenheim, ISTonne, and 
others), that extensive subacute and chronic diseases may occur in the anterior 
horns of the cord and lead to the development of extensive paralysis. The 
serological and general pathological conception of these cases is of course still 
wholly unsettled. 



SO-CALLED ACUTE 



ASCENDING 



SPINAL PAEALYSIS 



1021 



In the cases classed under this heading a paralysis, first of both legs and 
somewhat later usually of both arms, develops in a comparatively short time — 
in the course of some days, or weeks at most. It usually has no special cause 
or any severe initial symptoms. The patient complains at first of weakness 
in the legs ; he can no longer walk, and he is confined to the bed. A short time 
later the same disturbances appear in the arms, and lead to a more or less com- 
plete paralysis. More rarely the opposite condition obtains, that the arms are 
affected first and the leg's later, but the sensibility always remains wholly unaffect- 
ed, except at most for slight paresthesia, and there is also no pain, either spon- 
taneous or occurring on pressure. Soon after the paralysis an equally exten- 
sive atrophy develops, and a distinct loss of electrical excitability, running 
parallel to it; which passes over into a partial or, in all severe cases, a com- 
plete reaction of degeneration. The cutaneous and tendon reflexes are very 
much diminished and often entirely lost. The bladder and rectum, however, 
remain intact, and bed-sores never develop if the patient has proper care. We 
sometimes notice a striking diminution of the sweat secretion. In rare cases 
the muscles of the neck, the lips, the tongue, and the pharynx are attacked by 
the disease. 

After the paralysis has reached its greatest extent there is usually a pause. 
The condition remains stationary for months sometimes, and then a gradual 
improvement begins, which perhaps may go on to complete recovery ; but often, of 
course, the recovery remains incomplete, so that the patient has a more or less 
marked disturbance of function for life. The " middle form of chronic polio- 
myelitis " described by Erb, in which there is only a partial reaction of degenera- 
tion in the paralyzed muscles, almost always gives a good prognosis. The disease 
takes an unfavorable course, if the respiration be impaired through involvement 
of the respiratory muscles, or, if the patient can not swallow, through involvement 
of the muscles of deglutition, or if inhalation pneumonia set in. The autopsy 
then shows extensive degenerative inflammatory changes in the anterior gray 
columns of the cord with a great destruction of ganglion-cells, while we can 
usually discover only very slight 'changes (secondary degeneration) in the 
peripheral nerves. 

As a consequence of what has been said, we shall be compelled to make a diag- 
nosis of chronic poliomyelitis when extensive paralysis comes on with subsequent 
atrophy and electrical reaction of degeneration and without any neuritic symp- 
toms (pain!), and without disturbances of sensation or of the bladder. It is dis- 
tinguished from " spinal muscular atrophy " proper, by the fact that in this there 
is a slow atrophy, attacking fiber after fiber, so to speak, and that the atrophy and 
muscular weakness go absolutely parallel, while in chronic poliomyelitis the pa- 
ralysis precedes the atrophy, and whole muscles or muscular regions are affected 
from the start. 

The treatment is not absolutely hopeless, as is shown by the above description. 
A persistent electrical treatment is always most advisable. 



CHAPTER XI 

THE SO-CALLED ACUTE ASCENDING SPINAL PARALYSIS 

{Paralysis Ascendens Acuta. Landry 's Paralysis) 

In the year 1859 Landry described a disease under the name of " paralysie 
<ascendante aigue," which is chiefly characterized clinically by the fact that first 



1022 



DISEASES OE THE NERVOUS SYSTEM 



the lower and soon after the upper extremities, and finally a number of the 
muscular regions supplied by the medulla, are attacked by a rapidly advancing 
paralysis, while the sensibility and the functions of the bladder and rectum 
remain normal. In many cases the disease terminates fatally. Examination of 
the nervous system has so far, however, shown no lesion which can be regarded 
with certainty as the anatomical cause of the disease. Considering the continued 
and quite numerous observations of the disease, it seems questionable, at any 
rate, whether we can establish a uniform anatomical basis for it ( vide infra) ; but 
the clinical picture of Landry's paralysis is so striking that a comprehensive de- 
scription of it seems demanded. 

General Symptomatology. — Acute ascending paralysis attacks chiefly persons 
previously strong and healthy, in youth or middle life, somewhere between twenty 
and thirty-five years of age. Some cases also have been seen in children and older 
people. The disease seems to be more frequent in men than in women. 

The affection almost always begins with certain prodromata. These consist of 
general malaise, moderate febrile symptoms, headache, loss of appetite, and quite 
frequently of dragging and tearing pains in the back and the extremities. After 
these symptoms have lasted some days, or more rarely some weeks, during which 
they are either comparatively slight, or so severe that many patients are already 
confined to the bed, there usually comes on quite suddenly, or sometimes more 
gradually, a paresis, first of one leg, but very soon of both legs, which rapidly in- 
creases, and usually in a few days leads to an almost complete motor paraplegia. 

The paralysis is flaccid in almost all cases. The legs may be moved passively 
without any muscular resistance, and the muscles show neither active nor reflex 
tension. Their electrical excitability remains perfectly normal in many cases, 
but there is sometimes a rapid loss of faradic muscular excitability. It is not yet 
proved whether complete reaction of degeneration occurs. The reflexes, both 
cutaneous and tendon reflexes, seem to be diminished or wholly lost in the major- 
ity of cases, but some exceptions to this rule have been known. 

Sensibility is sometimes perfectly intact, but slight alterations do occur, and 
quite rarely there may be even marked anaesthesia. At times a noticeable delay 
of sensation is observed. We find no changes in the nerves of special sense. 
There is occasionally a slight oedema in the legs, which is perhaps to be regarded 
as a vaso-motor disturbance. The marked sweating, from which many patients 
suffer, is also worthy of mention. The bladder and rectum in most cases are not 
at all affected, or they present merely slight and temporary disturbances. 

A short time after the legs are attacked the arms also begin to be paretic. 
A marked motor weakness appears first in one, then in the other arm, and this 
may also increase to almost complete paralysis. The sensibility, the reflexes, and 
the electrical excitability show conditions like those in the lower extremities. 
The muscles of the trunk are also affected at the same time as, or still earlier 
than, the arms. The patient can no longer sit up in bed, turn on his side, or make 
similar movements. In some cases a paralysis of the muscles of the neck has also 
been observed. 

The third and last stage of the disease is characterized by the appearance of 
respiratory disturbances and bulbar symptoms. Manifest signs of a beginning 
respiratory paralysis appear; the respiration is labored and difficult, the move- 
ments of the diaphragm are impaired, and the paroxysms of coughing grow 
weaker. Disturbances in swallowing, difficulty in articulation, and paresis of 
the soft palate and the lips may set in. In a few cases a facial paralysis and 
disturbances of the ocular muscles have been observed. The condition grows 
worse acutely, and, as we have said, in many cases death ensues. 

Besides the symptoms thus far mentioned, referable to the nervous system, we 
find certain other symptoms in almost every case, which are less striking, but yet 



SO-CALLED ACUTE ASCENDING SPINAL PAEALYSIS 1023 



of greater significance in judging of the disease. The first of these is fever. The 
temperature is usually elevated from the beginning; it may temporarily show 
a considerable increase, up to 104° (40° C), and later it varies between 100° and 
102° (38°-39° C), but between times it may even sink to normal. Of the inter- 
nal organs the spleen shows the most frequent changes. It is usually swollen 
moderately, but appreciably. There is also sometimes a slight albuminuria. 

In the cases with a fatal termination the whole duration of the disease is some- 
times only a few days, and as a rule a week or two, or rarely more. Fortunately, 
however, all cases do not terminate fatally. The disease may come to a stand- 
still at any time, even if the most threatening symptoms be present. Then the 
paralysis shows no further advance, the disturbances present disappear, and recov- 
ery ensues after a course of several weeks. It is, of course, usually quite a long 
time before the patient again feels himself in possession of his full powers. 

Pathological Anatomy and Pathogenesis. — If we consider the whole picture 
of acute ascending paralysis, the idea is necessarily forced upon us that we have 
to do here with an acute infection or auto-intoxication of the body, with a pre- 
dominating localization in the motor nervous system. The beginning of the dis- 
ease with general malaise corresponds perfectly to the prodromal stage of many 
other acute infectious diseases. The fever, the acute splenic tumor, and the occa- 
sional albuminuria also can scarcely be explained in any other way, according to 
our present views, except by the above hypothesis. There are, of course, no 
definite and positive data as yet in support of this hypothesis. A notable case, 
published by Baumgarten, in which many bacilli, like those of splenic fever, 
were found in the spinal cord, is at present wholly unique. Further investiga- 
tions as to the anatomical changes in " acute ascending spinal paralysis " are 
still very desirable. In the earlier observations there is usually the statement of 
an " absolutely negative anatomical examination " ; but these statements usually 
refer only to the spinal cord. The peripheral nerves were formerly not examined 
at all; and yet, as we have long proclaimed and as is now quite generally ac- 
cepted, it is extremely probable from the clinical symptoms (pain, loss of electri- 
cal excitability, condition of the reflexes) that most cases of so-called Landry's 
paralysis are multiple neuritis (q. v.), and are nothing more than the most acute 
form thereof. Some recent anatomical investigations have already confirmed 
this hypothesis. 

It would, however, be distinctly false at present to identify acute ascending 
paralysis completely with multiple neuritis, for in some observations (R. Schulz 
and F. Schultze, von den Velden) extensive acute myelitic changes have also 
been found in the motor portions of the spinal cord (lateral columns, anterior 
gray columns). We must therefore wait for many more observations and not 
decide prematurely upon the nosological position of the disease. [Recent in- 
vestigations show that Landry's paralysis is an affection of the whole peripheral 
motor neurone, but that the ganglion-cells in the anterior horns show, as a rule, 
greater changes than the peripheral nerve-fibers. — K.] 

Diagnosis and Prognosis. — In every paralysis of the lower extremities begin- 
ning acutely and accompanied by general symptoms and fever we must consider 
the possibility of an acute ascending paralysis, but only the further course of the 
disease can decide the question. Inasmuch as merely a well-characterized clinical 
group of symptoms is meant by the above term, the diagnosis is always easy to 
make, with attention to the peculiarities given above. It is more difficult, how- 
ever, to decide accurately whether the case corresponds rather to the type of an 
acute multiple neuritis or to the type of an acute ascending spinal paralysis. We 
can judge as to this point only by careful attention to the single symptoms, espe- 
cially the condition of the sensibility (pains, anaesthesia), of the reflexes, and of 
the electrical excitability. 



1024 DISEASES OF THE NERVOUS SYSTEM 



The prognosis must at first be made with great reserve, and we must especially 
bear in mind the possibility of a rapidly fatal termination. If the first acute 
stage pass off fortunately and there be a decided cessation in the extension of the 
symptoms of paralysis, the prognosis is quite favorable, for we may then expect 
that the patient will be completely restored. 

Treatment. — We can not be certain whether an energetic " derivative treat- 
ment " is of advantage in the beginning of the disease. Dry cups along the verte- 
bral column are recommended, and even the use of the hot iron to the back. We 
would hardly advise the latter. It may be advisable, however, to prescribe 
inunctions with mercurial ointment, thirty to forty-five grains a day, as in anti- 
syphilitic treatment. Of internal medicines, we should try at the beginning sal- 
icylic acid or salicylate of sodium in large doses (30 grains, grammes 2, of 
salicylate of sodium three times a day), and also antipyrine. We may also try 
extract of ergot (ergotine) and perhaps iodide of potassium. It also seems to be 
a good plan to begin galvanic treatment early, applied to the spine and periph- 
erally. If alarming attacks of respiratory insufficiency occur, electrical ex- 
citation of the phrenic nerve and of the respiratory muscles sometimes affords 
relief to the patient. 

If the symptoms be arrested, electrical treatment and the use of baths may 
do most to hasten convalescence. 



CHAPTER XII 

NEW GROWTHS OF THE SPINAL CORD AND OF ITS MEMBRANES 

Pathological Anatomy. — Tumors of the spinal cord in the strict sense of the 
word are rare. The commonest primary new growth is the glioma, which arises 
from the neuroglia, and forms a cellular and vascular tumor. This is situated 
most frequently in the cervical or upper dorsal cord. It often develops at the 
beginning in the posterior half of the cord, but later it may attain a consid- 
erable length and a transverse diameter of several centimetres, so that the 
spinal cord in the part affected may have a considerable tumor-like thickening, 
or it may even be changed throughout almost its whole length into a thick, shape- 
less mass. Inside the glioma we sometimes find secondary haemorrhages and 
(myxomatous) softenings. Central gliosis is distinct from real glioma. The 
former never leads to any special enlargement of the cord (tumor formation), but 
to a gliomatous degeneration, and especially to an abnormal cavity formation in 
the cord, particularly in a longitudinal direction. We will speak of this impor- 
tant and by no means very rare disease more fully in a subsequent chapter. 

Of other rare new growths in the spinal cord we may mention solitary tuber- 
cles, syphilomata, and sarcomata. Solitary tubercle usually begins in the central 
gray matter. Cysticerci have also been repeatedly observed 1 in the spinal cord. 

In the spinal meninges have been found sarcomata, fibromata, lipomata, myxo- 
mata, and syphilomata. Sarcoma of the dura mater is the commonest and prac- 
tically the most important of these growths. It almost always seems to start 
from the endothelium on the inner surface of the dura, and it is then sometimes 
called endothelioma. Sarcoma of the dura has a great tendency to spread as a flat 
growth, so that it may finally surround a considerable portion of the cord with 
its mass of growth. Sarcoma is often multiple; thus it may co-exist on the spinal 
dura mater and at the base of the brain, etc. As a rule, it does not invade the 
pia mater or the substance of the cord itself. Lipoma develops on the outer sur- 



NEW GROWTHS OF THE SPINAL CORD 1025 



face of the dura, starting from the fatty tissue between the vertebral canal and 
the dural sac. A carcinoma arising from the vertebrae may also reach the spinal 
meninges by direct invasion. 

We know practically nothing of the_aetiology of most new growths in the spinal 
cord. In all probability there is an abnormal congenital predisposition of the 
tissues, which furnishes the germ for the subsequent development of the new 
growth. It is worthy of note that the onset of the first symptoms is very often 
preceded by an injury (fall on the back, etc.), which thus seems sometimes to give 
the first impetus to the formation of a tumor. 

Symptoms and Course. — New growths in the spinal meninges, especially sar- 
coma of the dura mater, are apt to cause at the beginning pronounced root symp- 
toms, and usually at first symptoms of irritation of the posterior roots. The first 
symptoms of the disease are therefore radiating pains, either persistent and burn- 
ing or paroxysmal and neuralgic, and paraesthesiae in certain root territories. 
There may also be local pain, a feeling of stiffness and pressure in the back, etc. 
There is rarely any characteristic tenderness over the spine. Anaesthesia and 
paralysis may also arise as pure root-symptoms, but only when the disease is 
extensive, since, as was mentioned above (page 921), the complete division of one 
sensory or motor root does not cause complete anaesthesia or paralysis in any 
region. Extensive paraplegic symptoms therefore point usually to an implication 
of the cord. The cord itself also suffers, as we have described more fully in the 
account of pressure paralysis from tuberculosis of the vertebrae (page 935). Only 
exceptionally does the growth itself invade the cord. The symptoms of spinal 
compression are exactly the same as in the other transverse diseases of the cord. 
The differential diagnosis between meningeal tumors and compression of the cord 
due to vertebral caries is therefore often very difficult, if we can detect no changes 
in the spine itself (Pott's boss). We must then pay chief attention to the general 
symptoms of tuberculosis (heredity, habitus, fever, other tubercular affections). 
If a meningeal sarcoma occurs as a metastasis or as one manifestation of multiple 
sarcomatosis, the discovery of a sarcoma in some other place (such as the skin) 
may put us on the right track in our diagnosis. 

In glioma of the cord itself the initial symptoms of sensory irritation may be 
almost wholly absent, or at least they may be only slight. A complicated type of 
spinal disease gradually develops, in which all the spinal symptoms may occur in 
the most varied combinations. The disease sometimes exhibits from the begin- 
ning the ordinary type of a transverse spinal paralysis. In such cases it is hardly 
possible to distinguish between a tumor and chronic myelitis. In other cases, 
however, certain peculiarities in the type lead us to suspect the possibility of a 
tumor. Among them especially is the early asymmetry of the symptoms on the 
two sides. Since a tumor may at first be confined to one half of the spinal cord 
(which scarcely ever happens in myelitis), the signs of a unilateral lesion of the 
spinal cord (vide infra, Chapter XVII) are often observed in tumors in a more or 
less pronounced fashion. Only later in the course of the disease does the clinical 
type of unilateral lesion gradually change to the ordinary transverse paralysis. A 
certain alternation in the symptoms, improvements, and new and quite sudden 
changes for the worse, are also noticed at times with tumors, a condition which 
is probably to be referred to changes in the fullness of the vessels, or to haemor- 
rhages in the substance of the tumor. The manner in which the disease pro- 
gresses is also to a certain degree characteristic. If we find on repeated exami- 
nations evident indications that the spinal affection is slowly extending upward, 
especially if the cutaneous anaesthesia is moving upward and the paralysis is 
invading higher muscular territories, this condition is decidedly in favor of the 
diagnosis of tumor, since it is far less frequently observed in other forms of dis- 
ease. We may also consider in diagnosis the fact that glioma often develops in 



1026 



DISEASES OE THE NEKVOUS SYSTEM 



the cervical cord, or at least gradually invades the cervical cord; consequently 
sensory disturbances and paralysis occur in the upper extremities in addition to 
the paraplegia of the legs. This is of rare occurrence in chronic myelitis, which 
is usually situated in the dorsal cord. The diagnosis of a tumor of the spinal 
cord, however, can at best be merely probable. 

The accurate determination of the seat of the tumor, the " segmental diagno- 
sis," is of great practical significance, if there is any question of operative treat- 
ment. It is evident that only new growths of the spinal meninges can be the 
subject of surgical interference. Such new growths have in a number of cases of 
late been operated upon successfully, but of course the number of cases in which 
a correct diagnosis can be made and an operation can be successfully performed is 
limited. We need not repeat here the details of a segmental diagnosis; they 
follow the general rules which hold for all lesions of the spinal cord (page 920) ; 
but we must once again remind the reader that total anaesthesia of a given 
cutaneous territory means not only an involvement of the corresponding posterior 
root as given in the diagram, but also an affection of the neighboring roots, espe- 
cially the two roots above. After determining the upper boundary of the anaes- 
thesia we should therefore always suspect that the upper boundary of the lesion in 
the cord is one or two segments higher than would correspond to the diagram, 
because the individual cutaneous territories are always in relation with several 
spinal roots. The same rule also holds when the segmental diagnosis is based 
upon the motor symptoms. The disregard of this relation, which was first clearly 
established by Sherrington, is the reason why formerly the location was usually 
put too low, even when the tumor itself had been correctly diagnosticated. In 
determining the upper boundary of the tumor, furthermore, we should consider 
not only the anaesthesia, but also the symptoms of sensory irritation. These 
very often manifest themselves above the anaesthetic zone and then point with 
considerable certainty to an irritation of the corresponding posterior roots by 
the upward growth of the tumor. The accurate determination of the position of 
the different spinal segments and roots in relation to the bodies and spinous pro- 
cesses of the vertebrae is also of great practical importance. In regard to this, we 
will refer to Fig. 125, page 928. 

A tumor of the spinal cord may last for many years. In new growths of the 
meninges the symptoms of sensory irritation alone may continue for several years 
before there are any well-developed transverse symptoms. Other cases, of course,, 
run a much more rapid course. The prognosis of tumors of the cord is wholly 
unfavorable unless there is a possibility of operative treatment; but, as we have 
said above, this presents itself in but few cases. Otherwise the treatment 
is merely symptomatic. If there is a suspicion of previous syphilis we should 
necessarily try inunction and the exhibition of iodide of potassium. In sarcoma 
arsenic in large doses is perhaps of some service. 



CHAPTEE Xm 
THE SYPHILITIC AFFECTIONS OF THE SPINAL CORD 

iEtiology and Pathology. — The affections of the spinal cord provoked by 
syphilis must be divided into two principal groups. The first group is formed by 
diseases in which a slow degeneration of certain systems of neurones develops in 
a somewhat obscure fashion under the influence of previous syphilitic infection 
(probably from the action of some toxine). These diseases are called most prop- 



SYPHILITIC AFFECTIONS OF THE SPINAL COED 1027 



erly " metasyphilitic " (so-called metasyphilis). Chief among them, as we have 
already seen, is tabes dorsalis (the metasyphilitic degeneration of the posterior 
root neurones), and also, probably, certain rare cases of degeneration of the 
lateral columns, and of combined systemic disease in the lateral and pos- 
terior columns (PyS, K1S, and the columns of Goll). The second group of syphi- 
litic diseases is to be classed as genuine tertiary syphilis in distinction from 
metasyphilis. These affections are characterized by the development of a specific 
gummatous new growth in the cord, especially in the membranes (meningitis 
gummosa) and in the blood-vessels (endarteritis syphilitica). This is usually 
quite extensive and not infrequently associated with corresponding syphilitic dis- 
ease in the brain. Since metasyphilis of the cord has already been discussed 
in another part of this work, there remains to be considered here only the specific 
syphilitic (gummatous) affections of the cord. 

Indications of syphilis of the cord may appear in six months to a year after 
the infection; but they develop more frequently in from two to five years after 
the infection, or even later. In only a few cases does a circumscribed gumma 
form, which then causes the symptoms of an intramedullary tumor. Diffuse gum- 
matous meningitis is far more common ; this almost always arises from the spinal 
pia mater, and only exceptionally from the dura mater (page 917). In such cases 
the spinal cord seems surrounded, in an irregular fashion, but to a considerable 
extent, by a newly-formed, vascular granulation tissue several millimetres thick. 
The meningeal blood-vessels are also almost always much diseased, their walls 
are thickened by endarteritic new formations, and their lumen obliterated or 
filled with thrombi. The posterior border of the cord is usually most affected. 
The disease usually has a considerable longitudinal extent. The region of 
the dorsal cord is often most affected, but in other cases it may be the 
cervical or lumbar cord, or sometimes the region of the conus medullaris and 
the cauda equina. The spinal roots especially are often surrounded by a thick 
sheath of newly-formed gummatous tissue. Rootlets of newly-formed tissue 
may extend from the pia mater into the substance of the cord, or the syphilitic 
new growth may extend to the vessels of the cord itself ; in such cases secondary 
tissue-changes (destruction of nerve-tissue, proliferation of neuroglia) develop 
as a result of the defective blood-supply of the tissue. In many cases certain 
secondary sequelae also develop in the tissues of the cord, similar to those we have 
become acquainted with in compression of the cord from tubercular new forma- 
tions on the dura mater (vide page 936). It is also worthy of mention that in 
a few cases genuine gummatous disease may apparently be associated with meta- 
syphilitic degeneration. 

Symptoms and Course. — It is evident that syphilis of the spinal cord can not 
afford any single definite type of disease on account of the multiple localization 
of the anatomical changes. We may say rather that syphilis of the spinal cord 
is characterized by the irregularity and the often unusual combination of its 
symptoms, and its changeable and varying course. From the different combina- 
tions of symptoms that occur we may best distinguish, relatively speaking, the 
following two forms of the affection: 

1. Chronic Gummatous Spinal Meningitis and Meningo-myelitis. — The dis- 
ease at first shows definite root symptoms, especially symptoms of irritation of 
the posterior roots : paresthesia, hyperesthesia, shooting pains, neuralgia. Asso- 
ciated with these we sometimes find well-defined local pain in the back or in the 
sacral region, pain on pressure and on movement of the vertebral column. Motor 
symptoms appear somewhat later as a rule, sometimes motor-root symptoms 
(atrophic paralyses in definite muscular territories, for example, in the muscles 
of the forearm and hand on one side or in the sacral distribution, etc.) ; or more 
frequently motor symptoms from implication of the cord itself; spastic paretic 



1028 



DISEASES OF THE NERVOUS SYSTEM 



symptoms in one or both legs, sometimes, in disease of the cervical cord, in both 
legs and one arm. Associated therewith are various, but usually slight, disturb- 
ances of sensibility, vesical disturbances, etc. If the region of the posterior col- 
umns and posterior roots be chiefly affected, affections resembling tabes may 
develop (syphilitic pseudo-tabes of Oppenheim). Not very rarely unilateral dis- 
ease may also present the more or less clearly-developed picture of Brown- 
Sequard's unilateral lesion. It is of course impossible to describe exhaustively 
all the combinations of symptoms that may be observed. 

The whole course of the disease is usually chronic and, as has been said, very 
variable. In mild cases we may sometimes see almost complete recovery under 
appropriate treatment, but this is unfortunately a rare event, since the secondary 
tissue necroses, the results of compression, obliteration of vessels, etc., are in- 
capable of complete restoration. We see improvement quite frequently, espe- 
cially with timely treatment, which finally passes into a stationary condition. 
We must be prepared for relapses, fresh exacerbations, and the onset of new symp- 
toms, which may also be cerebral. The disease may last for many — even twenty — 
years. The affection becomes directly fatal through the occurrence of dangerous 
complications (pyelo-cystitis) or severe attendant symptoms (apoplexy), etc. 

2. Syphilitic Myelitis and Syphilitic Spastic Spinal Paralysis. — In many 
cases syphilis of the spinal cord exhibits from the outset the symptoms of a 
myelitic affection. This form probably always arises from the vessels of the cord. 
The syphilitic endarteritis of the smaller vessels leads to a rapid or slow necro- 
sis of tissue and the symptoms of spinal disease which necessarily result there- 
from. The disease often develops as rapidly as an acute myelitis. A more or less 
complete paraplegia comes on within a few days. Only on careful inquiry do we 
sometimes learn that it has been preceded for some time by mild precursory symp- 
toms (weakness, paresthesias, etc.). In other cases the paraplegia develops more 
slowly, but yet within a few weeks or months. Since the anatomical lesion is 
very often in the dorsal cord, the paraplegia far most frequently shows the signs 
of spastic paralysis. Erb has therefore grouped certain cases under the name 
of syphilitic spastic spinal paralysis. This form of spinal syphilis, which in 
our experience is in fact very characteristic, is found especially in young 
persons of the male sex. Weakness, stiffness, and often a lively tremor (ankle 
clonus!) occur first in one leg and soon after in the other. The gait constantly 
grows more laborious, slower, and decidedly spastic-paretic. The sensory dis- 
turbances are at first very slight; and there is no pain. Later, on careful 
examination slight changes in sensibility are, of course, often to be found. Dis- 
turbances of the bladder are also rarely very prominent, but they are often plainly 
existent in a slight degree from the beginning. The condition may improve, espe- 
cially with timely treatment, but, for reasons already mentioned, a morbid con- 
dition may often remain stationary for years, or new symptoms even may ensue. 

Diagnosis. — So far as any diagnosis of syphilis of the spinal cord is possible, 
it is evident from what has been said. The chief rule is to consider the possibility 
of syphilitic disease in all spinal affections that are atypical from the beginning. 
If a previous infection is certain, or if, at least, it is rendered probable by the 
special antecedents, the diagnosis is the more warranted. Of course a previous 
infection often enough can not be established, even when there is certainly syph- 
ilis of the cord, and, on the other hand, other forms of spinal disease may, of 
course, occur in those who have been previously infected. The most characteristic 
features of syphilis of the cord have been mentioned above. Similar types of dis- 
ease may be produced by multiple sclerosis, by sarcomatosis of the spinal me- 
ninges, by tuberculosis of the vertebras, etc. We must therefore consider these 
affections chiefly in the differential diagnosis. Sometimes the success or failure 
of specific treatment may be of significance in diagnosis. 



SYRINGOMYELIA AND HYDROMYELUS 



1029 



Treatment. — In every case, even where there is merely a suspicion or a possi- 
bility of syphilitic disease of the spinal cord, we should institute at once a thor- 
ough antisyphilitic treatment. We think the best treatment is iriunction with 
mercurial ointment (grains xlv-lxxv, grammes 3-5, daily). Other physicians rec- 
ommend subcutaneous injections of corrosive sublimate, salicylate of mercury, 
etc. The inunction is almost always combined with the internal exhibition of 
iodine preparations, especially iodide of potassium (at first grains xx-xxx, 
grammes 1.5-2, and later still larger doses daily), iodide of sodium, or one 
of the newer iodine preparations, of which iodalbacid seems to us the best. [It 
is often necessary to give iodide of potassium in much larger doses. If the diag- 
nosis of syphilis be probable, it is advisable to begin with doses of half a drachm 
(grammes 2) or more three times a day, which should be increased rapidly 
until the patient is taking five or six drachms daily (grammes 20-25), and 
sometimes, as in cerebral syphilis, it may be necessary to push the dose to one 
or two ounces a day (grammes 30-60). — K.] If circumstances permit, it is 
well to combine inunction with a course at some bath (sulphur baths in Aix, 
Nenndorf, also Tolz, Hall in Austria, Wiesbaden, etc.). Every antisyphilitic 
treatment must be kept up a sufficient length of time and repeated after certain 
intervals, as is the general custom in the treatment of syphilis. Besides the 
specific treatment, the other therapeutic methods which are efficacious in chronic 
spinal affections also have their appropriate use (warm baths, mineral baths, gal- 
vanization). Individual symptoms (neuralgic pains, vesical troubles) require 
special attention. 

The properly conducted treatment of spinal syphilis may give results which 
are sometimes excellent and often at least satisfactory. We can understand from 
what has been said why our hopes are naturally only too often disappointed. 



CHAPTER XIV 
SYRINGOMYELIA AND HYDROMYELUS 

Pathological Anatomy and Pathogenesis. — The formation of abnormal cav- 
ities in the spinal cord is due either to a dilatation of the central canal (hydro- 
myelus) or to a peculiar process, which is called central gliosis, with the secondary 
formation of cavities (syringomyelia proper). The cases of genuine hydro- 
myelus are recognized by the fact that the cavity is found in the middle of the 
cord, corresponding to the position of the central canal, and that its walls are cov- 
ered by cylindrical epithelium. Slight degrees of hydromyelus, in which the 
dilated central canal has a diameter of a millimetre or a millimetre and a half, 
are not infrequently found. The dilatation usually extends over only one seg- 
ment o"f the cord. Greater degrees of hydromyelus, where the central canal is 
dilated to a diameter of half a centimetre or a centimetre and the longitudinal 
extent is greater, are much rarer. 

In regard to the origin of hydromyelus, we may assume, according to the 
teaching of Leyden, that the cause is quite generally some anomaly of develop- 
ment in the formation of the central canal. The hypothesis of Langhans, that 
processes of stasis in the central canal, such as compression of the upper end 
by a tumor in the posterior cranial fossa, may lead to hydromyelus, is certainly 
not applicable to the great majority of cases. 

The conditions are different in syringomyelia, which is of much greater prac- 
tical importance. In this affection, according to many investigators (Westphal, 



1030 



DISEASES OE THE XEEVOUS SYSTEM 



Simon, F. Schultze, J. Hoffmann, and others), the whole process apparently 
begins with a gliomatous new formation or transformation of tissue in the cen- 
tral portions of the spinal cord. This peculiar process, which probably starts in 
the ependymal cells about the central canal, is called central gliosis. It consists 
of a replacement of nerve-tissue by fibrous glia-tissue. The central gliosis, which 
extends toward either the posterior or the anterior horns, has a decided tendency 
to break down and thus to form secondary cavities, which unite with the central 
canal or remain independent, and these cavities may extend longitudinally in the 
central portions of the cord with numerous ramifications and projections. To this 
secondary formation of cavities we give the name of syringomyelia. In this con- 
dition the central canal itself hardly ever remains normal; it is usually dilated 
and shows many projections, reduplications, and the like, circumstances which 
clearly indicate that we must consider disturbances of development as factors in 
the origin of syringomyelia and central gliosis. We do not find any special en- 
largement of the cord in the nature of a tumor. Gliosis is thus distinct from 
true glioma formation (gliomatosis), but in some cases the distinction between 
gliosis and the formation of cellular glioma is ill-defined. In ordinary gliosis with 
syringomyelia, however, the cord appears normal externally, or, when the syr- 
ingomyelia is extensive, it may appear flabbier, saccular, and flattened in the 
parts affected. Only on section do we recognize, even with the naked eye, the 
cavity formation in the center or to one side in the gray matter and extending 
into the horns of the cord. Under the microscope we find about the cavity the 
newly-formed tissue, still proliferating peripherally and disintegrating toward 
the edge of the cavity. This tissue contains many newly-formed ependymal cells 
in Its central portion; toward the periphery the cells are fewer, and the tissue 
consists chiefly of a mesh-work of fine glia-fibers. We can not say definitely to 
what circumstances we may refer the destruction of tissue and the cavity forma- 
tion. Changes in the vessels, which are often found dilated, may perhaps play 
some part (haemorrhage, thrombosis, etc.). In most cases central gliosis and 
syringomyelia begin in the cervical cord and there attain their greatest extent; 
but they may extend downward in a lesser degree into the lumbar cord and 
upward into the medulla oblongata. 

We must probably always look for the final cause of gliosis and syringomyelia 
in a defective congenital constitution of the spinal cord. According to F. 
Schultze, injuries at birth in cases of difficult labor may perhaps lead to haemato- 
myelia and afford a basis for the later anomaly. Injury in later life is also fre- 
quently accused of producing the trouble. 

Clinical Symptoms. — Slight degrees of hydromyelus or of syringomyelia may 
be met with at autopsies as accidental findings which have given rise to no clin- 
ical symptoms whatever. Other cases of extensive cavity formation give rise to 
various complex forms of spinal disease, which usually escape correct interpre- 
tation during life. Thus we recall, for example, Spath-Schiippel's well-known 
case of general anaesthesia, a case under our own observation which presented the 
apparently pure type of spastic spinal paralysis, etc. 

Opposed to such isolated cases, however, the great majority of cases of cen- 
tral gliosis and syringomyelia of the cervical cord present an unusually character- 
istic picture, so that we can often make a diagnosis with absolute certainty. 
Since the investigations of E. Schultze and Kahler we know that this type is by 
no means rare. It is therefore certain that it was often seen in the past, but 
it was usually falsely interpreted. The fact that the gliosis begins as a rule 
in the center of the cervical cord and that, as it progresses, it must always 
involve at first the gray matter of the posterior and anterior horns on one 
or both sides, is the reason why the group of symptoms always occurs in a 
way that is generally very characteristic, although it may show some varia- 



SYKINGOMYELIA AND HYDKOMYELUS 



1031 



tions. It is seen especially in men in youth and middle age (between twenty 
and forty). 

The clinical symptoms of syringomyelia of the cervical cord develop very 
gradually, and almost always begin in the upper extremities — one arm usually 
being affected before the other. The symptoms observed in such cases may best 
be classed in three groups: 1. Motor weakness and muscular atrophy. These 
symptoms are dependent upon the involvement of the anterior horns in the pro- 
cess. The atrophy affects with especial preference the small muscles of the 
hand (interossei, thenar muscles), and also the muscles of the forearm, the del- 
toid, etc. Fibrillary twitchings and electrical reaction of degeneration are often 
found. The tendon reflexes are lost or else exaggerated, which may be easily ex- 
plained from the special localization of the process. 2. Disturbances of sensibil- 
ity are almost invariably associated with this muscular atrophy. The chief cause 
of these is always the involvement of the posterior horns in the process. The dis- 
turbances of sensibility almost always have 
this peculiarity, that the sensibility for pain 
and the temperature sense are at first always 
affected, while the simple sensibility for touch 
and the pressure sense may remain normal for 
a long time or throughout the disease. The 
fact that the patient is insensible to the influ- 
ence of pain or heat is therefore of special sig- 
nificance, because it may frequently lead to 
wounds, burns, etc., on the hands and forearms, 
which the patient may often never notice, and 
which therefore may heal badly. The disturb- 
ances of the temperature sense may affect 
either the sensibility to cold or the sensibility 
to heat, or both at once. 3. The third group 
of symptoms is made up of peculiar trophic 
changes. The above-mentioned external in- 
juries, caused by the analgesia, naturally play 
a large part in this connection (felons, bullae, 
phlegmon, etc.) ; * but we must also assume 
special trophic disturbances to explain many 
processes, especially the peculiar thickening of 
the bones sometimes observed, the atrophy of 
the fingers, etc. In many patients there may 

thus develop a very peculiar and characteristic deformity of one or both hands, of 
which the accompanying cut (Fig. 161) gives a good idea. The hand and fingers 
are thickened, and some fingers are shortened by atrophy of the phalanges. The 
most striking abnormal vaso-motor and secretory disturbances may also occur. 

In many cases the symptoms remain confined almost entirely to the upper 
extremities. They progress so slowly that many patients are able to do a certain 
amount of work for a long time ; but finally changes may also appear in the legs, 
-either simple paresis and spastic conditions or symptoms similar to those in the 
arms already described. These arise only when the process involves the gray 
matter of the lumbar cord. On the other hand, the disease may extend upward 




Fig. 161.— Syringomyelia of the cervical 
cord. Deformity of the hand, atro- 
phy of the interossei and of the adduc- 
tor pollicis. (Personal observation.) 



* The so-called Morvan's disease is nothing but syringomyelia, in which these trophic and inflam- 
matory changes are especially marked. [The large'number of cases coming under Morvan's observa- 
tion in a small district in Brittany suggest, however, that Morvan's disease may be rather an infectious 
neuritis, possibly due to leprosy, and therefore distinct from a syringomyelia with marked trophic dis- 
turbances. — TL] 



1032 



DISEASES OF THE NEBVOUS SYSTEM 



from the cervical cord, and then very characteristic bnlbar symptoms may ensue. 
The commonest bulbar disturbances are: partial loss of sensation in the region 
of the trigeminus, unilateral paralysis of the hypoglossus with unilateral atrophy 
of the tongue, paralysis of one vocal cord, unilateral paralysis of the accessory 
(weakness and atrophy of one trapezius and sterno-cleido-mastoid), paralysis of 
the soft palate, facial paralysis, abducens paralysis, etc. In many cases such bul- 
bar symptoms are much more prominent than the spinal symptoms. Abnormal- 
ities in the pupils and the fissura palpebrarum are seen in a few cases, even where 
the gliosis is limited to the cervical cord, and are to be explained by an involve- 
ment of the so-called cilio-spinal center. 

It is a remarkable fact that syringomyelia is very often associated with a more 
or less pronounced kyphoscoliosis of the spine. We are of the opinion that the 
kyphoscoliosis is not due to the syringomyelia, but that it is also an expression 
of abnormal conditions of development and growth in the vicinity of the medul- 
lary tube. 

The course of syringomyelia is very chronic, yet always unfavorable. Death 
finally ensues from some intercurrent disease, general weakness, pyelo-nephritis, 
or, as we have seen, from amyloid disease of the kidneys due to many suppurative 
processes. 

The diagnosis of typical cases of syringomyelia of the cervical cord is not dif- 
ficult if we once know the type. A careful examination of the sensibility prevents 
us from mistaking it for spinal muscular atrophy. Any combination of muscular 
atrophy in the hands with analgesia and disturbances of the temperature sense 
must awaken the suspicion of syringomyelia, as must all unusual trophic disturb- 
ances occurring in the hands, etc. If the three groups of symptoms mentioned 
above co-exist, we can be almost sure of our diagnosis. Only exceptionally can 
other processes in the cervical cord (such as compression following caries, as we 
have ourselves seen) produce a similar picture and give rise to confusion. The 
differential diagnosis between syringomyelia and leprosy may be more difficulty 
as the latter sometimes gives rise to a very similar type of disease ; but in such 
cases the special endemic conditions, the peculiar changes in the skin, , and finally 
the discovery of the specific bacillus, may enable us to make a correct decision. 

There is no special treatment for syringomyelia. The treatment must be 
symptomatic. We should remember, when there is analgesia, to warn the patient, 
of the possibility of injury. 



CHAPTEE XV 

SPIN" A BIFIDA 

(Hydrorrhachis. Myelocele. Meningocele) 

We give the name of spina bifida to a congenital fissure-formation on the pos- 
terior side of the vertebral arches, due to anomalies of development, and associ- 
ated with a hernia-like protrusion of the sac of the dura. The most frequent seat 
of the malformation is in the sacral and lumbar regions. Only rarely is the 
tumor so great as to hinder the birth of the child. Children afflicted with spina 
bifida are usually born normally, and not till afterwards do we find the tumor in 
the sacral region ; its size may be from that of a small nut to that of the fist or 
larger. The skin above the tumor is sometimes entirely normal, but in other 
cases very tense and reddened. If we have an opportunity to examine the tumor 
carefully post mortem, we usually find beneath the skin the protruded sac of the 
dura, and beneath it the arachnoid. Only rarely is the dura also fissured, so that 



SECOND AEY DEGENERATIONS IN THE SPINAL CORD 1033 

the sac is formed exclusively of the arachnoid. It is filled with a clear fluid 
which is precisely identical with the cerebro-spinal fluid. In rare cases there is 
also a dilatation of the central canal, hydromyelus ; then the substance of the 
cord is atrophied to a greater or less extent, and the central canal communicates 
directly with the cavity of the spina bifida. In other cases the condition of the 
cord is normal; sometimes its lower end is adherent to one spot of the sac. We 
must refer to the text-books of pathological anatomy in regard to the many fur- 
ther details of the anatomy and the history of development. 

In regard to the clinical symptoms of spina bifida, the condition of most chil- 
dren at first is perfectly normal, apart from the malformation. The tumor itself 
usually feels tense. If we exert pressure on it with the hand, we can often force 
part of its contents back into the vertebral canal. This causes an increase of the 
cerebral pressure, and we notice, besides the lessening of the spina bifida, a 
marked expansion of the fontanelles, and also the appearance of somnolence, 
contractions, and changes in the pulse and respiration, which demand a speedy 
interruption of this rather dangerous experiment. If such symptoms do not 
appear at all, we can conclude that the sac is completely constricted and closed. 

Only rarely, however, does the child's condition remain normal. The tumor 
usually shows a slow growth, and the results of pressure on the spinal cord 
or on the cauda equina gradually appear. Paralysis, anaesthesia, vesical dis- 
turbances, bed-sores, etc., develop, and these symptoms finally lead to death. Still 
more frequently the sac bursts, or its walls inflame, and this becomes fatal from 
the onset of a purulent meningitis. 

The prognosis of most cases of spina bifida is accordingly to be regarded as 
unfavorable, unless we succeed in curing the disease by surgical treatment. Re- 
covery has been brought about in many cases by methodical compression of the 
sac, and by puncture, with evacuation of the fluid and a subsequent injection of 
a solution of iodine to obtain an obliteration of the sac; but, on the other hand, 
the operative treatment of spina bifida is attended with many dangers, including 
liability to meningitis, so that we note frequent bad results as well as the favor- 
able ones. We can not here go into the details of the surgical methods for the 
cure of spina bifida ; they can be found in full in the text-books of surgery. 



CHAPTER XVI 
SECONDARY DEGENERATIONS IN THE SPINAL CORD 

Although the secondary degenerations in the spinal cord are chiefly interest- 
ing merely from an anatomical point of view, we must briefly describe them, 
because, in the first place, a clinical significance has been ascribed to them in cer- 
tain quarters, and also because the study of secondary degeneration has been the 
starting-point of all our present knowledge as to the systemic diseases of the 
spinal cord. 

1. Secondary Degeneration in the Spinal Cord after Cerebral Lesions. — We 
already know (compare page 834) that every lesion of the great motor ganglion- 
cells in the anterior cornua of the spinal cord, and every permanent break in con- 
duction in the motor nerves themselves, is followed by a secondary degeneration 
of the peripheral portion of the motor fibers. We assume as the reason for this, 
as we have seen, a " trophic influence " of the said ganglion-cells on the motor 
fibers arising from them, so that the latter degenerate when the conduction of 
that trophic influence is interrupted, or when the trophic ganglion-cells them- 



1034 



DISEASES OE THE NERVOUS SYSTEM 







selves are destroyed. Precisely analogous conditions exist for the first great por- 
tion of the motor conducting tract, the lateral pyramidal tract, from the cortex 
cerebri to the anterior horns of the spinal cord (vide Eig. 
137, page 986). The great ganglion-cells of the motor 
portion of the cortex cerebri also exert a trophic influence 
on the motor fibers arising from them, which extends to 
the end of these fibers — that is, up to but exclusive of 
large motor ganglion-cells of the spinal cord. This atro- 
phic influence may be understood if we regard the gan- 
glion-cell and its corresponding nerve-fiber as forming one 
complete unit and properly only a single cell, a neurone, 
and that therefore the process of the cell body (the " nerve- 
fiber ") can not possibly lead an independent existence 
when separated from the " ganglion-cell " — that is, from 
the nucleus of the cell body. If therefore there be disease 
situated in the motor portion of the cortex cerebri itself, 
or in any part of the motor tract in the brain (the motor 
fibers of the corona radiata, the internal capsule, the cms, 
or the pons), by which disease the conduction is inter- 
rupted — if there be disease there, we repeat, a secondary 
descending degeneration of the motor fibers ensues in the 
whole portion below, down to, but exclusive of, the anterior 
horns of the gray matter. The secondary descending de- 
generation of the pyramidal tract is found correspondingly 
in the crus, in the pons, and in the pyramid of the same 
side on which the focus of disease in the brain is situated. 
From this point we can trace the main part of the degen- 
eration below the decussation of the pyramids farther 
down the lateral column of the spinal cord on the opposite 
side (secondary degeneration of the lateral crossed pyram- 
idal tract) (see Fig. 162), while in many cases besides 
we find a slighter secondary degeneration in the anterior 
column of the spinal cord on the same side (secondary 
degeneration of the anterior uncrossed pyramidal tract). 
As we know from Elechsig's investigations, the relative 
amounts of the crossed lateral fibers, and the anterior 
fibers that remain uncrossed, vary in individual cases 
within certain limits. In the cases where no anterior 
pyramidal tract exists — that is, where all the motor fibers 
pass over to the lateral column of the opposite half of the 
spinal cord in the decussation of the pyramids — of course 
a descending degeneration in the anterior column is wholly 
wanting. We must add, however, that in some cases a 
small number of fibers seem to proceed uncrossed in the 
lateral column, so that accordingly we may also have a 
slight secondary descending degeneration in the lateral 
pyramidal tract of the same (affected) side (Pitres). 

2. Secondary Degeneration in the Spinal Cord in 
Transverse Affections of the Spinal Cord itself. — If a 
lesion be situated in any part of the spinal cord, by which 
more or less of its transverse section is affected, the in- 
terruption of conduction in these fibers is also followed by 
the appearance of secondary degenerations which may be 
made out both in a descending and in an ascending direc- 







Fig. 162.— Secondary de- 
scending degeneration 
of the pyramidal tracts 
in a primary lesion of 
the left half of the 
cerebrum. The lateral 
pyramidal tract of the 
right half of the cord is 
degenerated down to 
the lowest part of the 
lumbar region (1-8) ; 
the anterior pyramidal 
tract of the left half of 
the cord is degenerated 
to the beginning of the 
lumbar enlargement 
(1-6). 



SECONDARY DEGENERATIONS IN THE SPINAL CORD 1035 

tion (see Eig. 163). It is most frequently transverse myelitis, compression of the 
spinal cord, and tumors of the cord, which give rise to secondary degenerations. 
The latter, however, of course, are never due to the sort of lesion, but only to its 
seat, and to the interruption of conduction caused by it. 

The secondary descending degeneration affects the pyramidal tract in a fash- 
ion precisely analogous to that which we have also learned to recognize in sec- 
ondary degenerations after cerebral lesions; but since the primary affection 
usually affects the pyramidal tract on both sides, the descending secondary de- 
generation of course develops in both lateral pyramidal tracts, and also in the 
anterior pyramidal tracts, if they exist below the point of lesion. In general the 
area of the descending degeneration of the pyramidal tract is larger in transverse 
diseases of the spinal cord than it is in lesions of the brain. The principal reason 
of this is that lesions of the brain hardly ever destroy com- 
pletely all the motor fibers belonging to one half of the 
body. Eurthermore, in a transverse lesion of the cord 
certain other small systems of fibers of uncertain signifi- 
cance also degenerate downward: among these are a small 
zone of fibers lying internally to the lateral cerebellar tract 
and Gowers's tract (vide infra) and extending to the an- 
terior border of the cord near the anterior pyramidal tract 
(Lowenthal's " intermedian fasciculus of the ant ero -lateral 
column"), and also, very constantly, a small comma-shaped 
fasciculus in the middle of each posterior column, formed 
probably of descending collaterals of the fibers of the pos- 
terior columns (the so-called Schultze's comma, Eig. 163), 
which we can not usually trace very far downward. 

The secondary ascending degeneration, developing up- 
ward from the primary point of disease, affects several 
systems of fibers which conduct centripetally, the so-called 
columns of Goll (the internal portion of the posterior col- 
umns), and also two systems of fibers in the outer border 
of the lateral columns. The degeneration of the posterior 
columns is most extensive immediately above the point of 
interruption and gradually decreases upward (Fig. 163). 
We can readily understand this degeneration if we remem- 
ber that the fibers of the posterior columns are the ascend- 
ing fibers of the posterior roots, which have their origin in 
the cells of the spinal ganglia. Since the new fibers from 
the posterior roots which enter higher up are always ex- 
ternal to the fibers coming from the lower roots, the degen- 
eration must be limited more and more, as it ascends com- 
pletely, to the region of the columns of Goll. A secondary 
ascending degeneration in the posterior columns also fol- 
lows division of the posterior roots, and therefore, of course, injuries of the 
cauda equina. The secondary ascending degeneration in the lateral columns is 
made up of a smaller posterior and a broader anterior portion. The former is the 
lateral cerebellar tract discovered by Flechsig; its fibers arise from the cells of 
Clarke's columns in the lower dorsal cord, and therefore they must degenerate 
when separated from these cells. The fibers may be traced upward into the 
corpus restiforme, and then to the cerebellum. The bundle of fibers anterior 
to the lateral cerebellar tract, which also degenerate upward, is distinct from 
the lateral cerebellar tract in its development and its origin. It probably arises 
from cells of the posterior horns, and is called Gowers' tract or the antero-lateral 
ascending tract. Its termination and significance are still unknown. 




Fig. 163.— Secondary as- 
cending and descend- 
ing degeneration in a 
transverse affection of 
the upper dorsal re- 
gion. The columns of 
Goll and the direct 
cerebellar tracts are 
degenerated upward. 
The lateral pyramidal 
tracts are degenera- 
ted downward. 



1036 



DISEASES OF THE NERVOUS SYSTEM 



Although no clinical significance at all can be attributed to secondary as- 
cending degeneration, the theory first advanced by the French observers 
(Charcot and others) prevails almost universally, that secondary descending 
degeneration causes definite clinical symptoms. The secondary contractures 
and the increase of the tendon reflexes in the paralyzed limbs, occurring in 
hemiplegia, are especially referred to this. We shall see in a later section 
that this theory is by no means proved, and is even improbable, so that, in 
our opinion, the secondary descending degeneration also has no material clin- 
ical significance. 

3. Secondary Degeneration in the Spinal Cord after Amputations. — If we ex- 
amine the spinal cord of persons who have had an arm or a leg amputated some 
time before their death, we sometimes find that the entire corresponding half of 
the cord is smaller; but the diminution of the posterior column on that side is 
the most marked. On careful microscopic examination we can detect a slight 
but evident loss of fibers in the region of the column of Goll — that is, in the 
median portion of the posterior columns. We can also discover a slighter loss of 
fibers in the column of Goll on the other side (opposite to the amputation). We 
can not enter into a more detailed description here of this condition, which is 
of interest theoretically, but which need not be considered practically and which, 
furthermore, is in many respects not fully explained. 



CHAPTER XVII 

UNILATERAL LESION" OF THE SPINAL CORD 

(Bt'Oivn-tSequarcPs Spinal Paralysis) 

Unilateral lesion is not a definite disease of the spinal cord, but a peculiar 
group of symptoms, which occurs whenever an interruption of conduction is 
produced by any affection in one lateral half of the spinal cord. Since the symp- 
toms in these cases were first carefully studied clinically and experimentally by 
Brown- Sequard, we often call the type of disease in question " Brown-Sequard's 
paralysis." We see this paralysis in its purest form in injuries of the spinal 
cord. Almost perfectly exact sections of one lateral half of the spinal cord 
have been produced by stabs from a knife, a sword, etc. Tumors and syph- 
ilitic affections especially, and more rarely central gliosis, multiple sclerosis, 
hsematomyelia, compression of the cord in caries or cancer of the vertebras, 
etc., may also, during a certain period of their course, cause the symptoms of 
a more or less sharply defined unilateral lesion. 

The peculiar condition of the symptoms in unilateral lesion is easily explained 
by a consideration of the course of the fibers in the spinal cord. In the accom- 
panying diagram (see Fig. 164) the motor fibers from the anterior roots are 
marked v, the sensory fibers from the posterior roots, h. As is well known, the 
sensory fibers, In, pass at once into the opposite half of the spinal cord, and accord- 
ingly decussate with the corresponding sensory fibers of the other side.* The 
motor fibers, v, however, pass upward uncrossed on the side on which they enter 
the spinal cord, and mainly in the lateral column. If now, for example, there be 
situated on the right half of the spinal cord at a a lesion, e. g., a section of one 



[* More recent investigations by Mott render this theory of immediate decussation somewhat doubt- 
ful, and unilateral lesion may not always present the group of symptoms described below— K.] 



UNILATERAL LESION OF THE SPINAL CORD 



1037 



half the cord, the conduction of those motor fibers which come from the right side 
is interrupted, as well as the conduction of those sensory fibers which come from 
the left side. From this it follows that there must be motor paralysis on the same 
side of the body as the lesion in the spinal cord, and some degree of anaesthesia 
on the other side of the body. If the affection be situated in the dorsal or lumbar 
cord, the leg on the corresponding side is paralyzed, and the leg on the other side 
is anaesthetic. If the lesion be situated in the cervical cord, above the entrance of 
the nerves for the upper extremities, the arm and the leg on the side of the lesion 
are both paralyzed (spinal hemiplegia), while the arm and the leg on the other 
side are anaesthetic, but possess normal mo- 
tility; but strictly unilateral disease of the 
lowest end of the cord (the sacral cord and 
conus terminalis) may not give rise to the 
picture of a Brown-Sequard's unilateral 
lesion, because at this level no full decussa- 
tion of sensory fibers has taken place. At 
most we find a flaccid atrophic paralysis in 
one leg with a disturbance of sensation on 
the same side, and an anaesthesia of the 
scrotum, perineum, and penis on the other 
side, because the sensory fibers for this re- 
gion enter the lowest part of the cord, and 
therefore have their decussation the lowest. 

On more careful examination, further 
conditions of physiological interest appear. 
The sensibility on the side of the motor pa- 
ralysis is usually not wholly normal. In 
the first place, we sometimes find an evi- 
dent diminution of the muscular sense (the 
perception of passive movements), and in 
the second place the cutaneous sensibility 
is not always normal, but there is some- 
times a pronounced hyperesthesia for all, 
or at least for some, of the forms of irrita- 
tion. Slight pricks are very painful, and 
tickling the soles of the feet is felt with 
abnormal strength. Above the hyperaes- 
thetic territory in the skin we usually find 
a narrow anaesthetic zone (Fig. 165, b), and 
above this at times again a narrow hyper- 
£esthetic strip (see Fig. 165, c). The 
anaesthetic zone is easily explained. It corresponds precisely to the level 
of the lesion in the spinal cord — that is, to those sensory fibers coming 
from the same side, which are immediately involved as soon as they enter 
the cord; but a satisfactory explanation is entirely lacking for the appear- 
ance of the hyperaesthesia on the paralyzed side, and for the origin of the 
uppermost narrow hyperaesthetic zone. The reflexes, especially the tendon reflexes, 
are usually increased on the paralyzed side. There is often a vigorous ankle 
clonus, a symptom which must be explained by the loss of the reflex inhibitory 
influences coming from above. Definite statements are lacking as to the condition 
of the cutaneous reflexes. The cremasteric and abdominal reflexes are often 
absent on the paralyzed side, just as in cerebral hemiplegia (q. v.). In some 
cases ataxia has been observed on the side of the lesion, instead of paralysis ; this 
is apparently due to an affection of the posterior column on that side. Finally, 



/' 2 3 3 2 1 

It t f ti 




Fig. 164.— (From Erb.) Schematic representa- 
tion of the course of the main tracts in the 
cord, represented for a single pair of roots. 
v. Anterior roots, h. Posterior roots. 1. 
Paths for motor and vaso-motor conduc- 
tion. 2. Paths for muscular sense. 3. Paths 
for cutaneous sensibility on the right. 
1'. 2', 3'. The same paths' on the left. The 
arrows indicate the direction of physiologi- 
cal conduction. 



1038 



DISEASES OE THE NERVOUS SYSTEM 



we often find on the side of the lesion the signs of a vaso-motor paralysis, espe- 
cially a marked rise in the cutaneous temperature, even 2° (1° C), ov more. 

On the other side, opposite the lesion, the 
motility is normal. The disturbance of sensi- 
bility affects the sensibility to pain and tem- 
perature chiefly, while the sensibility to touch 
is usually wholly or almost wholly retained. 
The muscular sense (the perception of passive 
movements) is not affected, in contrast to the 
paralyzed side (vide supra). Above the anaes- 
thetic region we also find frequently a narrow 
hypersesthetic zone (see Eig. 165, c). The re- 
flexes are usually normal, or a little increased. 

The statements just made in regard to the 
sensory disturbances agree well with the rest 
of our knowledge as to the sensory conducting 
tracts. We know that only the posterior root- 
fibers which enter the posterior gray matter 
decussate in the cord (page 799), and that 
these fibers serve chiefly to conduct impres- 
sions of pain and temperature (compare page 
1031). The anaesthesia in unilateral lesions 
therefore affects chiefly these two qualities of 
sensibility. The muscular sensations are con- 
ducted by fibers which ascend uncrossed in the 
posterior columns. The disturbance of the 
muscular sense is therefore manifested, as has 
been said, upon the paralyzed side. There are 
apparently so many ways of conduction open 
for simple tactile sensations that these are 
only rarely much diminished. 

If other spinal symptoms (disturbances of 
micturition and defecation, neuralgic pains, 
muscular atrophy, changes in the electrical 
excitability, etc.) are associated with the 
symptom-complex just described, these symp- 
toms are dependent upon the special localiza- 
tion of the disease; for we must take special 
note that the clinical picture of a unilateral 
lesion may not be perfectly distinct, but we 
can often recognize only a few prominent 
features. 

We need add nothing as to the prognosis and treatment of unilateral lesion, 
because, of course, they are governed entirely by the form of the primary disease. 




Fig. 165. 



Schematic representation of 
the chief symptoms in unilateral le- 
sion of the left dorsal cord. (After 
Erb.) The oblique shading signifies 
motor and vaso-motor paralysis ; the 
vertical shading signifies cutaneous 
anaesthesia ; the dots signify cutane- 
ous hyperesthesia. 



PKOGEESSIVE BULBAR PARALYSIS 



1039 



IV.— THE DISEASES OF THE MEDULLA OBLONGATA 



CHAPTER I 

PROGRESSIVE BULBAR PARALYSIS 

( Glosso-labio-laryngeal Paralysis) 

Duchenne in 1860 described for the first time in complete detail the symptoms 
of a disease to which Wachsmuth subsequently gave the name of progressive bul- 
bar paralysis. Duchenne did not, however, recognize the true seat of the disease, 
and it was not until 1870 that Charcot in France, and E. Leyden in Germany, 
were enabled to confirm the suggestion of Wachsmuth that the lesion is a progres- 
sive degeneration and atrophy of the nuclei in the medulla oblongata. Since then 
our knowledge of the disease has rapidly increased, both from the clinical and the 
anatomical standpoints ; and Kussmaul and others have thoroughly investigated 
its relations to two other closely allied forms of disease — amyotrophic lateral 
sclerosis and progressive muscular atrophy. 

etiology. — We have scarcely any positive information about the cause of the 
disease. Heredity seems in general of slight importance ; but some observations 
indicate that the disease may also occur in families, so that we must probably 
assume in the last instance that the special cause of the affection is usually a 
congenital abnormality of the system of neurones which later become diseased. 
In some cases its origin is ascribed to catching cold, emotional excitement, trau- 
matic influences, or excessive bodily exertion. Perhaps it is sometimes occa- 
sioned by excessive use of the muscles to which the disease is chiefly confined, as 
in playing on wind-instruments ; but in many instances no possible external cause 
can be found. Men seem somewhat more liable to be attacked than women. The 
disease hardly ever appears until middle or old age — that is, after thirty-five. 
Only a few cases have been observed in childhood. 

Clinical History. — The symptoms are almost always very slow in their devel- 
opment. There may be mild premonitory symptoms — such as painful sensations 
in the back of the neck. Then there is a very gradual appearance of difficulty 
in articulation. Many words are pronounced indistinctly. The first trouble is 
noticed especially with letters in the utterance of which the tongue plays an es- 
sential part : E, R, L, S, G (hard), K, D, T, and 1\ T * It is easily seen that the 
derangement is not aphasic. There is no forgetting or confounding of the words 
or letters ; but the innervation of the tongue has become impaired. Long before 
the ordinary movements of this member are visibly embarrassed, the patient has 
lost the ability to make those more delicate manipulations of it which are essen- 
tial to normal speech. This disturbance of articulation is termed articulatory 
disturbance of speech (alalia or anarthria). 

By the time this has become somewhat marked, it is usually possible to detect, 
on close examination, that the tongue is beginning to atrophy. It seems flabby, 
thin, and less rounded. Here and there its surface presents furrows and depres- 
sions; and often the individual fasciculi exhibit active fibrillary contractions. 



[ * Except as otherwise specified, the letters and words used as examples here and later on are to be 
given the ordinary English pronunciation. — K.] 



1040 



DISEASES OE THE NERVOUS SYSTEM 



Just as in progressive muscular atrophy, the impairment of motion usually 
keeps equal pace * with the atrophy. The greater the atrophy, the less is the 
mobility. Einally it becomes quite impossible to project the tongue from the 
mouth or move it from side to side. The tongue lies fiat and limp on the floor of 
the mouth. Its surface is often diversified with furrows and depressions, contain- 
ing much desquamated epithelium or the like. Evidently any great impairment 
of motility in the tongue hinders not only speaking, but also chewing and swal- 
lowing. The organ can no longer bring out such portions of the food as get 
between the cheeks and the teeth, nor can it push the bolus backward within the 
grasp of the pharyngeal constrictors. 

Even before the atrophy of the tongue becomes extreme, analogous disturb- 
ances usually appear in neighboring groups of muscles. As a rule, the muscles of 
the lips are affected next after the tongue. The first thing the patient notices is 
a peculiar feeling of stiffness or tension in the lips. Movement becomes gradually 
more and more difficult ; and the patient becomes unable to pucker his lips so 
as to whistle. Speech is also noticeably interfered with, for now all those letters 
the pronunciation of which demands labial movements are very imperfectly artic- 
ulated, and at last they can not be uttered at all. These are O, A (long), P, E, B, 
M, and V ; and also the sound of double O, as in tool. It also becomes gradually 
evident that the lips atrophy. They grow thin, with sharp edges and wrinkled 
skin. Fibrillary contractions are not infrequently visible. 

This atrophy of the lips (orbicularis oris) is followed by atrophy and paresis 
of some of the other muscles of expression supplied by the lower division of the 
facial nerve. The general facial expression of a patient with bulbar paralysis 
thus comes to bear a very characteristic stamp : the mouth remains half open, and 
seems to be broadened, the corners of the mouth are drawn down, and the 
lower lip hangs down, so that the whole aspect is persistently lachrymose. Even 
in laughing, the lower half of the face relaxes comparatively little; while the 
region supplied by the upper division of the facial nerve, and the movements of 
the eyeball, remain as a rule perfectly normal. 

The third group of muscles affected are those of the pharynx and larynx. 
The soft palate becomes paretic, and produces further trouble in swallowing. 
Quite often the liquid ingesta are regurgitated through the nose. The voice 
becomes nasal. The production of many sounds, and in particular of B and P, 
is now impossible, since, in addition to the labial paresis, a portion of the essen- 
tial current of air escapes through the nostrils. This explains why the letters 
mentioned can sometimes be pronounced better if the nose be compressed. The 
paralysis of the constrictors of the pharynx impedes deglutition more and more, 
till the impairment of nutrition becomes extreme. 

The enfeebled action of the laryngeal muscles is betrayed, in the earlier 
stages of the disease, by a certain weakness and monotony in speaking. Modula- 
tions of the voice, and the production of the higher notes, as in singing, are no 
longer possible. If the innervation of the larynx becomes still more impaired, it 
becomes a very serious matter. If the arytenoid cartilages do not press together 
firmly on swallowing, the entrance to the larynx is inadequately closed, and food 
is often swallowed the wrong way. Liquid and even solid ingesta get into the 
larynx, and excite a violent cough; or, being inhaled into the air-passages, they 
cause bronchitis or lobular pneumonia. The paralysis may reach such a degree 

* At the commencement of the disease the paralysis may possibly seem greater than the atrophy, 
so far as the latter can be detected. Nor would it be impossible for a primary lesion of the nuclei of 
nerves to result in a paralysis before the secondary descending degeneration had become completely 
developed, or for the degeneration to begin in the corresponding central neurones. On the other 
hand, it must be borne in mind that numerous individual fibers in the lip or tongue might be already 
atrophied before the eye or the touch could appreciate any change in bulk. 



PEOGEESSIVE BULBAK PAEALYSIS 



1041 



that the voice is at best a hoarse whisper. With the laryngoscope we can see that 
the vocal cords are paralyzed. The inability to close the glottis tightly is ex- 
tremely unfavorable, for it renders the patient unable to cough vigorously. Mu- 
cous accumulations may therefore come to be the source of extreme dyspnoea. 

The catalogue of symptoms is not yet ended. As we have seen, the muscular 
atrophy of the tongue and lips can invariably be detected. That of the pharyn- 
geal and laryngeal muscles can not be demonstrated during life, although it is to 
be found post mortem. Inasmuch as the process is one of genuine degeneration 
with consequent atrophy, the affected fibers ought to give the reaction of degener- 
ation to electricity; but this is difficult of actual proof, just as it is in progressive 
muscular atrophy, because numerous healthy fibers lie side by side with the 
degenerated ones. Still, in an advanced case, careful examination will usually 
bring out an evident degenerative reaction here and there in the tongue and lips. 

The disturbance of reflex action is often striking. Usually the reflexes are 
greatly diminished or even absent, so that one can tickle the root of the tongue 
and the epiglottis without causing the patient to gag. In a few instances the 
facial muscles exhibit an increase of tendon reflex, as can be shown by tapping 
upon the tendons, the periosteum of the jaws, or the bridge of the nose. This 
behavior reminds one of the condition of the muscles in amyotrophic lateral 
sclerosis (q. v.). 

Exceptionally, still other muscular groups are involved. Of such disturbances, 
the most frequent is in the region supplied by the motor branch of the trigeminus, 
impairing mastication. The impairment of these muscles now combines with the 
labial and lingual atrophy to render chewing almost impossible. In very rare 
cases the ocular muscles are also involved, with resulting ptosis and strabismus. 

All the symptoms thus far enumerated are exclusively motor. Sensation is 
perfect to the end. The sensibility of the skin of the face and of the mucous 
membrane of the tongue and mouth, as well as the sense of taste, are unimpaired. 
Disturbances of sensation in the distribution of the trigeminus, and more or less 
deafness, have been reported in one or two cases ; but there is some doubt about 
the observations. It does, however, seem certain that secretory and vaso-motor 
derangements are frequent. Salivation deserves especial mention. In many 
cases of bulbar paralysis it is a constant symptom, so that the patient is obliged 
to keep a pocket-handkerchief to his mouth, to catch the fluid as it dribbles away. 
This is due, to a certain extent, to the fact that the secreted saliva can not be 
swallowed, and, as the lips do not shut tightly, it naturally escapes from the 
mouth; but volumetric examinations have rendered it pretty certain that the 
amount of saliva is abnormally large. The explanation of this has not been 
determined. Nor as yet do we know much about the vaso-motor disturbances. 
Many patients complain of a feeling of heat and " boiling " in the head. We 
may also mention in this connection that occasionally, toward the close of the 
disease, the pulse becomes very rapid (140-160). This is probably due to paralysis 
of the vagus. 

The course of the disease is invariably protracted. The order in which the 
symptoms appear is, as a rule, that in which they have just been described. The 
atrophy and paresis appear first in the tongue, then in the lips and the neighbor- 
ing muscles of the face, and lastly in the muscles of the soft palate, pharynx, and 
larynx. Still, there may be some deviation from this. Usually the progress of 
the disease is very gradual. There may be an apparent arrest of the trouble ; or 
less often there are quite sudden exacerbations. When all the different symptoms 
are well developed, the clinical picture is unusually characteristic. The peculiar 
immobility of expression; the broad, slightly gaping mouth, with the atrophied 
lips; the almost unintelligible speech, low, monotonous, and labored; and the 
inability to swallow — these often betray the disease at once. The last stage of 
66 



1042 



DISEASES OE THE NERVOUS SYSTEM 



the illness is the more distressing, in that the intelligence remains to the end 
entirely unclouded. 

The entire duration of the disease is usually several years — perhaps two to five. 
If death is not caused by some intercurrent trouble, it is brought about in one of 
three ways : either through inanition, due to the increasing difficulty of degluti- 
tion; or through pulmonary complications — namely, bronchitis, lobular pneu- 
monia, or gangrene, as a result of food passing down the trachea ; or through sud- 
den asphyxia or cardiac failure. 

Pathology. Nature of the Disease, and its Appearance as a Symptom of 
Progressive Muscular Atrophy or of Amyotrophic Lateral Sclerosis. — If we seek 
the anatomical lesion corresponding to the group of symptoms above depicted, we 
shall find, on microscopic examination of the nervous system, in all cases of this 
description, a typical disease of the medulla oblongata. The ganglionic nuclei 
and the nerves (compare the accompanying anatomical diagram, Fig. 166), corre- 
sponding to those muscles which we have found to undergo atrophy in bulbar 
paralysis, present distinct evidences of degeneration. This is most readily dem- 
onstrated in the nucleus of the hypoglossus. The ganglionic cells have some of 
them entirely disappeared, while others are greatly atrophied. The connective 
tissue is increased in amount, and the walls of the blood-vessels traversing the 
nucleus are thickened. In the earlier stages there are often many cells which 
contain granules of fat. The same changes, though perhaps less pronounced, are 




Fig. 166.— The position of the nuclei of the cranial nerves. The medulla oblongata and the pons are sup- 
posed to be transparent. The nuclei of origin (motor) are black, the terminal nuclei, (sensory) are red. 
(From Edinger.) 



exhibited by the common nucleus of the vagus and accessorius, that of the facial, 
and sometimes also that of the glosso-pharyngeal nerve. The other nuclei are 
perfectly normal. We never find a diffuse " inflammation," but in every case a 
primary degeneration of the nuclei, which spreads no farther. 

Starting from these nuclei, the degeneration and atrophy may be seen to 
extend into the nerve-fibers which issue from them. The roots of the hypo- 
glossus, vagus, accessory, and facial nerves can often be seen by the naked eye to 
be diminished in size and of a gray color. The microscope always shows a partial 
atrophy of their fibers. Einally, there is a corresponding atrophy of muscles of 
the tongue, lips, and other parts. We need not enter into detail, for the histo- 
logical conditions are precisely those seen in the muscles of the trunk and ex- 
tremities in the spinal form of progressive muscular atrophy. 

Thus we find progressive bulbar paralysis perfectly analogous with progressive 
muscular atrophy. The motor nuclei in the medulla oblongata are the motor and 



PEOGEESSIVE BULBAE PAEALYSIS 



1043 



trophic centers of the bulbar nerves and of the muscles which these nerves supply. 
The relation is precisely the same as exists between the anterior cornua of the 
spinal cord on the one hand, and the spinal nerves and the muscles which they 
innervate on the other. In both diseases there is a degenerative atrophy of the 
individual neuro-muscular elements, the so-called neurones (consisting of nerve- 
cells and peripheral nerve-fibers), and their corresponding muscular fibers. In 
both diseases the atrophy and the functional disability of the muscles keep pace 
with each other, and in both the affection is limited strictly to the motor tract, 
sensibility suffering no impairment whatever. Certain questions about bulbar 
paralysis are as unsettled as similar ones about progressive muscular atrophy. 
It is uncertain whether the primary degenerative process is limited to the bulbar 
nuclei, and the degeneration of the nerves and muscles is to be regarded as sec- 
ondary; or whether the entire motor apparatus, from the ganglionic cell to the 
muscular fiber, is simultaneously attacked ; or, finally, whether the atrophy begins 
in the muscle and involves the corresponding nerve-fiber and nerve-cell only in 
its further progress. We think it improbable that these points will be cleared 
up very speedily. Their solution would seem to be only of theoretical interest. 

We certainly must recognize, however, the essential identity of progressive 
bulbar paralysis and progressive muscular atrophy. The resemblance becomes 
even more striking if we consider that very frequently both diseases are present 
simultaneously. Often, after a case of progressive muscular atrophy has lasted 
for some time, the symptoms of bulbar paralysis also appear. On the other 
hand, an illness may begin with bulbar symptoms, and later on be complicated by 
atrophy of the muscles of the extremities — almost always seen first in the arms. 
If cases of this sort come to autopsy, we find a combination of the anatomical 
lesions of both diseases; in addition to the degeneration of the nuclei in the 
medulla oblongata, there is marked atrophy of the ganglionic cells in correspond- 
ing places in the anterior gray cornua of the spinal cord. 

Progressive bulbar paralysis has as close a relation to amyotrophic lateral scle- 
rosis (vide page 986) as to progressive spinal muscular atrophy. Amyotrophic 
lateral sclerosis is at first situated, as a rule, only in the portions of the motor 
conducting system, including the pyramidal tracts, which supply the extremities ; 
but finally there is very often an involvement of the motor bulbar nuclei — that is, 
bulbar paralysis sets in. It seems justifiable, therefore, to say that these three 
diseases — progressive bulbar paralysis, progressive spinal muscular atrophy, and 
amyotrophic lateral sclerosis — differing as they do in the localization of their 
lesions, are yet closely allied. They are to be regarded as manifestations of one 
morbid process which is probably essentially the same in its pathology and seti- 
ology. We do not know the special cause of this process of degeneration. In 
many cases, although perhaps not in all, we must finally assume a congenital 
weakness of the affected nerve territory. Such a defective nerve territory suc- 
cumbs prematurely to the injurious influences which either are associated with 
the normal functions themselves or act upon them from without in some other 
fashion. At any rate, there is always a primary chronic degeneration of portions 
of the main motor conducting tract, in one or another area and varying extent. If 
we accustom ourselves to regard these three groups of symptoms as really identi- 
cal, we shall be less puzzled by the slight variations which different cases may 
present than if we attempt to differentiate the disorders too nicely on account of 
unessential variations. 

Diagnosis. — The diagnosis of a typical case of progressive bulbar paralysis has 
no difficulties, if we only hold firmly to the definition of the disease and its symp- 
toms as above depicted. Upon careful examination of the other muscles, and con- 
sideration of the course of the disease as a whole, we shall be able in each case to 
determine whether the bulbar trouble is the sole disease, or merely a part of a 



1044 



DISEASES OE THE NERVOUS SYSTEM 



more extended degeneration of the motor tract. If there are no symptoms but 
those referable to the medulla oblongata, we must bear in mind that the phe- 
nomena of genuine progressive bulbar paralysis may be closely simulated by other 
bulbar diseases. The acute troubles, such as thrombosis or haemorrhage, although 
they produce similar symptoms, can easily be differentiated by the manner of 
their appearance, contrasting with the invariably slow development of genuine 
bulbar paralysis. It is, however, much more difficult to eliminate gradually form- 
ing tumors situated in the medulla oblongata or its vicinity. Here prolonged 
observation is frequently needed, until finally such phenomena appear as are for- 
eign to typical bulbar paralysis. Such symptoms are disturbances of sensation 
and invasion of the upper division of the facial, the nerves of special sense, and 
the ocular muscles. The same is true of that rare trouble, diffuse sclerosis of the 
medulla oblongata. 

It should also be mentioned that bilateral cerebral trouble may occasion so 
complete a paralysis of the tongue and lips, according to Lepine and others, as to 
simulate bulbar paralysis. Such cases have been termed " glosso-labio-pharyngeal 
paralysis of cerebral origin," or pseudo-bulbar paralysis. Indeed, in rare in- 
stances, a similar group of symptoms seems to be referable to unilateral cerebral 
disturbances. This is explained by assuming that the muscles involved upon both 
sides receive at least a portion of their motor nervous fibers from the same hemi- 
sphere. And yet in most of these cases of pseudo-bulbar paralysis the exclusion 
of the genuine disease is possible, because certain variations from the typical 
course of the disease are pronounced enough to set us right. Thus there is an 
apoplectic onset or repeated apoplectiform attacks. The paralysis is not perfectly 
symmetrical. There is also paralysis of the extremities on one or both sides. The 
lips and tongue react normally to electricity without much atrophy, or there are 
marked signs of mental weakness. In most cases there is an extensive arterio- 
sclerosis at the bottom of the whole morbid process, for the sclerosis of the cere- 
bral arteries often leads to multiple foci of softening or to multiple haemorrhages. 

Prognosis and Treatment. — Despite the unfavorable prognosis of progressive 
bulbar paralysis, we must at least try to check the progress of the disease. Elec- 
tricity may perhaps be regarded as the most promising means to employ. To in- 
fluence the seat of the trouble, galvanization is chiefly used. The poles are applied 
to the two mastoid processes, every day if possible, for two or three minutes, and 
the current is repeatedly reversed. We may also galvanize the sympathetic 
nerve and the affected muscles of the lips and tongue. Upon the muscles the 
faradic current may also be tried. When deglutition begins to be impaired, it is 
an excellent thing to excite the action of swallowing, by galvanism. For this the 
anode is placed upon the nape of the neck, and the cathode upon one side of the 
larynx. At every cathodic closure (KaS), or every time that the cathode is 
passed across the side of the larynx, there is a reflex act of deglutition. The cur- 
rent should be of medium strength. 

It may be well to prescribe further a resort to treatment by baths, or the 
" cold-water cure " may be cautiously tried, but we should not expect either of 
these procedures to have any special influence on the disease. The same internal 
remedies are recommended as in the chronic diseases of the cord, especially argen- 
tic nitrate, ergotine, and potassic iodide. For salivation, atropine may prove 
beneficial, in pills of tfo of a grain (gramme 0.0005), three or four to be taken 
daily. 

The way of giving nourishment is important if deglutition is impaired. We 
should try carefully to avoid having the food go down the wrong way, lest pul- 
monary complications ensue. It is therefore wise not to defer the use of the stom- 
ach-tube too long, through which we may introduce milk, eggs, wine, and the 
various infant foods. 



BAKER FORMS OF CHROXIC BULBAR BARALYSIS 1045 

In the distressing close of the disease, narcotics must be exhibited to lessen 
the patient's suffering, at least as far as we can. 



CHARTER II 

THE RARER FORMS OE CHRONIC BULBAR PARALYSIS, PROGRESSIVE 
OPHTHALMOPLEGIA AND ASTHENIC BULBAR PARALYSIS 

1. Brogressive Ophthalmoplegia 

As we have seen, the form of chronic bulbar paralysis described in the pre- 
vious chapter as " typical,'' is practically limited in its effects to the distribution 
of the hypoglossus, the labial division of the facial, and the pharyngeal muscles. 
Bossibly the reason it extends no farther is merely that death is so speedy. But 
there are a few rare cases where the chronic degenerative process comes to in- 
volve other motor nuclei, together with the corresponding nerve-fibers and muscles. 
Of course the clinical phenomena of these cases vary from the ordinary; and yet 
there is no real reason to distinguish them from common bulbar paralysis, par- 
ticularly as all sorts of transitional forms are to be observed. Thus, we have our- 
selves noticed that there is sometimes a symmetrical and slowly progressive 
paresis of the upper division of the facial, and in particular of that portion which 
supplies the cheek, complicating the glosso-pharyngeal paralysis. In other cases 
we have seen the degeneration attack from the start the entire distribution of 
the facial, gradually producing a complete " diplegia facialis^ Sometimes, also, 
the ordinary symptoms of bulbar paralysis are accompanied by disturbances in 
the area of distribution of the ocular nerves, probably the result of degeneration 
of the corresponding nerve-nuclei (see Fig. 166, page 1042). 

What seems very remarkable is that the process may be confined entirely to 
the ocular muscles. A. von Graefe named this condition progressive ophthalmo- 
plegia. Another name is " anterior bulbar paralysis." In this form a bilateral 
paralysis of all the external ocular muscles progresses with extreme slowness and 
is perfectly symmetrical. The movements of the eye are therefore impaired in all 
directions. Diplopia is never present. The pupil reacts to light, and almost 
always the power of accommodation is preserved. Finally both eyeballs become 
absolutely motionless, and there is a well-marked though incomplete ptosis. There 
is, beyond a doubt, a progressive degeneration of the nuclei and fibers of the cor- 
responding nerves — that is, the abducens and motor oculi; but with these the 
process may stop, spreading no farther. We have ourselves lately met with a 
patient who presented total bilateral ophthalmoplegia, in whom the condition had 
existed without the slightest change for fifteen years. Besides the oculo-motor 
paralysis the muscles of the face (Fig. 167) and even those of the body are some- 
times involved. On the other hand, in a few cases the process seems to be lim- 
ited to only a part of the oculo-motor nerves (as the abducens). 

The diagnosis of genuine progressive ophthalmoplegia is usually easy, if we 
hold strictly to the definition of the disease as a degeneration of the motor nuclei 
and nerves exclusively (that is, completely analogous to progressive spinal mus- 
cular atrophy and bulbar paralysis). We shall thus avoid confusing it with those 
cases in which progressive ophthalmoplegia occurs as one symptom of a compli- 
cated morbid process of quite a different sort. Thus we must bear in mind par- 
ticularly that tabes and general paralysis may lead to complete ophthalmoplegia. 
To these cases may be added those that follow syphilitic infection. Multiple 



1046 



DISEASES OE THE KEEVOTJS SYSTEM! 



sclerosis may also lead to almost complete ophthalmoplegia ; and, finally, the 
same symptom- complex has been observed as a post-diphtheritic nervous disease. 

The progressive ophthalmoplegias which develop after birth are also to be 
distinguished from the congenital defects in the movements of the eyes. Com- 




Fig. 167.— Progressive ophthalmoplegia. Paralysis of both eyeballs kwith bilateral ptosis. Weakness of 
both facial nerves. (Erlangen Medical Clinique.) 



plete external ophthalmoplegia (that is, paralysis of all the external ocular mus- 
cles) has been repeatedly observed as a congenital condition, and also congenital 
bilateral abducens paralysis, congenital ptosis, etc. Autopsies of such cases are 
still lacking. There are probably defective conditions of the corresponding nerve- 
nuclei, and perhaps of the nerves or muscles also. 

2. Asthenic Bulbar Paralysis. Pseudo-paralytic Myasthenia 

TVe will speak at this point of a very remarkable and peculiar type of disease, 
the milder forms of which were first described by Erb, and the severe and fatal 
forms by Oppenheim. The symptoms of the affection consist of ptosis, paresis of 
the facial muscles, and disturbances of mastication, swallowing, and talking. On 



RARER POR^IS OF CHRONIC BULBAR PARALYSIS 1047 



more careful observation it is seen that these symptoms are only in part uniform 
and persistent, but that they are due chiefly to an extremely rapid fatigue and 
exhaustion of the affected muscles (Goldflam). Such a patient can, for instance, 
utter a few sentences quite plainly, but, if he continues to talk, his speech grows 
more indistinct and inarticulate, and finally it becomes an incomprehensible 
lalling. The same thing is seen in chewing and swallowing: the first mouthfuls 
are chewed and swallowed in quite the normal fashion, but in a few minutes it 
becomes wholly impossible to take any more food. Besides these " bulbar " symp- 
toms, which at first are the most striking, we also see very similar symptoms in 
the muscles of the extremities ; usually the same rapid fatigue progressing to the 
most complete failure of their function. One of our patients, if she had pre- 
viously rested, could go up a flight of stairs very well, but on the second attempt 
she had to take hold of the banisters, and the third or fourth attempt failed com- 
pletely on account of the complete muscular weakness that ensued. 

As Jolly has found, we can detect this same abnormal fatigue by continued 
faradic stimulation of the muscles. 

This clinical condition permits us to draw the conclusion that there is no 
permanent and complete atrophy or degeneration of the mctor apparatus as a 
basis for the clinical symptoms ; and, in fact, in those cases in which death finally 
ensued (in one or two years) from choking, insufficiency of respiration, etc., the 
autopsies have thus far been wholly negative (hence the term " bulbar paralysis 
without anatomical lesion "). This is also the reason why in this affection de- 
cided improvement or even complete recovery may occur after the disease has 
continued for several months, if the functional impairment of the affected nerve 
territory again disappears. In order to express this distinction between the 
bulbar paralyses due to coarse anatomical changes and the merely functional 
disease now in question, we have proposed for the latter the name of " asthenic 
hulbar paralysis" We must, however, note that the disease is not limited exclu- 
sively to the territory of the bulbar nerves, although the bulbar disturbances are 
usually most prominent in the clinical picture. On the other hand, there are 
apparently some cases where the abnormal fatigue and the consequent symptoms 
occur only in the extremities, without any implication of the bulbar muscles. 
Por this condition the name proposed by Jolly, "pseudo-paralytic myasthenia," 1 
is more suitable. 

Prom what has been said above, the prognosis is to be regarded as not abso- 
lutely unfavorable, but recurrences are to be dreaded even when recovery has 
apparently set in. The treatment is first of all to provide the greatest physical rest 
and care for the patient. If it is difficult to take food, nourishment must be given 
cautiously by the oesophageal tube. AVe may try mild massage and galvaniza- 
tion of the muscles, and central galvanization of the spinal cord and medulla 
oblongata. Internally we have given strychnine, arsenic, and phosphorus, without 
any perceptible benefit. On the hypothesis that the trouble was perhaps de- 
pendent upon some chemical-toxic influence, the cautious use of sweating has 
also been recommended. 

[Family Periodic Paralysis. — Goldflam has described a peculiar affection, 
first carefully studied by Westphal, which merits brief mention. It consists of 
recurring attacks of paralysis, most marked in the legs, associated with loss of 
reflex and electrical excitability, without mental or sensory symptoms and with 
intervals of perfect health. Thirty-five out of fifty-three cases occurred in three 
families, but the families showed no special signs of nervous degeneracy. The 
attacks are apt to begin at puberty, and they are also apt to come on during sleep 
after some unusual muscular exertion. The frequency of the attacks varies 
greatly, from one or two in a lifetime to several times a week. The average dura- 
tion of the individual attack is from ten to forty-eight hours. The attacks begin 



1048 



DISEASES OE THE NERVOUS SYSTEM! 



somewhat gradually, -usually in the legs, and they may increase to complete paraly- 
sis of all the muscles of the limbs, body, and neck. The cranial nerves are rarely 
involved. The deep reflexes are abolished, and the plantar reflex is often absent. 
There is a quantitative diminution of electrical reactions, sometimes amounting 
to complete abolition, but there is no reaction of degeneration. The mechanical 
irritability of muscles and nerves is also lost. In two cases the heart became 
enlarged during the attack. The sphincters are not affected. The pathology is- 
wholly unknown. Golchiam believes that the trouble is in some way connected 
with the muscular dystrophies. The prognosis is good so far as life is concerned, 
but the attacks usually recur through life. Treatment is unavailing. — K.] 



CHAPTER III 
ACUTE AND APOPLECTIFORM BULBAR PARALYSIS 

1. H-EMORRHAGE INTO THE MEDULLA OBLONGATA AND THE PONS 

Hemorrhage into the medulla oblongata and the pons is much more frequent 
than into the spinal cord, but it is much rarer than cerebral haemorrhage. As to 
its production, the same views are held as will be considered in detail under cere- 
bral haemorrhage, in the next section. In the first place, there is probably always 
some disease of the blood-vessels — that is, atheroma or miliary aneurism — and 
then some factor productive of increased arterial tension. There may be cardiac- 
hypertrophy, nephritis, excessive bodily exertion, or alcoholism. Xow and then 
injuries of the occiput are followed by an effusion into the medulla. It is not rare 
to have secondary and usually small ecchymoses in acute inflammation of the 
spinal cord (vide infra), and in purulent meningitis, or in connection with new 
growths which are richly vascular. 

The anatomical conditions produced by bulbar haemorrhage are so completely 
analogous with those of cerebral haemorrhage that the reader may safely be 
referred to the succeeding section about these also. The size of the lesion varies 
greatly. Bleeding extensive enough to affect the greater part of a transverse sec- 
tion is more frequent in the pons than in the medulla oblongata. If the blood 
is poured out close under the floor of the fourth ventricle, as has been repeatedly 
observed, it may break into the ventricle. If death be not speedy, the blood is 
mostly absorbed, and in its place develops either an " apoplectic scar " or an apo- 
plectic cyst. 

There may be slight prodromata, but the real symptoms of bulbar haemorrhage 
are very sudden. There is almost always a pronounced apoplectic seizure. The 
patient has a shock, falls down, and becomes dizzy or even unconscious. In other 
cases there may be headache, vomiting-, tinnitus aurium, and clonic spasms, or 
even a typical epileptiform attack. 

In most cases death is speedy, if not immediate. This is probably due in every 
instance to grave lesions of the respiratory and circulatory centers, rendering 
continued existence impossible. Sometimes the initial symptoms abate, where- 
upon the local results of the lesion become appreciable. 

The first characteristic feature of bulbar paralyses now manifests itself, that 
disturbances are particularly great in the distribution of the bulbar nerves, 
while in cerebral apoplexy they never appear in the same way. Another point 
is, that these paralytic symptoms are combined with paralysis of the extremities 
in a peculiar way, as a result of the anatomical relations. Eor the same reason, 



ACUTE AND APOPLECTIFORM BULBAR PARALYSIS 10I£ 



the order of the paralysis in the extremities may also be peculiar. Of the bulbar 
paralyses we may mention more or less complete paralysis of the tongue, and a 
consequent difficulty in articulation (anarthria) ; frequent inability to swallow; 
and paralysis in the distribution of the accessorius, facial, and trigeminus. If 
there is a lesion of the pyramidal tracts in the pons or medulla, we have paralysis 
of the extremities in addition to the specific bulbar symptoms. If the hemor- 
rhage be extensive, all four extremities may be more or less completely paralyzed ; 
but in most instances the paralysis is unilateral. In the larger number of haemor- 
rhages into the pons there is crossed paralysis. The paralysis of the extremi- 
ties is upon one side, and that of the facial is on the other side. This is a great 
aid to diagnosis. It is easy to see how this happens if we bear in mind that 
the cerebral fibers of the facial cross at a point certainly much higher than the 
decussation of the pyramids, in which latter place the motor fibers of the ex- 
tremities cross. 2s~ow a haemorrhage may be situated in one side of the pons, 
above the decussation of the pyramids but below that of the facial. This would 
occasion (vide Fig. 168, y) a paralysis of the facial on 
the same side with the lesion, and of the extremities upon 
the opposite side; but if the lesion be higher, above the 
place where the facial crosses over, all the paralytic symp- 
toms would be on the opposite side of the body (vide 
Fig. 168, x). 

In other, rarer instances we observe similar combina- 
tions; only some other bulbar nerve replaces the facial, 
such as the hypoglossus or abducens. In a few cases the 
lesion is at the very decussation of the pyramids. This 
is extremely rare in haemorrhage, though somewhat more 
frequent in troubles of a different nature. The result 
may be that the motor fibers for one extremity are cut off 
before they cross, and those of the other extremity after 
they have crossed. Thus is produced the rare phenome- 
non of a crossed hemiplegia — i. e., paralysis of the arm 
on one side and of the leg on the other. 

Disturbances of sensation in the skin of the paralyzed 
extremities sometimes result from trouble in the pons, 
but they are very seldom extreme, and they can not be 
made available for making out the exact locality of the 
haemorrhage, since the course of the sensory fibers through 
the upper extremity of the spinal cord is still almost un- 
known. The anaesthesia sometimes observed in the distribution of the trigeminus 
is of more value, as this may be due to a lesion of the nucleus or root of the- 
nerve. 

There are other symptoms, which are indeed rare, but which bear an impor- 
tant relation to certain nervous centers of the medulla. Thus, there may be 
| marked respiratory disturbance; the pulse may become rapid or irregular; there 
may be vaso-motor derangement, as shown by a rise of the cutaneous temperature 
and by a subjective sensation of warmth; and occasionally there are temporary" 
albuminuria and glycosuria. The temperature of the body is generally normal at 
first, or nearly so; but in case of a fatal termination it often rises greatly, even 
to 107.5° (42° C.) or higher. 

As to the prognosis of bulbar haemorrhage, speedy death has been repeatedly 
observed, as we have said. If the immediate effects be successfully withstood, the 
prospect becomes more favorable. The effusion is gradually absorbed, the symp- 
toms of compression abate, and there is a steady progress toward comparatively 
good or even perfect health. More often, however, some of the paralytic symp- 



L R 




Fig. 168.— Diagram of focal 
diseases in the pons. 
L. Left. B. Right. P. 
Pons. Mo. Medulla ob- 
longata. DP. Decussa- 
tion of the pyramids. 
E. Fibers to * the ex- 
tremities. F. Facial 
fibers, x. Lesion in the- 
upper half of the pons. 
y. Lesion in the lower- 
half of the pons. 



1050 



DISEASES OF THE NEKVOUS SYSTEM 



toms remain stationary, either in the distribution of the bulbar nerves (the 
lingual or pharyngeal), or in the extremities, as shown by persistent hemiplegia. 
If this latter be the case, the subsequent contractures and other symptoms are the 
same as in ordinary cerebral hemiplegia. 

The diagnosis of bulbar haemorrhage is based upon the apoplectic onset, and 
upon the presence of specific bulbar symptoms, such as disturbance of speech and 
of deglutition, and, most characteristic of all, if it occur, a crossed hemiplegia. 
The differential diagnosis between embolism and haemorrhage can hardly ever be 
made with certainty (vide infra). 

The treatment, not only of the seizure but of the persistent paralysis, should 
conform to the principles which will hereafter be set forth in describing the 
treatment of cerebral haemorrhage. If the bulbar nerves present obstinate symp- 
toms, we must employ the same means as in chronic bulbar paralysis, the most 
effective being electricity. 

2. Embolism and Thrombosis of the Basilar Artery 

The medulla and pons receive their blood chiefly from branches of the anterior 
spinal, vertebral, and basilar arteries. These branches penetrate the anterior 
median fissure and then proceed to the nerve-nuclei. A far smaller portion of 
the circulation flows through the " arteries of the roots." These are minute off- 
shoots of the lateral branches of the basilar and vertebral arteries, which enter 
the cord at the roots of the nerves and penetrate to the corresponding nuclei. 
According to Duret, the nuclei of the hypoglossal and accessory nerves are sup- 
plied from the anterior spinal and vertebral arteries ; those of the vagus, glosso- 
pharyngeal, and auditory nerves by branches of the upper end of the vertebral 
arteries; and the nuclei of the facial, trigeminus, and the three nerves to the 
ocular muscles by branches of the basilar. There may be individual exceptions to 
these rules. Occlusion by embolism or thrombosis of the arteries just named 
must occasion a secondary softening in corresponding portions of the medulla, 
and it is, therefore, a not very infrequent cause of apoplectic, or at least very 
rapidly developing, bulbar paralysis. 

The causes of thrombosis or embolism in the arteries just mentioned are the 
same as we shall consider minutely when treating of cerebral softening. Emboli 
are most frequent in cardiac disease. They occur only in the vertebral arteries, 
oftenest in the left one, and are never primary in the basilar artery; but an 
embolus may be enlarged by thrombosis after lodging in one of the vertebral arter- 
ies, and then block up the basilar. Thrombosis is of more frequent occurrence, 
and results from chronic changes in the arteries, mainly atheroma or syphilitic 
endarteritis. The latter disease, one favorite locality for which is the basilar 
artery, is the commonest cause of acute softening of the pons. 

The anatomical condition is likewise similar to that in cerebral softening 
(q. v.). In the region which is deprived of arterial blood by the occlusion of the 
affluent vessel, the acute anaemia entails necrosis and disintegration of tissue. A 
spot of " softening " results, made up mainly of vestiges of nervous tissue and 
numerous cells filled with granules of fat. 

When the basilar artery is blocked up, the symptoms appear very suddenly. 
There is either an apoplectic seizure, or at least a very rapid development of pa- 
ralysis (occupying only a few days). The symptoms of the first onset are, in all 
essential points, those of bulbar or even of cerebral apoplexy. Although there is 
usually no marked loss of consciousness in apoplectic bulbar paralysis, yet no 
great diagnostic significance can be assigned to its absence. The sudden obstruc- 
tion of the basilar artery produces such a disturbance of the circulation even in 
anterior portions of the brain as may suspend consciousness. In some few in- 
stances this circulatory derangement may even give rise to choked disk, as seen 



ACUTE AND APOPLECTIFORM BULBAR PARALYSIS 1051 



by the ophthalmoscope. Often there are noticeable respiratory and cardiac symp- 
toms, such as Cheyne-Stokes respiration, and rapid pulse. 

If death be not immediate, and we are therefore enabled to make out the symp- 
toms due to the local disturbance, we usually observe the same phenomena as have 
just been described under bulbar haemorrhage. There is sometimes paralysis of 
all the extremities, but usually there is trouble only upon one side. Then we 
have the characteristic crossed hemiplegia. The facial nerve or the nerves of the 
ocular muscles may be paralyzed. It has repeatedly happened that the paralysis 
seemed at first much greater upon one side, but after a few days changed over to 
the opposite one. This must be due to changes in the circulation ; the thrombus 
grows larger, or a collateral circulation is developed. The specific bulbar symp- 
toms are the familiar ones of all bulbar derangements — namely, lingual paralysis 
with resulting difficulty in articulation, pharyngeal paralysis, and rarely deafness, 
as a result of lesion of the acoustic center. Of course, the severity and extent 
of all these symptoms must vary according to the location and size of the spot of 
softening. 

The prognosis of cases of this sort is almost always unfavorable. Death 
results in a few days at latest. It is often ushered in by a high temperature. 
Exceptionally, there is a transition into a chronic form. 

We need say nothing about treatment, except that the same remedies are 
employed as in other acute bulbar diseases. 

3. Acute Inflammatory Bulbar Paralysis 

(Acute Bulbar Myelitis. Multiple Bulbar Neuritis) 

" Acute bulbar paralysis," in the stricter sense of the term, means a form of 
disease where marked symptoms of bulbar derangement appear acutely — that is, 
within a few days or weeks. The anatomical lesion is probably an acute inflam- 
mation of the medulla oblongata. It is a rare disorder, and its aetiology is doubt- 
ful. There are usually mild prodromata : vertigo, headache, and, in one case of 
our own, painful sensations in the back of the neck. Evident bulbar symptoms 
very quickly follow. Usually the first of these is dysphagia. !Not only is deglu- 
tition impaired, but the paresis of the soft palate and of the laryngeal muscles 
allows liquids to enter the nostrils or the larynx. The tongue also becomes grad- 
ually paralyzed, speech becomes indistinct, and, if the soft palate be involved, 
nasal. 

Sometimes the extremities also become paretic, as a result of the extension of 
the disease to the region of the pyramids ; but in many instances the extremities 
remain unaffected to the end. Paralyses of the facial nerve and of the ocular 
muscles are somewhat more frequent. The temperature is sometimes a little ele- 
vated (100°-102°, 38°-39° C), but not always. The pulse is almost invariably 
rapid ; in our patient it was 148. 

The prognosis is apparently always bad. Often death takes place in four to 
eight days, or it may be not till the end of two or three weeks. It is invariably 
preceded by all the tokens of paralysis of respiration. In our case there was well- 
marked paralysis of the diaphragm at the end. 

As yet, few autopsies have been reported. Generally the medulla presents no 
macroscopic changes. Exceptionally, it can be seen to be softened and mottled 
with minute haemorrhages. The microscope detects abundant evidence of inflam- 
mation : granule-cells, infiltration with nuclei around the blood-vessels, thicken- 
ing of the walls of some of the blood-vessels, small extravasations, swollen axis- 
cylinders, etc. It should also be borne in mind that precisely similar clinical 
phenomena seem often to be referable to peripheral changes, such as multiple 
neuritis affecting the bulbar nerves. 

The treatment of acute bulbar paralysis is, of course, almost hopeless. In 



1052 



DISEASES OF THE KEKVOUS SYSTEM 



early stages we should apply counter-irritation to the nape of the neck; and we 
might prescribe mercurial inunction. It might be well to employ the con- 
stant current, applied at the back of the neck, and also in such a manner as to 
excite the movements of deglutition. We found injections of strychnine useless. 
Toward the end, narcotics are indispensable. 



CHAPTEK IV 
COMPRESSION OF THE MEDULLA 

Acute compression and other injuries of the medulla are due most frequently 
to fracture or dislocation of the atlas and axis. As is well known, dislocation of 
the axis, or backward dislocation of the atlas, usually causes instant death. 

Gradual compression is seen in chronic disease of the bones around the me- 
dulla, in caries and tumors of the occiput and of the first two vertebrae. Enchon- 
droma of the base of the skull; new growths of the sphenoid, at its junction 
with the occipital ; tumors of the dura ; and sometimes even tumors of the cere- 
bellum — may all excite by their pressure the gravest bulbar symptoms. We 
should also mention aneurism of the vertebral artery at its upper end, and of the 
basilar, as capable of doing similar harm. In all these cases the main cause of 
disturbance is undoubtedly the mechanical pressure, either directly destroying 
the nervous tracts or interrupting the transmission of nervous influences; but 
the circumstances may be further complicated by haemorrhages, and sometimes 
perhaps by inflammation of the medulla itself. 

The clinical phenomena of gradual bulbar compression resemble those of spinal 
compression, in that they usually begin with symptoms of irritation in the distri- 
bution of those nerves the roots of which are first affected. There are neuralgia 
of the trigeminus, twitching of the facial muscles, tinnitus aurium, etc. If the 
compression becomes greater, there are more serious bulbar symptoms : disturb- 
ances of speech and deglutition, paralysis of the tongue, soft palate, face, and 
very likely motor (paretic or ataxic) and sensory symptoms in the extremities. 
Usually we also see general cerebral symptoms, such as vertigo, headache, vomit- 
ing, and sometimes epileptiform convulsions. 

We can not, of course, draw up a definite and rigid list of symptoms, since 
both the individual symptoms and the general course of the disease exhibit great 
variations according to the way in which the compression is brouglit about. The 
diagnosis can be made in those cases only where some serological factor such as 
trauma or caries of the vertebras is known to exist. Aneurism of the vertebral 
artery is said by Moser sometimes to give rise to a loud systolic murmur heard 
between the mastoid process and the spine. In all other cases we can seldom do 
more than surmise the truth. Slow compression is distinguished from genuine 
progressive bulbar paralysis chiefly by the course it pursues — that is, there are 
initial symptoms of irritation — by the greater complexity of the clinical phenom- 
ena, such as sensory lesions and hemiplegia, and sometimes by the asymmetry of 
certain symptoms. If the anterior part of the medulla is compressed in the region 
of the pyramids, there may for a time be no bulbar symptoms, but merely motor 
symptoms in the extremities. These are chiefly paretic or spastic. 

The prognosis is almost always bad, as can be inferred from the nature of the- 
causative disease. Death is brought on either by inhalation-pneumonia, or by 
paralysis of respiration. Treatment must be purely symptomatic, and should fol- 
low the same rules as in progressive bulbar paralysis. 



HEMATOMA OF THE DURA MATEE 1053 



V.— THE DISEASES OF THE BRAIN 



SECTION I 

Diseases of the Cerebral Meninges 
CHAPTEE I 

HEMATOMA OF THE DURA MATER 

{Internal Hannorrnagic Pachymeningitis) 

iEtiology and Pathology. — Hematoma of the dura mater is the name given 
to effusions of blood found on the inner surface of the dura mater. These effu- 
sions are of considerable area, but of moderate thickness, and are usually encap- 
sulated. There has been much discussion as to their mode of origin, and views 
still differ. One is that the haemorrhage is the primary lesion, and that the 
connective-tissue membranes are developed only by the organization of the clot. 
This conception was originally the prevailing one, but was opposed by Virchow, 
who was led by the results of his own investigations to maintain that the haemor- 
rhage was always secondary. The primary process he believed to be a peculiar 
sort of inflammation — " hemorrhagic pachymeningitis." This gave rise to a new 
growth of richly vascular connective tissue, into which the haemorrhage took 
place. Of late, however, the tendency is again to regard the haemorrhage as the 
initial change, at least in certain cases, and to refer it to an affection of the walls 
of the blood-vessels which diminishes their power of resistance. 

The mildest forms of internal pachymeningitis present a delicate membrane 
upon the inner surface of the dura mater, quite easily separable, of a reddish 
color, and dotted with numerous red and brownish spots. These spots are due to 
minute haemorrhages and collections of haematoidine. The membrane itself is a 
delicate interstitial tissue, traversed by numerous wide capillaries. 

In more advanced cases the thickening is much greater. There are usually 
several layers, the newest and most superficial being nearest the brain. The old- 
est, which is in apposition with the dura mater, is composed of connective tissue 
that has already become rather firm and fibrous. It is evident from this lamellar 
structure that the whole process goes on by fits and starts. The clinical course of 
the disease will be seen from what follows to agree well with such a view. The 
effusions are sometimes very extensive, even larger than a hen's egg, and exercise 
no slight pressure upon the underlying cerebral parenchyma. The haemorrhage 
always takes place inside the mass, or between its layers. The effusion may, how- 
ever, break through the innermost layer, so that the blood flows into the arach- 
noideal spaces ; this is known as " intermeningeal apoplexy." 

The favorite location of the haematoma is the parietal region. It is some- 
times found at the base of the brain, in the posterior or middle fossa. Occasion- 
ally the haematoma is bilateral. 

Haemorrhagic pachymeningitis is not a rare disease. It is sometimes found to 
exist in a moderate degree in chronic cardiac, renal, or pulmonary cases, which 
come to autopsy. Usually there have been no special symptoms, the lesion being 
discovered incidentally. It has been found in like manner in connection with 



1054 



DISEASES OE THE NERVOUS SYSTEM 



a great many acute infectious diseases, such as typhoid fever and small-pox. It is 
a more important and more frequent complication in other chronic cerebral dis- 
eases, in particular such as induce marked atrophy of the brain as a whole. It is 
especially common in general paralysis of the insane and in other forms of de- 
mentia. In the apparently primary hemorrhagic pachymeningitis chronic alco- 
holism is the commonest and most important causal factor. In hard drinkers it is 
not very unusual for the haematoma to be so extensive, if it occurs at all, as to 
cause grave cerebral derangement. Very likely changes in the vascular walls, 
such as atheroma and fatty degeneration, contribute an important part to the re- 
sult in such patients. Injury is a second important cause. We have seen a case 
of haematoma of the dura with a fatal termination in a patient who some months 
before had received very severe blows on the head in a fight. Haematoma may also 
occur in all diseases where there is a general hsemorrhagic diathesis. Thus it is 
seen in pernicious anaemia, leukaemia, and scurvy. Here certainly the haemor- 
rhage is the primary event. 

As might be inferred from the etiological factors enumerated, the disease is 
found chiefly in advanced life, and much oftener in men than in women. 

Symptoms. — Not infrequently a haematoma of the dura is found post mortem, 
which had during life been entirely unsuspected. Either the haemorrhage was 
not extensive enough to cause any symptoms, or the brain exercised that remark- 
able tolerance which it sometimes shows even when there are wide-reaching 
lesions ; or such symptoms as may have existed escaped particular notice, in the 
severity of the more general symptoms (of typhoid fever or some similar disease). 
But in other cases hemorrhagic pachymeningitis excites grave symptoms, al- 
though they are seldom so characteristic as to reveal the diagnosis ; for individual 
cases vary greatly, according to the size of the haemorrhages, their location, and 
the frequency of their recurrence. 

Almost always the beginning of the disease is rather sudden. It may even be 
like an apoplectic seizure. The symptoms are referable partly to the general 
effect of the haemorrhage upon the brain, and partly to the exact locality of the 
haemorrhage. The more general symptoms comprise headache, impairment of 
intelligence (that is, stupor or even complete coma), slow or irregular pulse, vom- 
iting, and contracted pupils — all being symptoms of cerebral compression. Now 
and then we even find choked disk. Other phenomena are added to the above 
when the haematoma occupies its usual position, upon one side and in the neigh- 
borhood of the motor cortical region, or central convolutions. The hemiplegic 
symptoms are not infrequent, such as hemiparesis, and, from the irritation which 
the effusion produces in the motor centers, twitchings and convulsions in one half 
of the body. Sometimes these symptoms are limited to a single extremity or to 
the distribution of the facial nerve. Aphasia has been repeatedly observed when 
the haemorrhage was near the island of Reil. If the effusion increases, the motor 
disturbance becomes correspondingly aggravated, and it may become bilateral. 
Sensation is usually little impaired. 

The further course of the disease varies greatly in different cases. In the 
worst cases there is speedy death, usually ushered in by deep coma. In others, the 
first symptoms are followed by improvement, although mild indications of cere- 
bral pressure persist, such as headache or vertigo, or else local symptoms, such as 
hemiparesis. It is possible for the effused blood to be absorbed, and complete re- 
covery to ensue; but usually new haemorrhages and corresponding symptoms 
arise. It is precisely this appearance of the symptoms in separate attacks, this 
frequent recurrence of severe cerebral disturbances, that is characteristic of haem- 
atoma of the dura mater. As already intimated, the way in which the anatomical 
lesions develop explains this perfectly. Thus the disease may drag on for months 
and years, sometimes improving and sometimes getting worse again. Then some 



PURULENT MENINGITIS 



1055 



attack at last proves fatal. Arrest and actual improvement are still possible even 
in the later stages, although, often the features of the case have meanwhile under- 
gone essential alteration because of the progress of some causative disease. In 
general, the clinical phenomena of hematoma of the dura are often complicated 
and obscured by the co-existence of the primary disease. 

The diagnosis is therefore difficult. The main points may be recapitulated as 
follows : First, the existence of etiological factors, such as alcoholism, previous 
injury, or chronic cerebral disease; second, the sudden onset, and also the abrupt 
appearance of further symptoms, the alternation of rapid aggravation and im- 
provement ; and third, the existence of symptoms which experience has taught us 
to refer mainly to the cortex of the brain, namely, unilateral convulsions, mono- 
plegic paresis and contractures, and contracted pupils. Nevertheless, frequent 
errors in diagnosis can not be avoided. 

Treatment. — The possibility of therapeutic interference being successful is 
very small. In apoplectic shocks, ice to the head is useful ; and if the patient be 
robust, it may also be advisable to use local depletion, by leeches on the temples or 
behind the eaTs. It is also customary to prescribe some such drug as senna or 
calomel for " intestinal depletion." 

If the first onset is successfully withstood, the main points in the further 
treatment are general hygienic and dietetic directions, so as to guard as far as 
possible against fresh hemorrhages. Alcohol and excessive bodily or mental 
exertion should be forbidden. Of course, paralysis or other persistent disturb- 
ances may call for special attention. 



CHAPTEE II 

PURULENT MENINGITIS 

{Purulent Cerebral Leptomeningitis. Meningitis of the Convexity') 

Etiology. — Purulent inflammation of the dura mater has no clinical impor- 
tance, for it is very rare, and occurs only as the result of the extension of disease 
from neighboring parts. We shall accordingly consider below purulent inflam- 
mation of the pia mater only. One important variety of this disease has already 
been discussed (see page 111 et seq.) as one of the infectious diseases, under the 
name of epidemic cerebro-spinal meningitis. There we saw also that the occa- 
sional sporadic cases of primary or " idiopathic " meningitis are probably identi- 
cal serologically with those of epidemic meningitis. In all other instances, puru- 
lent meningitis is a secondary disease — that is, the specific pus coccus (usually 
the streptococcus pyogenes), which excites the purulent inflammation, originates 
in some other organ primarily, and affects the meninges only secondarily. We 
should, therefore, seek most carefully in every case of purulent meningitis, at 
the bedside and more particularly at the autopsy, to discover the way by which 
the pathogenic virus reached the meninges. We have no right to say that the 
case is one of primary meningitis, strictly so called, until we have made a most 
careful examination with a negative result. From a clinical standpoint, it is true 
that many cases of secondary meningitis do seem as if they were primary, be- 
cause not infrequently the real primary disease excites insignificant symptoms, 
or perhaps no symptoms at all. 

Secondary purulent meningitis is due most frequently to disease of the cranial 
bones, and in particular to disease of the petrous portion of the temporal bone, 
with the auditory apparatus therein contained. If we consider the anatomical 



1056 



DISEASES OE THE NERVOUS SYSTEM 



Telations of the middle and internal parts of the ear, we can easily understand 
why inflammation in them is not infrequently followed by meningitis. Usually 
it is a caries of the petrous portion of the temporal bone, itself due to an otitis 
media, which leads to an irruption into the cranial cavity. This is especially apt 
to take place through the thin vault of the tympanic cavity. It may also extend 
from the mastoid cells, or by direct propagation along the sheaths of the acoustic 
or facial nerves, or along the vessels which lie in the petroso-squamous suture. 
The dura is first attacked, and then the pia. In many instances, the neighboring 
venous sinuses (transverse, cavernous, and superior petrosal) transmit the in- 
flammation, being first attacked by a suppurative thrombo-phlebitis. Again, ex- 
ceptionally, a purulent inflammation in the upper part of the nasal cavity or in 
the orbital cavity (panophthalmitis) may lead to meningitis. 

Another and frequent source of meningitis is found in the various in- 
juries of the cranium. In the great majority of these cases there is an open 
wound, admitting infectious agents which are suspended in the air. The suppura- 
tion often commences in the spongy texture of the diploe, thence extending to the 
dura and pia, either directly or by way of a purulent thrombosis of some sinus 
into which the veins of the diploe enter. It was, indeed, often affirmed in the 
past that we could have a traumatic purulent meningitis without any open 
wound ; but this is not easily explained, according to our present views as to the 
origin of purulent inflammations. There are probably in every case small wounds 
•of the skin, which are perhaps overlooked. The statements are also to be rejected 
that the heat of the sun's rays, striking upon an uncovered head, may excite 
purulent meningitis. In most cases of fatal sunstroke we find marked hyperaemia 
of the meninges, but no inflammation. 

Meningitis may have an intra-cranial origin; it is sometimes the sequel of 
-cerebral abscess. ~No matter what starts the abscess, if it extends to the surface 
of the brain, it causes a more or less extensive purulent meningitis at that point. 
An abscess may burst into one of the lateral ventricles, and the infection be car- 
Tied from that point to the pia at the base of the brain. 

All the cases thus far contemplated allow of the explanation that the inflam- 
mation reaches the meninges by direct extension; but there is another group of 
<cases where the agent that infects the pia mater originates at some distant part of 
the body, and is probably conveyed by the blood or lymph currents. These cases 
are often termed metastatic meningitis. 

Of this sort is the secondary meningitis seen in connection with genuine lobar 
pneumonia, a combination already discussed (see page 215). The meningitis is 
also sometimes a complication of empyema, rarely of pyaemia and septicaemia, or 
ulcerative endocarditis, and very rarely of typhoid fever and the acute exanthe- 
mata (small-pox, scarlet fever), and of acute articular rheumatism. In each case 
we must, of course, determine whether the meningitis may not have a connecting 
link between itself and the primary disease, such as otitis in scarlatina, or sec- 
ondary empyema in typhoid fever. 

Pathology . — For the pathological anatomy of purulent meningitis, we may 
refer mainly to the statements made on page 112, under epidemic meningitis, for 
the lesions are similar. The only way to determine whether a meningitis is sec- 
ondary or primary is by finding or failing to find disease in neighboring or remote 
parts, for example, pneumonia. The seat of the meningitis will vary according 
to that of the primary inflammation, if there be any. If the meningitis is due to 
caries of the petrous bone or to an injury of the skull, the purulent exudation is 
usually most abundant in the immediate neighborhood of the primary lesion, 
between the pia and arachnoid. Thence it gradually extends along the surface of 
the brain, sometimes chiefly on the convexity and sometimes at the base. But in 
general it may be said that both the secondary and the metastatic varieties of 



PURULENT MENINGITIS 



1057 



meningitis as a rule affect the convexity, although this is by no means invariably 
the case. This rule explains why these cases are sometimes termed meningitis of 
the convexity, in contrast to tubercular meningitis, which latter, as we shall find, 
has a preference for the base of the brain, and hence is called basilar menin- 
gitis. The spinal pia mater is sometimes simultaneously attacked, but not so 
constantly as in primary, or epidemic meningitis. The brain is almost always 
involved — the inflammation extends along the vessels which dip from the pia 
mater into the cerebral parenchyma. It is not a rare thing to find minute ab- 
scesses or ecchymoses in the interior of the brain. The whole parenchyma is usu- 
ally moist, ©edematous, and of a doughy consistency. The meningeal exudation 
exerts upon the brain a pressure which gives rise to important symptoms ; by it 
the superficial cerebral convolutions are often considerably flattened. The lateral 
ventricles almost always contain more or less sero-pus. 

Clinical History. — So varied are the primary diseases which may entail a men- 
ingitis, that it is hardly possible to make a sketch of the disease which would suit 
all cases. If the meningitis comes on during the course of pyaemia, pneumonia, 
or some other severe illness, its proper symptoms are often inextricably confused 
with those of the primary trouble; and when the skull or the brain has been 
mechanically injured, it is very hard to determine whether a meningitis has been 
excited, because the trauma may of itself produce such serious effects. The fol- 
lowing description, therefore, applies chiefly to cases of apparently primary men- 
ingitis, or to cases where the meningitis, although secondary, is well marked. 

The beginning in such cases may be sudden, or it may be somewhat insidious. 
Sometimes the grave symptoms appear almost at once, accompanied by a chill and 
high fever. Sometimes there are for a time indefinite and more or less ambigu- 
ous prodromata, but almost always it is the headache which first attracts atten- 
tion. This grows worse with more or less rapidity, and almost always becomes 
very violent. Exceptionally it may be insignificant. Not infrequently it varies 
considerably, being much worse at some hours or on some days than on others. 
The location of the pain is sometimes frontal, sometimes occipital, and sometimes 
over the whole head. Next in prominence to the headache, particularly in the 
later stages of the disease, is the mental disturbance. The patient complains of 
vertigo, becomes dull and stupid, or begins to wander. The delirium may be ex- 
tremely violent, but usually there is depression rather than exaltation, and the 
stupor merges into coma. That the headache still continues may be inferred from 
the frequent raising of the hand to the head and the grimace of pain whenever 
the head is moved, until finally the coma becomes so profound that even these 
reflex actions cease. 

Usually these general cerebral symptoms are attended by others referable to 
the particular locality affected. The neck is rigid. This is most marked when 
the posterior fossa and the medulla are affected. Then there are all sorts of 
paralytic or irritative symptoms in the distribution of the cranial nerves, mainly 
due to lesions of the nerves where they emerge from the base of the brain; there 
is derangement of the oculo-motor nerves, as shown by paralysis or nystagmus ; the 
pupils are unequal, or are contracted or dilated, and do not react to light; there 
is paresis of the facial, or trismus, or grinding of the teeth. All these symptoms 
may be equally pronounced in other forms of meningitis. Sometimes we can 
detect optic neuritis with the ophthalmoscope. Other symptoms are due to cere- 
oral disturbance, often apparently located chiefly in the cortex. Thus there may 
he twitchings of individual muscles, or even genuine convulsions in one or 
more limbs, or paralysis of one extremity or of half the body. Sometimes the 
autopsy explains these phenomena, but often we fail to find any marked ana- 
tomical lesion to correspond to them, and are obliged to ascribe them to circu- 
latory or functional derangement. 
67 



1058 



DISEASES OE THE NERVOUS SYSTEM 



Of the remaining symptoms, the fever is most important. Almost always the 
temperature is decidedly elevated, not infrequently reaching 104° or 105° (40°- 
40.5° C). The fever is, however, very irregular. There may be repeated chills 
with great elevations of temperature. The pulse is generally rapid, and often 
somewhat irregular. Exceptionally it is less frequent than normal, because of 
cerebral compression. Vomiting is not a rare symptom, particularly at first. 
There is almost invariably constipation, and the abdomen is often tense and con- 
cave. The urine is scanty, and often contains a trace of albumen. Secondary 
diseases are sometimes found post mortem, such as lobular pneumonia, due to 
inhalation of food during the comatose state. 

The entire course of the disease occupies only a few days in very acute cases, 
and scarcely ever exceeds a week or ten days. The termination is almost sure- 
to be fatal. In the few cases of recovery which have been reported the diagnosis 
is doubtful. In most instances deep coma precedes death, though sometimes it is- 
ushered in by convulsions. There is often a great rise of temperature (107.5°, 
42° C, or higher) before the close of life. 

Diagnosis. — The diagnosis of purulent meningitis is sometimes pretty evi- 
dent ; but it may be very obscure, so that we can not always avoid confounding it 
with other severe acute diseases, such as typhoid fever, pyaemia, and general- 
tuberculosis. In general the most characteristic symptoms of any variety of men- 
ingitis are intense headache, rapid onset of grave cerebral disturbances, delirium 
and insensibility, stiffness of the neck, and disturbances in the distribution of 
the cranial nerves (especially impaired motion of the eyeball and optic neuritis). 
These last, although often slight, are generally present; and in connection with 
these separate symptoms we must also always consider the whole course of the 
disease and any aetiological factors which may exist. Typhoid fever is excluded 
by its usually slower onset, the greater delay in the appearance of grave cerebral 
symptoms, the rose-spots, the greater size of the spleen, the characteristic stools, 
and the peculiar fever-curve. It may also be of importance in diagnosis that in 
typhoid fever there is usually no leucocytosis of the blood, since in purulent 
meningitis the number of leucocytes in the blood is increased. Severe septic 
and pyaemic diseases, including ulcerative endocarditis, likewise excite cerebral 
disturbances which might be misleading, but these diseases are to be recognized 
by their aetiology (external wounds, abortion, etc.), cutaneous ecchymoses, septic 
retinitis, swelling of the joints, and repeated rigors. Uraemia may also simulate 
meningitis. Sometimes the character of the urine, and the predominance of con- 
vulsions, will set us right, but not always. We may state in conclusion that every 
one who sees many cases must (like ourselves) repeatedly have met with 
patients presenting the symptoms of a severe and acute cerebral affection appar- 
ently primary, without demonstrable cause, and seeming to justify a diagnosis 
of meningitis, but yet yielding post mortem no signs of disease beyond "hyper- 
emia," " oedematous swelling," and similar changes of only secondary importance.. 
We are as yet wholly unable to explain such cases. 

Granting that meningitis exists, what variety is present? The aetiology is a 
great help in answering this question. We should endeavor to learn whether 
there has been traumatism or some old ear trouble. It is well to employ the aural 
speculum. We can not say that a patient has epidemic meningitis unless several 
cases occur simultaneously, although herpes is very characteristic, as it appears 
only exceptionally in other varieties. [Lumbar puncture may sometimes be of 
assistance in the diagnosis. — K.] Usually tubercular meningitis also can be 
diagnosticated only by means of the aetiology. Its symptoms, of course, are in 
almost all particulars identical with those of purulent meningitis. Sometimes,, 
however, tubercles can be detected in the choroid by means of the ophthalmoscope^ 
Eor further particulars see the next chapter. 



TUBEECULAE MENINGITIS 



1059 



Prognosis. — The prognosis of purulent meningitis is almost invariably wholly 
unfavorable, as follows from what has been said above. In the reported cases 
of recovery from meningitis the diagnosis must be determined with the greatest 
caution, but it is not impossible that sporadic cases of epidemic diplococcus men- 
ingitis may terminate favorably. We may also state that sometimes in severe 
infectious diseases " meningitic " symptoms may appear which lead us to fear 
the worst, but which finally disappear. In acute purulent inflammation of the 
middle ear, especially in the young, meningitic symptoms (headache, stupor) 
sometimes set in, which also seem threatening, but which disappear. It is, of 
course, usually impossible to determine positively the anatomical processes in 
such cases. 

Treatment. — The treatment of the different forms of meningitis varies but 
little. Locally, the favorite remedies are ice applied to the head, which should 
be shaved if practicable, and local depletion by means of leeches behind the ears 
or on the temples. Many physicians recommend cutting off the hair and rubbing 
in antimonial ointment, or applying ethereal tincture of iodine. We have never 
tried this. Cool baths with douching can not be employed unless the patient can 
be moved without too much pain. For violent pain or great restlessness we must 
use narcotics. The best is morphine subcutaneously. We can not hope for much 
benefit from other internal remedies, such as iodide of potassium or calomel. 

Prophylaxis demands, above all, prompt recourse to the otologist for aural 
trouble of any kind, and strictly antiseptic treatment of all injuries of the skull. 
Even in cases of meningitis that have already begun, surgical interference 
(trephining the mastoid, etc.) may perhaps often check the advance of the inflam- 
mation and lead to recovery. 



CHAPTEE III 

TUBERCULAR MENINGITIS 

{Basilar Meningitis) 

iEtiology. — Tuberculosis of the leptomeninges is always a secondary affec- 
tion — a sequel to previously existing tubercular disease of some other organ. 
Why the pia mater should be so often singled out for secondary infection with 
the tubercular virus, or what path that virus traverses to reach the pia, 
we can hardly say. We can merely state what the other tubercular diseases 
are, which, as experience shows, entail tubercular meningitis most frequently. 
These primary affections may be of themselves productive of grave clinical 
phenomena, the meningitis merely adding to the complexity of the pic- 
ture. Again, the primary trouble may not have betrayed itself at all, or its 
symptoms may have been long ago arrested, so that the meningitis seems to be 
a primary disease. In some cases even the most careful examination will fail to 
detect the origin of the trouble. 

Tubercular meningitis is oftenest a sequel to pulmonary tuberculosis. It may 
appear as a terminal complication in cases of advanced phthisis, or it may come 
on while the signs of pulmonary disease are as yet very slight. ISText in order as a 
causative affection comes tubercular pleurisy. This origin is not infrequent. As 
we have already seen, most cases of apparently primary pleurisy are due to tuber- 
cle. This statement is supported by the fact that it is not very exceptional for the 
symptoms of tubercular meningitis to supeiwene suddenly upon what had seemed 
to be genuine convalescence from pleurisy. In children, and sometimes in adults, 
the virus may be carried to the meninges from cheesy, tubercular, bronchial or 



1060 



DISEASES OE THE NEKVOUS SYSTEM 



mesenteric glands, or from tubercular or " fungous " disease of the bones or 
joints. Another danger to adults is tubercular disease of the genito-urinary 
apparatus. It should also be noticed that a single large tubercle in the brain may 
lead to miliary tuberculosis of the meninges. In short, we see that it is not 
impossible for any tubercular infiltration, wherever situated, to communicate 
infection either to the meninges alone (in some remarkable way), or simul- 
taneously to them and many other organs. In this latter case, where in all proba- 
bility the blood carries the virus through the system, the meningitis is merely 
a part of a general miliary tuberculosis (see page 261), while in the former case 
the reason why the meninges are exclusively or primarily affected depends upon 
the special form of the infection; but we are almost wholly ignorant of the way 
by which the tubercle bacilli reach the meninges. We are ourselves disposed to 
suspect that, in many cases at least, the infectious material first enters the 
arachnoid sac of the spinal cord through the lymph sheaths of the nerves (e. g., 
the intercostal nerves), and thence extends upward to the base of the brain. 

We sometimes hear the attack ascribed to such causes as over-exertion, mental 
excitement, traumatism, etc.; but we need hardly say that these can not be 
properly regarded as serological factors, and that usually they are merely coin- 
cidences. Age, however, does have an influence; children are much oftener at- 
tacked than adults, although the latter also are liable to the disease. 

Pathology. — As in tuberculosis of serous membranes, so in tuberculosis of the 
pia, there are two effects of infection to be distinguished from each other: (1) 
the development of the specific new growth — that is, of miliary tubercles; and (2) 
the inflammation. The relative degree of these two varies. Sometimes the 
tubercles are very abundant and the inflammatory exudation comparatively 
scanty; and in other cases the inflammation is considerable, although relatively 
few tubercles are discoverable. The tubercles are usually found in greatest 
number along the course of the larger blood-vessels, and therefore chiefly in the 
furrows and clefts of the surface of the ^rain, in the fissure of Sylvius, at the 
chiasma, the pons, the medulla, and the cerebellum. And, in general, the base of 
the brain is usually more affected than the convexity — hence, as we have said, the 
name of " basilar meningitis." There are, however, exceptions to this rule. We 
very often find that the region supplied by one or more arteries suffers above 
other parts; this must be due to the manner of infection. The inflammatory 
lesions consist of hyperemia, usually well marked, and a sero-gelatinous exuda- 
tion of variable amount. That this exudation is partly cellular can always be 
proved by the microscope, and often even macroscopically from the great cloudi- 
ness of the pia ; but still we seldom find enough to justify us in calling the pro- 
cess one of genuine purulent inflammation. Small haemorrhages into the pia are 
quite often found. The brain itself is usually flattened from the pressure of the 
meningeal exudation. Often the inflammation involves the brain-subst°nce 
itself, as shown microscopically by tubercles, inflammatory changes, and capillary 
haemorrhages. The ventricles usually, although not invariably, contain a hydro- 
cephalic effusion. This led earlier observers to term the disease " acute hydro- 
cephalus." The effusion is serous, but generally turbid from cellular constituents, 
and not infrequently tinged with blood. The choroid plexus is engorged, and it 
may present tubercles. The spinal cord, in the majority of cases, shares in the 
tubercular disease. Here, too, we find inflammation of the pia and miliary 
tubercles. 

Clinical History. — Tubercular meningitis almost always begins with a pro- 
dromal stage, which is often brief, but which may last one or two weeks, or even 
longer. The patient may be apparently well (vide supra) until this comes on, or 
he may have already shown signs of some other tubercular affection. He now 
feels somewhat ill at any rate, and begins to complain of headache, worse at some 



TUBERCULAR MENINGITIS 



1061 



times than at others. There is anorexia and very often constipation. Another 
frequent prodrome is an attack of vomiting, which may or may not recur. Sleep 
is disturbed, either by the headache or by a certain general restlessness. We have 
occasionally met with cases where the illness began with pronounced mental dis- 
turbance. The patient became irrational and said and did queer things, and then 
a few days later there appeared distinctive meningeal symptoms. In two pa- 
tients, who were hard drinkers, the disease began just like delirium tremens. 

After an initial period of variable duration, the general health becomes more 
and more impaired. The headache increases. The patient takes to his bed, begins 
to be delirious, and soon presents well-marked symptoms of grave brain trouble. 
Intelligence becomes more and more impaired. The patient is sleepy, and he can 
be roused imperfectly by the voice, if at all. At the same time he is usually quite 
restless at first, grasping at invisible objects in the air, picking the bed-clothes, 
and continually moving his legs. The delirium may be low or noisy; the patient 
may keep up a constant singing, screaming, or whistling. The persistence of 
the headache even in this stage is shown by the facial contortions and complaints 
of the sufferer, whenever there is a temporary approach to consciousness. There 
is also, as a rule, decided tenderness in the nape of the neck on pressure, fre- 
quently accompanied by great stiffness of the neck. Sometimes there is stiffness 
of the entire spinal column, and pain in the same. This is certainly due to the 
coincident spinal meningitis. 

Another group of symptoms in the distribution of the cranial nerves are iden- 
tical with those seen in other forms of meningitis. Ptosis is not infrequent, 
on one or both sides, due to paresis of the motor oculi. There is strabismus, 
either internal or external. Symptoms of irritation of the nerves governing the 
movements of the eye are very frequent, especially in the early stages of the dis- 
ease. Thus we see slow involuntary lateral movements of the eyeballs, and some- 
times nystagmus. The pupils are often unequal; they may be enlarged or con- 
tracted, and often they undergo marked and repeated variations in size. The re- 
action of the pupils to light is usually sluggish, and it may be absent. With the 
ophthalmoscope we find not infrequently neuritis, or choked disk. In some in- 
stances, but not in all, we find also tubercles in the choroid, which, of course, 
greatly assists diagnosis. Sometimes there is occasional twitching in the distribu- 
tion of the facial nerve, or a slight tonic contraction, or again paresis on one side. 
The natural explanation of all these phenomena is that the nerve-trunks are inter- 
fered with at the base of the brain, either by the pressure of the exudation or 
by participation in the inflammatory process, or by the minute hemorrhages 
which sometimes take place into the sheath of the nerves. 

Disturbances in the extremities may be caused by various lesions. Motor 
symptoms of irritation are apparently referable for the most part to changes in 
the cortex of the brain. We see occasional twitching of larger or smaller groups 
of muscles, or rarely convulsions. These latter may be unilateral, or limited 
to a single extremity. Sometimes there is well-marked paresis of one half the 
body or paralysis of one limb, or there may be aphasia, although it is only in a 
part of the cases that we find post mortem any lesion which explains these symp- 
toms. In most cases, however, there is a particularly large collection of tubercles 
in certain places upon the cortex cerebri, occasioning a local compression or an 
inflammatory oedema, which in its turn excites the phenomena mentioned. Some- 
times the brain-substance itself is found in a state of red softening underneath 
these spots. Another not very rare symptom is a peculiar stiffness of the limbs, 
due either to direct irritation or to reflex action. The reflexes in the lower ex- 
tremities are generally exaggerated at first, but later on become diminished, and 
finally abolished. The reflexes upon one side may be more vigorous than upon the 
other. As to sensation, it is hard to reach definite conclusions, because of the 



1062 



DISEASES OF THE NERVOUS SYSTEM 



patient's stupor. Sometimes there is well-marked cutaneous hyperesthesia, prob- 
ably referable to an implication of the spinal cord in the process. 

The behavior of the pulse and temperature is interesting. The temperature 
is usually elevated, but often only to a slight extent — that is, varying between 
100.5° and 102° (38° and 39° C). Often the temperature falls quite low, only to 
rise again, the alternations being at irregular intervals. Exceptionally the tem- 
perature may remain high (104° F., 40° C.) most of the time. Toward the end 
there is usually a decided change in temperature, either upward or downward. 
In many instances there is a very low temperature before death; in two cases we 
have seen a temperature of 87.8° (31° C). Or the temperature may rise to 106° 
(41° C.) or higher just before death. The pulse is often abnormally slow in the 
early stages of the disease, even numbering only 40 to 50 beats per minute. This 
is referable without doubt to the increased intra-cranial pressure. Later on the 
pulse becomes small and rapid. The transition may be very sudden. The vagus 
is at first irritated, and then paralyzed. The pulse is often irregular. 

Respiration is generally moderately accelerated. If the breathing is very 
deep and rapid, we should always think of simultaneous miliary tuberculosis of 
the lungs. Toward the close of the disease the respiration often assumes the 
Cheyne- Stokes type : there is a long pause, followed by very superficial and gentle 
respiration, which gradually grows deeper and deeper, then diminishes again, 
and is succeeded by another complete pause. This symptom is always most omi- 
nous, for it indicates that the excitability of the respiratory center is already 
greatly impaired. 

Symptoms referable to still other organs are few. Vomiting is rare in the 
later stages of the disease. The abdomen often presents a " boat-shaped " concav- 
ity, as the result of tonic muscular contraction, and is hard and tense. There is 
almost always constipation. The spleen may be somewhat enlarged. The urine 
sometimes contains a trace of albumen. On account of the drowsiness, it is usu- 
ally voided in the bed or retained in the bladder. Almost invariably there is rapid 
marasmus. 

The entire duration of tubercular meningitis varies somewhat, chiefly because 
of the varied length of the first stage. When the disease is once fully developed, 
the illness seldom lasts more than three to ten days longer. Frequently the 
illness is divided into three stages : 1. The stage of cerebral irritation, with head- 
ache, stiff neck, vomiting, and delirium; 2. The stage of cerebral compression, 
due chiefly to the hydrocephalus, and causing drowsiness, slowness of the pulse, 
paralysis of the oculo-motor nerves, hemiplegia, etc. ; and 3. The paralytic stage, 
presenting deep coma, relaxation of the previously contracted muscles, accelerated 
pulse, and marked variations of temperature. Such a division is too diagram- 
matic to correspond accurately to the real phenomena, but it will, nevertheless, 
often aid us in getting a general idea of the course of the disease. 

The termination of tubercular meningitis seems to be inevitably fatal. 
Sooner or later the patient loses consciousness completely, his pulse grows very 
small and rapid, his respirations irregular and intermittent (Cheyne-Stokes), his 
temperature, as we have said, either rises high or falls far below normal, and, 
finally, death is ushered in by a paralysis of all the vital functions. A few 
physicians have reported cases of recovery ; but was the diagnosis correct ? While 
we would by no means absolutely deny that recovery from tubercular meningitis 
might occur, it would certainly be very difficult to prove, in any particular in- 
stance, that such a thing had happened. 

Tubercular Meningitis in Children. — The disease is so prone to attack chil- 
dren that it seems desirable to subjoin a few remarks about the peculiarities of 
the affection as observed in them. 

Often the little patient is pale and weakly, with tubercular antecedents; but 



TUBERCULAR MENINGITIS 



1063 



sometimes apparently healthy and vigorous children are attacked. Tubercular 
meningitis may be the sequel of measles, whooping-cough, or some other disease, 
which has occasioned the development of the tubercular process. Usually the 
severer symptoms are preceded by a rather long prodromal stage (a week or ten 
days), which often does not forebode the severity of the disease that is begin- 
ning. The child looks pale, has a poor appetite, grows thin, is restless in his sleep, 
is out of humor and cries during the day, is often tired and sleepy, does not play 
naturally, the tongue is coated and the bowels constipated. The second stage is 
generally ushered in by headache and vomiting. The headache is not very often 
violent; but children complain with remarkable frequency of pain in the abdo- 
men and chest. The cause of this symptom is unknown. The pulse is almost 
invariably slow, often somewhat irregular and whirring (that is, as if it trembled 
beneath the finger), and it frequently undergoes surprisingly rapid changes in 
rate — for example, varying twenty or more beats inside of a few hours. Very 
early the child becomes dull and drowsy. Frequently it emits a peculiar deep 
sigh, or that sudden loud scream or " cephalic cry " which physicians long ago 
learned to recognize and fear. The symptoms referable to the cranial nerves and 
the nervous disturbances in the limbs are similar to those seen in adults. Strabis- 
mus is almost constant. Very often there are trismus, and a distinctly audible 
grinding of the teeth, most distressing to the by-standers. Trousseau laid weight 
upon the appearance of red spots (taches cerebrates) upon the skin after it has 
"been mechanically irritated; but these have no diagnostic value. They are due 
to increased reflex action, and are seen in all sorts of acute diseases. The fever 
is irregular throughout and generally, as in adults, not very high, 100° to 102° 
(38°-39° C). Respiration is usually rapid, and often is irregular. 

The change from bad to worse is almost always announced by a rapid increase 
in the pulse-rate, to 160 or 200. The child becomes completely comatose. Very 
often there are repeated epileptiform convulsions, either universal or affecting 
single extremities. Death is usually preceded by a decided rise in temperature. 

Diagnosis. — When the symptoms are pronounced, the diagnosis of meningitis 
is easy, and we have merely to determine just what variety is before us. That 
the disease is due to tuberculosis is never to be ascertained by means of the 
meningeal symptoms themselves, but is rendered possible only by the aatiology, 
if that be discoverable. Here, as in all tubercular diseases, we have chiefly to re- 
gard (1) heredity and (2) the evidence of previous or existing tubercular affec- 
tions in other parts of the body. Under this second head are to be considered 
scrofula, diseases of the bones and joints, pulmonary tuberculosis, pleurisy, and 
tuberculosis of the genitals or of the choroid. If our search be unsuccessful, we 
may sometimes get a hint of the truth from the general appearance of the pa- 
tient : for example, he may be pale, or narrow-chested. And, again, the absence 
of trauma, aural disease, or epidemic meningitis will make tuberculosis more 
probable. 

In its early stages, or when it varies from the usual course, tubercular menin- 
gitis may be very difficult to diagnosticate. This is particularly true when the 
patient is a child. The early malaise and vomiting are treated as " ordinary 
gastric catarrh " until the grave cerebral symptoms disclose the mistake in diag- 
nosis. In such cases we should be careful not to disregard the initial slowness 
and irregularity of the pulse. This alone should make our prognosis guarded. 
The fever may be prominent at the commencement, and tempt us to call the case 
one of incipient typhoid fever; and, indeed, the correct diagnosis is often impos- 
sible until the disease develops further. In regard to this, see the preceding- 
chapter on purulent meningitis, where the exclusion of severe septic diseases and 
of uraemia is also considered. 

Before the autopsy we must remain in great uncertainty as to the number 



1064 



DISEASES OE THE NERVOUS SYSTEM 



and distribution of the tubercles, the existence of a large effusion into the lateral 
ventricles, etc. We are often amazed at the post-mortem examination by the 
apparent insignificance of the lesions. Paralysis of the cranial nerves (eyes, 
face) implies that the base of the brain is gravely affected. If such symptoms are 
absent, and there are mental disturbances, and symptoms of motor irritation dis- 
played in the extremities, we are led to infer meningitis of the convexity. If the 
nervous disorder be mainly unilateral, we may assume that one hemisphere is 
more affected than the other. 

Treatment. — However hopeless the prospect, we are nevertheless bound to 
employ all the remedies at our command, as in other forms of meningitis. Above 
all, we should be thorough in applying ice to the head, and we may also try in- 
unctions of iodoform ointment to the shaven scalp, and lukewarm baths, with 
douching. The inunction of mercurial ointment (especially on the head, neck, 
and back) has also been recommended. The most common internal remedies are 
calomel — half a grain to a grain (gramme 0.03-0.05) for a child every two hours — 
and infusion of senna. Iodide of potassium may also be freely given, fifteen 
grains daily to a child, and two or three times as much to an adult. Whether 
it does any good is extremely doubtful. If the patient is very restless, narcotics 
are indispensable. Stimulants are often given in the last stage of the disease, 
but generally without effect. 

About prophylaxis, we need merely refer to the general statements on page 
254, in regard to prophylaxis from the various tubercular diseases. 



CHAPTER IV 
THROMBOSIS OF THE CEREBRAL SINUSES 

Etiology and Pathology. — The sinuses of the dura mater sometimes present 
a thrombosis, under circumstances similar to those which induce the same process 
in other veins. The most frequent occasion for such thrombosis is marasmus, 
however brought about, with the accompanying feebleness of circulation. This 
is the explanation of those not very rare cases found among wretched and ill- 
nourished children in the first year of life, and also in patients with phthisis, 
cancer, etc. We must note in particular that in severe anaemic conditions (espe- 
cially in chlorosis) sinus thrombosis is comparatively common. 

Half way between marantic thrombosis and the inflammatory variety imme- 
diately to be described, come those cases which are seen in typhoid fever and 
other severe acute infectious diseases. Here the specific virus apparently plays 
an important part (just as in thrombosis of the femoral vein), although very 
likely the cardiac weakness also promotes the thrombosis. 

Genuine inflammatory thrombosis (thrombophlebitis) — that is, thrombosis in 
connection with real phlebitis of the sinus — is almost always due to the extension 
of inflammation from some neighboring part. The most fruitful cause is sup- 
puration in the petrous portion of the temporal bone, the result of otitis or caries. 
This spreads to the walls of the transverse or petrosal sinuses, which are close by. 
Also wounds, necrosis, or other affections of other cranial bones may excite throm- 
bosis ; likewise, although seldom, deep-seated inflammation of the soft parts of the 
head and face, large furuncles or erysipelatous abscesses, may produce the same 
result. The reason why sinus thrombosis may arise from the causes last men- 
tioned lies in the fact that the external veins of the skull are also connected with 
the sinuses of the dura mater by means of the emissary veins of Santorini. It is 



THEOMBOSIS OF THE CEBEBEAL SINUSES 



1065 



easy to understand that purulent thrombophlebitis of the cerebral sinuses is 
often found associated with purulent meningitis or brain abscess. 

Thrombosis due to marasmus is most frequently found in the superior longi- 
tudinal and transverse sinuses, while the inflammatory variety usually occupies 
either the transverse, petrosal, or cavernous sinuses. Of course the thrombus 
may grow out from its original sinus into neighboring- ones. Important clinical 
symptoms are caused by secondary venous stasis in the veins which empty into 
the occluded sinus. These symptoms are most pronounced when the longitudinal 
sinus is affected; objectively, we find the meningeal veins which lie on the surface 
of the brain distended and tortuous; and often there are extensive meningeal 
ecchymoses. Even the cerebral parenchyma beneath shows distinct evidence of 
passive congestion, and minute capillary haemorrhages have been repeatedly 
found in it. 

Symptoms. — In some instances moderate thrombosis of the cerebral sinuses 
has been found post mortem, although there had been no symptom suggesting it 
before death. In other cases the thrombosis does excite undeniable cerebral dis- 
order, but the symptoms are so general and ambiguous that the most we can do 
is to suspect the existence of the clot without being at all certain about it. Sinus 
thrombosis in marantic children usually causes coma, stiffness of the neck and 
back, strabismus, nystagmus, and sometimes clonic spasms in the face and limbs. 
The symptoms in adults are similar, comprising headache, drowsiness, occasion- 
ally delirium, sometimes coma, and varying symptoms of irritation or of paraly- 
sis in the distribution of the cranial nerves (nystagmus, strabismus, trismus) 
and in the extremities. But even all these symptoms are insufficient to make 
the diagnosis certain. They must be re-enforced by certain other phenomena 
more distinctly referable to the peculiar circulatory disturbances occasioned 
by the thrombosis. Occlusion of the cavernous sinus sometimes excites well- 
marked symptoms of stasis in the ophthalmic veins. Thus the retina may be 
seen through the ophthalmoscope to be passively congested, there is oedema of 
eyelids and the conjunctiva, the eyeball is unusually prominent, and the frontal 
vein is distended. In case of an inflammatory thrombosis, the periphlebitic swell- 
ing may cause symptoms in the distribution of the neighboring nerves, especially 
paresis of the oculo-motor or abducens, or trigeminal neuralgia. In thrombosis 
of the transverse sinus an ©edematous swelling is occasionally seen behind the 
ear, near the mastoid process. If the clot projects into the petrosal sinus or even 
actually into the internal jugular, the lower part of this vein collapses. And inas- 
much as the external jugular can empty itself with unusual ease into the unfilled 
internal jugular vein, the external jugular is also affected and becomes less 
prominent upon the affected than upon the normal side. Sometimes it is even 
possible to feel the thrombus in the internal jugular. Such thrombosis causes 
pain and swelling in the neck on the affected side. When the superior longi- 
tudinal sinus is blocked up, there are symptoms of nasal engorgement (epistaxis), 
and distention of the veins about the temples, which veins are connected with the 
longitudinal sinus by emissary veins. We must confess, however, that all these 
special symptoms are comparatively rare, and often difficult of demonstration 
even when present. 

Primary thrombosis of the transverse sinus with extension of the clot into the 
venae magnae Galeni, thus causing internal hydrocephalus, has been repeatedly 
observed in the chlorotic. The clinical picture consists of the rapid onset of 
severe cerebral symptoms (headache, vomiting, somnolence), which rppidly pro- 
gress to deep sopor and lead to death in a few days. When unilateral paralysis 
and symptoms of motor irritation occur (choreic twitchings, epileptiform 
attacks), they are due in part to haemorrhages from stasis in the brain substance. 

The symptoms become more complex where there is a suppurative phlebitis, 



1066 



DISEASES OF THE NERVOUS SYSTEM 



because there are usually pysemic symptoms as the disease progresses. Thus, 
there may be rigors and high fever, pulmonary abscess, suppurative arthritis, etc. 
We have already mentioned the combination of thrombosis of a sinus with puru- 
lent meningitis or brain abscess. 

The prognosis is almost always bad, both because of the nature of the causa- 
tive disease and because of the grave cerebral derangement or the secondary 
pyaemia. Spontaneous recovery may occur, but it is rare. The nervous symptoms 
may last at times only a week or two, but they may extend over several months. 

Treatment in most cases must be purely symptomatic. Only when a purulent 
sinus thrombosis follows ear disease can surgical interference give very satisfac- 
tory results. The details of such treatment are to be found in the text-books of 
operative aural surgery. 



SECTION II 
Diseases of the Brain-Substance 

CHAPTER I 

DISTURBANCES OF CIRCULATION IN THE BRAIN 

(Cerebral Hypercemia. Cerebral Ancemia) 

It is presumable that so sensitive an organ as the brain is much influenced 
even by slight disturbances of circulation ; but as yet we have comparatively little 
knowledge of the production and character of such disturbances, their very exist- 
ence being very difficult to demonstrate. There are many instances where marked 
cerebral symptoms justify the assumption that the brain is in some abnormal 
condition, where yet there are many arguments against any marked ana- 
tomical lesion. Here we surmise that there is some circulatory derangement, 
although we have no actual and direct arguments to rely upon. For example, 
we refer to this cause certain cases of headache, of sensations of pressure in the 
head, of vertigo, of general hyperesthesia, and of that protean and nevertheless 
easily distinguishable disease known as cerebral neurasthenia (q. v.). At present, 
however, we can not determine how far circulatory disturbances are actually con- 
cerned in these cases, or of what kind they are, or whether there may not be 
purely functional disease of the brain entirely independent of changes in the 
blood-vessels. 

Certain groups of cerebral symptoms, which come on in paroxysms, seem the 
most clearly referable of all to circulatory disturbance. There can hardly be a 
doubt that the phenomenon known as fainting or syncope is due to sudden cere- 
bral anaemia. As is well known, fainting is usually the result of a clearly demon- 
strable cause. Frequent and familiar causes are emotional excitement, terror, 
unusual psychical impressions (like the sight of blood), trie influence of great 
heat, or great physical strain, as by long standing. The condition of the stomach 
has certainly a great influence in many cases. There are many persons who, if 
they go long beyond the usual time without eating (particularly if they go with- 
out breakfast), are very liable to syncope. Some individuals are especially sub- 
ject to fainting fits. Such persons are often slight and anaemic (for example, 
convalescents), but some are in appearance robust and vigorous. Many children 
are subject to fainting. 

The immediate cause of the cerebral anaemia in all these cases is doubtful. 
Mental excitement is usually supposed to lead, in fainting, to a contraction of the 



DISTURBANCES OF CIRCULATION IX THE BRAIN 1067 



minute cerebral arteries. It is not, however, impossible that in these cases also, as 
in others, sudden cardiac weakness is one factor, although, if so, it is strange 
that we never see a trace of cyanosis. Where the attack is apparently connected 
with unusual conditions of the abdominal organs we are reminded of the relations 
of the splanchnic nerve to the heart (Goltz's experiment of beating the belly of a 
frog), and of the possibility that the brain might be left anaemic if the abdominal 
vessels suddenly dilated and absorbed a large proportion of the whole blood- 
supply. 

The symptoms of an ordinary fainting fit are known to every one. There are 
usually certain prodromata. The person begins to " feel badly." Dizziness comes 
on, the senses are confused, the patient gapes, the ears ring, there are spots be- 
fore the eyes or total darkness, the floor seems to move, and surrounding objects 
begin to spin around. All this is almost always accompanied by nausea, and 
sometimes there is actual vomiting. If the person can lie down promptly the 
attack is sometimes averted without complete loss of consciousness. Otherwise 
there is unconsciousness for a time varying from some minutes to even a half- 
hour or longer. What is most noticeable, even in the beginning of the attack, 
is the pallor which overspreads the face and often becomes extreme, and is 
the visible expression of the coincident cerebral anaemia. Very often the face 
and body are bathed in cold perspiration. The pulse is usually small and rapid. 

There is no real danger in an ordinary attack. The most important therapeu- 
tic measure is to lay the patient horizontal as soon as possible, to favor the 
return of blood to the brain. Mild stimulants should also be employed ; the face 
should be sprinkled with cold water, the temples rubbed with vinegar or cologne- 
water ; brandy or wine should be administered. We can overcome a tendency to 
fainting fits only by strengthening the constitution. 

The results of chronic cerebral anaemia are observable when the cerebral con- 
dition is part of excessive general anaemia. Almost all cases of chlorosis, per- 
nicious anaemia, and acute anaemia from loss of blood (as in ulcer of the stomach) 
display most plainly the symptoms of cerebral anaemia. The phenomena are 
essentially the same as in syncope, only less in degree. Consciousness is main- 
tained, except in the worst cases. A sort of persistent drowsiness, however, 
often attended by frequent gaping, is one of the most constant symptoms. The 
patient is most distressed, as a rule, by loud tinnitus aurium, persistent nausea, 
and sometimes by obstinate headache. All these symptoms are aggravated, and 
often increase to an actual attack of fainting, if the patient sits up in bed, and 
are least marked when he lies as quietly as possible in a horizontal position. 
The treatment of this condition is of course identical with that of the causative 
disease and the general anaemia. 

Cerebral hyper aemia, like cerebral anaemia, may be either chronic or paroxys- 
mal. Of the chronic variety we know almost nothing. It seems doubtful, to say 
the least, whether there is really a " general plethora," or whether the headaches 
and vertigo of which " full-blooded " persons complain are due to hyperaemia of 
the brain. Nor have we any direct proof that the cerebral symptoms resulting 
from chronic poisoning (alcohol, tobacco, etc.), or from persistent mental over- 
exertion, are brought about by hyperaemia, as some assume, rather than by func- 
tional disorder of the nervous elements themselves. 

These conditions, which are called attacks of " cerebral congestion " or " rush 
of blood to the head," are often referred to the sudden onset of cerebral hyperae- 
mia. There is a more or less sudden appearance of general excitement, with a 
sensation of warmth in the head and neck, strong pulsation of the carotids, a red 
face, general hyperaesthesia and irritability, headache, vertigo, tinnitus, spots be- 
fore the eyes, and nausea. An attack lasts half an hour to an hour. In severe 
cases there may be maniacal excitement, or there may be stupor and drowsiness 



1068 



DISEASES OE THE NERVOUS SYSTEM 



and other symptoms of lowered intellectual activity, resembling a slight apoplectic 
attack (see a later chapter). The special cause of such attacks, however, is usu- 
ally obscure. It is, indeed, very probable that in these attacks vaso-motor dis- 
turbances play a part (dilatation of the cerebral vessels from vascular paralysis 
or from irritation of the vaso-dilator nerves) ; but it is very questionable whether 
these vascular changes are really the primary diseased state, rather than the 
result of some other different morbid condition. Possibly we have to do some- 
times with epileptic states, or more frequently with one manifestation of general 
nervousness, neurasthenia or hysteria (q. v.) with primary mental disturb- 
ances (anxious ideas, etc.). 

In treating " congestion " we should keep the patient as quiet as possible, with 
head and shoulders raised; and, secondly, we should endeavor to draw the blood 
away from the brain. This purpose will be served by hot foot-baths, sinapisms 
applied to the chest and the calves, and such purgatives as senna or colocynth. 
It is also beneficial to apply cold to the head. In a severe case it is proper to put 
leeches to the temples or the mastoid processes. 

To prevent, as far as possible, the recurrence of the attacks, we must have 
regard to the whole mental and physical constitution of the patient. We may 
mention, as of chief importance, diet (no alcohol) and a course at some watering- 
place, or cold-water treatment. 



CHAPTER II 

GENERAL PRELIMINARY REMARKS UPON THE LOCALIZATION 
OF CEREBRAL DISEASES 

( Topical Diagnosis of Cerebral Lesions) 

The physiological relations of the brain are such that the symptoms of cere- 
bral disease are determined to a greater extent by the locality than by the nature 
of the lesion. If, for example, there arises at any place a break in the con- 
tinuity of the cerebral motor tract, the result, as we already know (see page 831), 
is hemiplegia upon the opposite side of the body. The result is precisely the 
same, whether the interruption be due to a haemorrhage, an abscess, a new 
growth, or an embolic softening. If in any way the function of the motor fibers 
is suspended, then the necessary sequence in every case is a paralysis of definite 
extent and definite characteristics. Much the same may be said of many other 
symptoms which appear when there is a lesion of one or more definite places, but 
which are never referable to a special abnormal process, regardless of the portion 
of brain thereby affected. 

However self-evident these simple statements may appear, it required a long 
time for them to gain universal acceptance among physicians. The chief cause 
of this was the conception entertained by the older physiologists in regard to 
the functions of the brain. Elourens, in 1842, taught that functionally all parts of 
the cerebrum were alike, and therefore any one part could act vicariously for any 
other; and this view had numerous adherents among physicians, as well as physi- 
ologists. It was nevertheless experience at the bedside and the autopsy-table 
which first led to observations and discoveries irreconcilable with this view. 
Above all, it was the lesions found in aphasia which forced men to localize one 
particular cerebral symptom as due to an affection of one particular spot in the 
brain. In 1861 Broca announced that the appearance of aphasia is always due to 
a lesion of the left third frontal convolution; and this was the starting-point 
of the doctrine of localization in general. Nine years later (1870) appeared the 
famous treatise of Fritsch and Hitzig detailing successful attempts at excitation 



THE LOCALIZATION OF CEKEBKAL DISEASES 1069 



of the surface of the brain in animals, and thus overthrowing the old idea that 
the gray cortical substance could not be irritated. It was shown that excitation 
of certain places in the cortex is followed by muscular contractions in well-defined 
portions of the opposite side of the body, so that we are justified in assuming the 
existence of a number of cortical centers, which are quite limited in extent. 
These results were soon confirmed by numerous observations in cerebral pa- 
thology in man; and to-day our information about the motor functions of 
the cerebral cortex forms the best-known portion of the doctrine of cerebral 
localization. Of late years successful work has been done in this exceedingly 
difficult field by Meynert and Flechsig among anatomists ; Ferrier, Munk, Goltz, 
and other physiologists; and such pathologists as Charcot and his pupils, Noth- 
nagel, Wernicke, Hughlings Jackson, Horsley, and others. It is true that we 
are only just beginning to know something about the subject. There are numer- 
ous contradictory views asserted, and numerous questions unanswered. The fol- 
lowing summary, therefore, is to be regarded merely as expressing the prevailing 
opinions now existing. Much in it will surely be altered in the course of time; 
but still this doctrine of special localization of the various cerebral functions 
marks out in general outlines the only foundation upon which we can hope to 
erect a system of cerebral pathology and diagnosis. In the following sketch we 
shall, for practical reasons, put the results of clinical observations upon man in 
the foreground, and merely speak incidentally of the corresponding experimental 
achievements. This will be the quickest way to gain acquaintance with the 
practical points in the diagnosis of what Griesinger called the " focal diseases"; 
and then, when we take up the separate varieties of cerebral disease, we shall 
have these general remarks to refer to. 

1. The Motor Region of the Cortex Cerebri 

Clinical observation and the results of experiment both teach that a part 
of the cerebral cortex is distinct from the rest, inasmuch as it is the exclusive 
seat of motor functions. This " motor region " (vide Figs. 169 and 170) 




Fig. 169.— Lateral aspect of the brain (from Ecker). The gyri and lobules are in Roman type, the sulci 

and fissures in italics. 



1070 DISEASES OF THE NERVOUS SYSTEM 



is made up chiefly of the two central convolutions (gyri centrales anterior et 
posterior, in Fig. 169), and the paracentral lobule (vide Fig. 171), which lies on 
the median surface of the cerebrum. To a slight degree the motor region also 
embraces the neighboring portions of the frontal convolutions and the upper 
parietal convolutions. It is also anatomically different from the other regions of 




Fig. 170.— Lateral aspect of the brain (after Ecker). The motor region of the cortex, consisting of the 
anterior and posterior central convolutions, as well as of the paracentral lobule shown in Fig. 171 . is 
shaded. 

the cortex, as Betz was the first to point out, for it alone possesses certain large 
pyramidal ganglion-cells, which must certainly be regarded as the same motor 
ganglion-cells from which the fibers of the pyramidal tract arise (vide supra, page 
829). However extensive the destructive processes which attack other parts of 
the surface of the brain, provided they do not involve these particular convolu- 
tions, they cause no paralytic symptoms; while all diseases which destroy any 
considerable portion of the " motor " region inevitably result in a motor disturb- 
ance on the opposite side of the body. 

We can distinguish still further in different regions of the cortex special 
centers for the various groups of muscles, but we must take special note that the 
individual centers are not sharply distinguished from one another, but that they 
overlap. Thus the different centers which are associated have an intimate con- 
nection, which also seems necessary physiologically. The center for the move- 
ments of the facial muscles (facial region), lies, as it would seem, at the lower 
end of the central convolutions, and particularly of the anterior central convolu- 
tion. Near by, probably somewhat lower, is found the center for the movements 
of the tongue. This center probably extends to the foot of the third frontal con- 
volution, so that on the left side it is accordingly in close proximity to the special 
motor-speech center (vide infra). The center for the movements of the arm lies 
somewhat higher than the center for the facial, occupying roughly the middle por- 
tion of the anterior and probably the posterior central convolutions. The center 
for the lower extremity is found partly in the uppermost portions of the central 



THE LOCALIZATION OF CEREBRAL DISEASES 1071 



convolutions, but apparently lies for the most part in the paracentral lobule. The 
center for the movements of the trunk probably lies in front of the leg center in 
the most posterior portion of the upper frontal convolution and also on the 
median surface of that convolution (the so-called marginal gyrus, the median 
portion of the upper frontal convolution). 

Within these great cortical centers for the chief portions of the body (leg, 
arm, face, tongue) there is a much more accurate localization for individual 
groups of muscles, and perhaps even for individual muscles. This fact has been 
established especially by the interesting experiments of excitation of the cortex 
of monkeys by Ferrier, Horsley, and others. Pathological observations and 
occasional attempts at excitation of the cortex which have been practiced on man 
after trephining or in extensive cranial defects arising from injury or disease, 
have shown that the conditions in man are in general quite the same as in the 
higher apes. Within the leg center lie special centers for the toes and foot, chiefly 




Fig. 171.— Aspect of the median surface of the cerebrum, which is shown when the two hemispheres are 
separated from each other by a sagittal section. B. Corpus callosum. The differences in the t3'pe 
have the same meaning as in Fig. 169. The paracentral lobule, as a part of the motor region of the 
cortex, is shaded. (Copied from Ecker, only the paracentral lobule is made more sharply prominent 
than in the original.) 

above and especially in the posterior central convolution. Then come the centers 
for the movements of the knee, and then those for the movements of the hip. 
In the paracentral lobule are found chiefly the centers for the thigh and the 
pelvic and glutseal muscles. Within the arm center and for the most part above 
— that is, toward the leg center — are the centers for movements of the shoulder 
and elbow. Farther downward come the centers for the movements of the hand 
and fingers, chiefly in the anterior central convolution. The separate position of 
the center for the thumb is especially noticeable ; this is in the posterior central 
convolution, adjoining the centers for the facial muscles. Farther downward 
lie the centers for the upper facial territory above the centers for the muscles of 
the mouth and lips. In the lowest part of the central convolutions and in the 
adjacent portions of the two lower frontal convolutions lie the motor centers for 
movements of mastication (the centers for closing the mouth are said to lie above 
those for opening the mouth), and for the movements of the tongue and vocal 
cords. The exact position of these centers in man is not yet definitely known. 
The centers for the associated movements of the eyes to one side seem to be quite 
scattered. We elicit these movements (usually coincident with a corresponding 



1072 



DISEASES OE THE NERVOUS SYSTEM 



turning- of the head) on irritation of the posterior portion of the frontal lobe 
adjoining the region of the centers for the arm and face; but, on the other hand, 
pathological observations favor the existence of a center for associated movements 
of the eyes in the region of the angular gyrus {vide infra). This multiple locali- 
zation is perhaps explained by the fact that the movements of the head and eyes 
are closely associated both with all complicated activities of the hand and with 
the functions of sense (listening, looking at objects). The diagram on page 
1073 (Fig. 173), from a drawing by C. K. Mills, gives a review of all these 
details. 

The topical diagnosis of diseases in the motor region of the cerebral cortex 
is based upon the following considerations : 

In the first place, we have already remarked (page 831) that the relative posi- 
tions of the motor centers for the face, arm, and leg are such as to allow readily 
of isolated paralysis of any one of these portions of the body — that is, " mono- 



Fig. 172. — (Drawn according to Ecker.) Explanation of the topographical relations between the surface of 
the brain and the skull, c. Fissure of Rolando. HC. and VC. Posterior and anterior central convolu- 
tions. S. Si and Sn. Fissure of Sylvius. P 1 P 2 . Upper and lower parietal lobes. O. Occipital lobe. 
Cb. Cerebellum. T. Temporal lobe. F. Frontal lobe. 

plegia." In fact, we already possess a long series of observations where circum- 
scribed lesions in the motor area of the cortex produced paralysis of one side of 
the face, or of one arm or leg, and of no other part. Such paralysis is termed 
monoplegia of the face, the arm, or the lower extremity. It follows, from what 
has been said, that even during life we can state, with considerable accuracy, 
the spot on the surface of the brain where the disease must be situated. Still 
more frequently, a combined paralysis of two portions of the body is to be ob- 
served as a result of cortical lesion; the commonest is a simultaneous paralysis 
of the arm and face; more rarely we see the arm and leg paralyzed together. On 
the other hand, we may feel certain, from the position of the motor centers, that 
no single center of disease could paralyze simultaneously the leg and the face, 
while the arm escaped injury. As a matter of fact, no such combination has ever 
been observed. It is also worthy of note that the muscles that always act 
bilaterally (frontal muscles, muscles of mastication, eye muscles, vocal-cord 




THE LOCALIZATION OF CEREBEAL DISEASES 1073 



muscles, etc.) have also a bilateral innervation. A unilateral focus of disease 
in any center, therefore, does not cause paralysis of these muscles. 

Besides this limitation of the paralysis to one portion of the body just dis- 
cussed, localized disease of the cortex has another very characteristic feature. In 
it the symptoms of irritation of the motor centers are noticeably frequent. There 
are tonic and clonic spasms, which, like the paralysis, not infrequently affect 
one arm, or the arm and half the face. Sometimes, however, they involve 
the entire half of the body. These paroxysmal spasms are termed " cortical 
epilepsy," partial epilepsy, or Jacksonian epilepsy; for the movements are just 
the same as in genuine epilepsy. Numerous cases of disease have taught us 
that such circumscribed epileptiform attacks occur only in affections of the motor 
cortex. They furnish still more definite information as to the precise locality of 




Fig. 173.— Localization in the cerebral cortex. 



the lesion; for spasms in the distribution of the facial nerve imply that mainly 
the lower third of the central convolutions is affected; of the arm, the middle 
third; and of the leg, the upper portions of the same. If we have the opportunity 
to observe such attacks of partial cortical epilepsy accurately, we can almost 
always determine that the twitching begins in quite a limited muscular terri- 
tory — for example, in the face, the thumb, etc. The attack often begins with 
a slight sensory aura (paresthesia in the part of the body affected) ; then fol- 
lows a tonic muscular contraction which soon passes into a decided clonus. From 
this point the twitchings extend, and always in the order corresponding to the 
local arrangement of the different centers which lie next to one another. It is 
therefore always of importance in diagnosis to determine in what group of 
muscles the twitchings begin, because we can thus decide that the corresponding 
cortical center is the chief seat of the morbid affection. In the muscles inner- 
vated bilaterally (the frontal muscles, the eye muscles, the muscles of mastication, 
etc.) the convulsions also occur bilaterally. In very severe attacks the spasm 
finally involves the other half of the body, the irritation being conveyed through 
the fibers of the corpus callosum to the corresponding cortical motor centers of the 
08 



1074 



DISEASES OE THE NEEVOUS SYSTEM 



other hemisphere. The twitchings usually persist the longest in the muscles first 
affected. In the attacks of circumscribed cortical epilepsy there is no disturbance 
of consciousness, but if the convulsion extends to both halves of the body, there is 
usually loss of consciousness, or at least a decided clouding of consciousness. The 
individual attacks last only a short time — about one or two minutes. After they 
cease there usually remains a very transitory motor weakness or even complete 
paralysis in the muscles most affected, which is in a degree the indication of ex- 
haustion of the affected center. Temporary disturbances of speech are often 
associated with right-sided Jacksonian epilepsy. The relation of convulsions to 
permanent paralysis varies greatly. Often, for example, when there is haemor- 
rhage into the central convolutions, violent unilateral convulsions come on 
simultaneously with the paralysis. In the case of tumors and other lesions 
which develop slowly, partial epileptiform spasms will often appear quite a long 
time before there are persistent symptoms of paralysis. Finally, it is not rare 
for epileptiform attacks to occur repeatedly in regions that are already paralytic. 
Either of the occurrences described in the two preceding sentences are particu- 
larly strong evidence that the cortex cerebri is diseased. Besides the pronounced 
epileptic attacks, disease of the motor region of the cortex may give rise to less- 
violent symptoms of motor irritation, such as occasional twitching, rhythmical 
twitching, tonic contraction, etc. 

About the condition of sensation when there is cortical paralysis we know as- 
yet very little. The experimental researches of Munk and the anatomical inves- 
tigations of Flechsig and others have led to the conclusion that the termination 
of the sensory tract of the lemniscus, the so-called sensory sphere, is in part in 
the same cortical region as the motor cortical centers. We might, therefore, be- 
inclined to suppose that a disturbance of sensation would invariably accompany 
cortical paralysis in man also, but about this point clinical observations do not 
yet give perfectly harmonious results. From our own experience, however, we 
believe that we can say that sensory disturbances are far more common than was- 
formerly supposed. It is a remarkable fact, however, that the sensibility for pain 
and temperature is hardly ever affected, but the disturbances involve the simple 
sensations of touch and especially the stereognostic sense (recognition of objects 
by touch, see page 795). Disturbances of the muscular sense and ataxic disturb- 
ances have also been repeatedly observed in diseases of the motor cortical region. 

2. The other Parts of the Cortex Cerebri, except the Center for Speech 

1. Frontal Convolutions. — Unilateral disease of the anterior portion of the- 
brain may be quite extensive without causing notable disturbance of any kind. 
Certainly the greatest part of the upper two frontal convolutions have no motor' 
functions. It is, however, maintained that the posterior portion contiguous to 
the anterior central convolution, called the foot of the frontal convolutions, does 
contain motor centers. We have stated above (page 1071) that the motor centers 
for the muscles of the trunk are situated in the upper frontal convolution, espe- 
cially on its median aspect. This is the reason why a decided swaying of the 
trunk in walking and in standing (just as in cerebellar ataxia, vide infra) has. 
been repeatedly observed in diseases of the frontal lobe, especially in tumors. 
The third (lowest) frontal convolution on the left side has, as we shall soon see,, 
an undoubted connection with the motor processes of speech. 

There is a quite generally accepted opinion that the cortex of the frontal por- 
tion of the brain is to be regarded as the " seat of the higher psychical functions."' 
Some few cases are on record where extensive bilateral lesions of these parts had 
for their only manifestations mental symptoms (loss of mental functions, changes 
in character, the so-called morbid wittiness, Witzelsucht, etc.) without any other- 
disturbances. In general paralysis also, and in other forms of dementia, the pre- 



THE LOCALIZATION OF CEREBKAL DISEASES 1075 



dominance of atrophy in the frontal lobe is very striking, so that it is actually 
very probable that the frontal lobe has a close relation to the higher mental 
processes. Nevertheless, we can not emphasize too much the fact that, at present, 
we have no certain knowledge about the precise form of this relation or of the 
nature of the physical functions. 

2. Parietal Convolutions. — We know but little about the functions of the 
cortex of the parietal lobe, and the symptoms which might indicate disease of 
that portion of the cerebrum. According to Flechsig, a large part of the sensory 
tract of the tegmentum ends in the parietal cortex. We might therefore expect 
decided disturbances of sensibility in diseases of the parietal lobe, but unequivocal 
clinical and anatomical evidence in support of this hypothesis is still almost 
wholly lacking. Observations on the occurrence of motor disturbances in diseases 
of the parietal cortex are somewhat more numerous. Centers for associated 
movements of the eyes seem to be situated in this region (in the angular gyrus). 
In diseases of this region we may often observe an interesting symptom of irrita- 
tion, the so-called " conjugate deviation " — 
that is, the simultaneous turning of the head 
and eyes to one side. The angular gyrus is 
also said to contain a center for the ocular 
portion of the facial (orbicularis oculi mus- 
cle) and the levator palpebrse superioris; 
but of course these statements have not been 
universally accepted. 

3. Occipital Convolutions. — The clinical 
and experimental investigations of the last 
few years have all shown that the occipital 
portion of the cerebrum contains the cortical 
center for visual sensations. It is here, in all 
probability, that the fibers of the optic nerve 
terminate in the cortex cerebri. A glance 
at the accompanying diagram (Fig. 174) 

.,, , . -| , , I,. , Fig. 174.— Diagram of the course of the optic 

will make it easy to understand the disturb- fibers in the chiasma. 

ances of vision which result from lesions 

of the occipital lobe. L represents the left eye and R the right, Ch the optic 
chiasma, where, as is now certain, some of the fibers of the optic nerves cross to 
the opposite side. The fibers (distinguished by a broken line) from the outer 
or temporal half of each retina extend, without crossing, into the correspond- 
ing optic tract (Tract, opt.), while those from the inner or nasal half of 
the retina cross over in the chiasma. The right occipital lobe, for example, 
comes in this way to receive the fibers from the outer half of the right 
retina and from the inner half of the left. If the right occipital lobe becomes 
disorganized, then the images formed upon the parts of the retinaa just named, 
belonging to the left half of the field of vision, are unperceived. With each eye 
the patient sees only such objects as lie in the right half of his field of vision, 
and is blind to all that lies upon his left. This sort of visual disturbance, where 
each eye becomes blind to the same " homonymous " portions of the- field of vision, 
is termed hemianopsia, or hemiopia. A lesion of the right occipital lobe causes, 
therefore, left-sided hemianopsia, and, vice versa, destruction of the left occipi- 
tal lobe entails right-sided hemianopsia* 

[* When hemianopsia is due to a lesion between the chiasma and the pulvinar and geniculate 
body (second optic neurone, vide infra, page 1089), the pupil does not react when light is thrown on 
the blind half of the retina, although it does react when light is thrown on the sound half ( Wernicke's 
" hemiopic pupillary reaction"). When hemianopsia is due to a lesion between these ganglia and the 
cuneus. (third optic neurone) this hemiopic reaction does not occur.— K.] 




1076 



DISEASES OF THE NERVOUS SYSTEM 



The anatomical evidence is still very contradictory as to the precise localiza- 
tion of the visual center. Disturbances of vision are found most constantly 
in diseases of the cuneus and the first occipital convolution. In this region the 
sensations of light as such seem therefore to take their rise. In diseases of the 
medullated layers of the occipital lobes and their vicinity (angular gyrus) — that 
is, of the connecting tracts between the occipital cortex and other cortical regions 
— we sometimes observe the interesting symptom of so-called " soul blindness " 
(Munk). This disturbance is when the patient can still see objects, but can not 
recognize what they signify. He no longer knows what to do with them, or he 
uses them in the most utterly wrong way. He no longer recognizes his acquaint- 
ances by their appearance, but only by the sound of their voice. In diseases of 
the left occipital lobe the connections between the optic impressions and ideas 
of language may sometimes be solely affected; then there develop optic aphasia 
and alexia; the patient recognizes objects, but he can not name them. He can not 
read or copy, but he can write very well spontaneously and from dictation (com- 
pare the following section). 

4. Temporal Convolutions. — The relation of the temporal lobe to hearing is 
apparently analogous with that of the occipital lobe to vision. Destruction of the 
posterior half of the superior temporal convolution, according to some observa- 
tions, is apparently capable of causing actual deafness in the opposite ear; but 
the trouble usually disappears in a very short time. Each auditory nerve is there- 
fore probably connected with both temporal lobes. It is much more certain than 
these observations of actual disturbance of hearing, that diseases of the [left] 
superior (first) temporal convolution cause so-called word deafness (" soul deaf- 
ness ") — that is, the loss of comprehension of spoken language. We will return 
again to this condition, which is usually associated with motor aphasia. 

We may observe, in conclusion, that the olfactory nerve probably ends in the 
gyrus uncinatus and the parts adjacent (Fig. 171, page 1071), so that we may 
assume that that is the center for smell. 

[The sensori-motor centers in the Rolandic region, and the special centers for 
vision, hearing, and smell which have just been described, occupy only about one 
third of the area of the cerebral cortex. Flechsig has found that the fibers con- 
nected with these areas assume their myeline sheaths at an early period of 
foetal life, while the fibers connected with other regions become myelinized much 
later. These other regions he regards as association centers, and believes that 
they are especially concerned in the higher intellectual functions. The anterior 
association centers, embracing the anterior portions of the frontal convolutions 
and the gyrus rectus, are supposed by him to be the chief centers for ideas of 
personality. The posterior association centers include the precuneus, the 
parietal convolutions (except the posterior central convolution), all portions of 
the occipital cortex except the visual area, and all portions of the temporal cortex 
except the auditory and olfactory areas. These centers are supposed to be the 
centers for ideas referring to the external world. The island of Reil and the 
parts adjacent form the middle association center. Flechsig's hypotheses have 
been strongly opposed, especially on the anatomical side. It is doubtful whether 
the projection and the association centers in the cortex can be so definitely dis- 
tinguished, but the hypotheses thus advanced have also some clinical and patho- 
logical support, and they present a rich field for further investigation. — K.] 



THE LOCALIZATION OF CEEEBEAL DISEASES 1077 



3. The Centers of Speech and the Disturbances of Speech 

(Aphasia and Allied Conditions) 

The Various Forms of Aphasia, and their Anatomical Localization. — As we 

remarked at the very beginning of this chapter, the peculiar derangements of 
speech observed in many cerebral diseases were the first symptoms which were 
found to be caused by a distinctly localized cerebral lesion. For the better under- 
standing of this extremely interesting subject, it is necessary that we should 
enter somewhat minutely into the processes connected with normal speech. 

Incitement to speech — that is, to the oral expression of our thoughts to others 
— comes either from an internal impulse or from external causes which excite 
this impulse. Speech always requires internal mental activities — the presence of 
ideas and their transformation into that which we wish to communicate by 
speech. Where there are no conceptions there can be no words. The demented 
person is silent, because, like the newborn infant or the brute, he has nothing to 
say; but, on the other hand, the impulse to speak must also be present. In 
melancholic insanity we sometimes observe persistent loss of speech, not from 
any lack of something to say, but because there is no incitement to the act, or 
because inhibitory influences immediately repress any tendency to utter words. 
If we take for granted that the mental material for speech exists, then the trans- 
formation of this material into actual speech is a result of the following compli- 
cated processes, the disturbance of which, individually, produces the various 
forms of aphasia. 

In the first place, the speaker must be acquainted with the word which ex- 
presses the mental conception. If, for instance, he wishes to tell another the 
name of some animal, he must know the appropriate word — " dog," " sparrow," 
" frog." This knowledge, which, as far as our mother tongue is concerned, we 
all acquired in childhood, may, as experience shows, be lost again in case of cere- 
bral disease. Just as we may ourselves forget a word momentarily, or as any 
healthy person may, at the sight of an animal that is perhaps rather rare, be 
" unable at the minute to think of its name," so in disease one may forget all or 
a greater or less number of words. Such a patient sees a dog, and knows well 
enough that it is an animal possessed of such and such qualities, but he has 
forgotten its name. The association between the conception " dog," and like- 
wise between the perception of a dog by the eye, and the appropriate vocal repre- 
sentation " dog," is lost. This condition is termed amnesic or sensory aphasia, 
because it is due to complete or partial loss of the memory for words. The 
patient knows perfectly well what he wishes to say, but the words escape him. At 
the same time, in cases of pure amnesic aphasia, the power of repetition is unim- 
paired. As soon as we say " dog " to the patient, he repeats the word perfectly 
well; and sometimes he also perceives that this is really the correct word; but in 
other instances, although the word is correctly repeated, the patient does not 
become conscious of its meaning {vide infra "word deafness "). 

If we examine cases of amnesic aphasia more carefully we may notice by what 
special sensory perceptions the memory of the lost word can be eventually called 
back. Although the mere idea alone does not call the proper word back to con- 
sciousness, the sensory perception (so far as we have to do with external objects) 
may often by association recall the corresponding word. It is, of course, most 
frequently the visual perception which recalls the memory of the word. If this 
association also fails we speak of an optic-amnesic aphasia. In other cases 
auditory impressions (e. g., the ticking of a watch, the note of a musical instru- 
ment) may restore the recollection of the proper word, or, in other cases still, 
sensations of touch, taste, or smell. All these associations between given percep- 
tions and the corresponding verbal representations may be destroyed at the same 



1078 



DISEASES OF THE XEEYOUS SYSTEM 



time or one by one, or they may be partially retained. Sometimes it is only 
by the simultaneous action of different sensory impressions — e. g\, perceptions 
of sight and touch — that the idea of the word can again be recalled to con- 
sciousness. 

Of great interest are certain cases where there is only partial amnesia. These 
have been repeatedly observed. Thus a patient forgot nothing but his own name, 
remembering all other words perfectly; or the loss of words may be confined to 
but one language, the patient being still able to express himself tolerably well in 
another tongue. In a case observed by Graves, the patient still knew the initial 
letter of all words ; if, for example, he saw a cow, he would know that the corre- 
sponding word began with C, and would look under C in a dictionary till he found 
the word. 

Among the amnesic disturbances, we may also class the dissolution of closely 
associated sequences of words, as are found, for example, in the order of numbers, 
in the names of the days of the week, the names of the months, familiar prayers, 
etc. Although such sequences of words which have been practiced from childhood 
may on the one hand (vide infra) greatly facilitate the pronunciation of the indi- 
vidual words, on the other hand the connection often becomes so loose that the 
patient may repeat the whole list very well after any person, but he can not recite 
it spontaneously. Such tests often show most interesting peculiarities. Thus we 
have repeatedly noticed, for example, that aphasic patients can repeat the names 
of the days of the week very well in their ordinary sequence, but that it is very 
hard to say them backward. Many . patients find great difficulty in counting 
backward. 

If the memory for words be retained, the next requisite for speaking is the 
transfer of the word image into such action of the muscles of our organs of speech 
as is calculated to produce the word in question as an actual sound. This motor 
process is so complicated that an extremely accurate co-ordination of movements 
is demanded for the correct pronunciation of the word. Man therefore possesses 
a separate center, in which this transfer of the word image into the motor pro- 
cesses of speech takes place. If this center be diseased, there again results a loss, 
or at least a greater or less impairment, of speech. The patient is in this case 
well aware of the word he wishes to say, but he can not pronounce it. He has, 
if we may use the expression, forgotten the movements that are essential to 
speaking. His tongue and lips are not really paralyzed, but the patient no longer 
knows how to make use of them for talking. He has reverted to the condition of 
childhood, before he had learned to talk. The patient often makes the greatest 
effort to speak. The word he wishes to utter " keeps hovering before him " ; he 
moves his mouth in the most striking manner, but brings out only an occasional 
sound, and that incorrect. This commonest form of speech disturbance is known 
as ataxic aphasia. Of course it is equally impossible for the patient to repeat 
a word after some one else. He keeps his eyes fixed on the mouth of the speaker, 
and endeavors to imitate the motions of his mouth, but he is either partially or 
totally unable to reproduce the sound. 

Ataxic aphasia exhibits many degrees of intensity. On the one hand there are 
cases of complete aphasia, where the patient can utter only such separate sounds 
as " a," " e," etc. And, on the other hand, there are also mild cases where there 
are merely errors in pronunciation. Such cases may best be termed " ataxic " 
aphasia. The patient pronounces many words correctly, but with others there 
are such mistakes as the transposition of individual letters, the misplacement or 
omission of letters, or, finally, the adding on of letters. For example, he will 
say thens instead of then, widow instead of window, dipter instead of dipper, hefd 
instead of held, wrelster instead of wrestler, and belnow instead of below. This 
mildest form of ataxic disturbance is termed "stumbling over syllables" (Sil- 



THE LOCALIZATION OF CEREBEAL DISEASES 1079 



bernstolpern), or "literal ataxia/' Patients sometimes affix the same inappro- 
priate termination to many words ; for example, a woman used to count : " onen, 
twoen, threen, fouren, riven/' etc. In most instances the patient can pronounce 
some words tolerably well, others only imperfectly and with difficulty, and still 
others not at all. Usually the patient gradually learns a few common Avords and 
expressions (e. g., " good morning ") by means of persistence in repeating them 
as they are uttered by another, so that he pronounces them better and better. 
TThat is very remarkable, and not so very rare, is that a patient will be able when 
in a passion to pronounce a word, such as an expression of anger, an oath, or an 
exclamation, perfectly well, because it is done to a certain extent involuntarily, 
while he can not utter the same words if he wishes to say them. One patient 
under our observation always said " well." in answer to the question, " How are 
you? " but she was wholly unable to repeat the word " well " by itself when asked 
to do so. Association also often exerts an appreciable influence; for example, a 
patient who finds it absolutely impossible to pronounce " six," utters it with 
perfect distinctness if he begins to count from one, in the ordinary way, up 
to six. "When patients have at last managed to say the right word, they some- 
times stick to it — that is. they continue to repeat this word when they should say 
something else. In many severe cases of motor aphasia the whole capacity for 
speech is limited to a few syllables or a few brief phrases, which always appear 
as soon as the patient makes any attempt to speak (so-called monophasia). 

A patient of our own could for a long time utter nothing but the meaningless 
words, "seller sag ich namlich selber" (self say I namely self). The entire 
verbal thesaurus of another (female) patient whom we saw consisted of the 
meaningless sounds " bibi " and " eibibi." Still a third could say only " tinne, 
tinne." The patient is quite well aware that what he says is wrong, but. despite 
all his efforts, every attempt to speak excites these same sounds. It produces a 
comical impression to see the patient use the same invariable word, with all sorts 
of facial expression. Thus the woman mentioned above begged for things, with 
" bibi," in a coaxing tone, while sometimes she would give vent to violent anger 
with a loud " bibibibi." 

Amnesic (sensory) aphasia may also vary greatly in degree. It is only rarely 
observed in its pure form, but it is usually associated with motor aphasia. The 
amnesic (sensory) aphasia does not always consist of the complete loss of memory 
of words, but very often merely of a disturbance of the firm bond of association 
between ideas and their corresponding words. Patients with sensory aphasia 
therefore very often confuse their words or form entirely false and senseless 
words (so-called paraphasia). Such a patient may talk a long while without 
conveying any idea to the listener, inasmuch as he says " brush " instead of 
" bed," or " gove " instead of " give," etc. It is a very interesting fact that in 
paraphasia the influence of certain associations are often manifest. The patient, 
for instance, utters a wrong word which has a certain resemblance in sound to 
the right one. begins with the same syllable, etc. Purely ideal associations some- 
times also play a part: thus one of our patients called a white handkerchief 
" snow," etc. 

The aphasic disturbances thus far described all refer to the power of speech — 
that is, to the uttering of ideas aloud, but we now come to the description of 
the disturbance in the understanding of speech, which is often associated with 
this or which in rare cases may occur by itself. This disturbance consists of the 
patient's inability to understand the words spoken to him, although he can 
hear them well. The word when heard no longer excites in his consciousness 
the appropriate idea. The patient is not really deaf, for he hears everything, 
but he no longer understands what he hears, and he has forgotten what the words 
signify. The vernacular sounds to him as a foreign language, of which he knows 



1080 



DISEASES OF THE NERVOUS SYSTEM 



nothing or of which he has learned but little, would to a well man. This con- 
dition is best termed, according- to Kussmaul, " word deafness " or " soul deaf- 
ness." Wernicke . also calls word deafness " sensory aphasia," which does not 
seem to us to be quite correct, since word deafness — that is, the defective under- 
standing of speech — is not identical with the inability to speak in consequence of 
the loss of ideas of • speech (amnesic or sensory aphasia in the stricter sense). 
Amnesic aphasia and word deafness are of course very often associated from allied 
reasons, but it may very well be the case that a patient has forgotten the word 
for an idea, but that he at once recognizes its significance as soon as he hears 
it. Word deafness is in a certain sense a higher degree of verbal amnesia. A 
healthy person often can not find the word for an idea in a foreign language,, 
but the idea comes to him at once if he hears the word. It is much harder to 
speak a foreign language than to understand it. 

Slighter degrees of word deafness are very often (we might say almost always) 
associated with motor aphasia. We must, however, search for them carefully, 
preferably by giving the patient certain commands (to point to certain objects 
or parts of the body, to perform certain acts), avoiding any suggestive help by 
signs or expression, and seeing whether he understands what is said and acts 
accordingly. We may also test him by holding an object in front of him and 
calling it by various wrong names and then finally giving it the correct name. 
We thus see whether the patient gives any sign of recognizing the correct name 
or not. The detection of word deafness is usually limited, however, to concrete 
nouns, certain verbs or adjectives, but it is hardly practicable to examine for 
word deafness for any other words (many abstract words, adverbs, etc.), espe- 
cially when the patient is also aphasic. We very often notice, therefore, that 
aphasic patients understand very well the usual brief questions directed to them, 
but that they are quite unable to follow with complete understanding any long 
speech, anything that is read to them, etc. They often fail to understand be- 
cause the rapidity of perception is much impaired. We have seen patients who 
understood any question or sentence only after the words had been repeated 
several times. In such patients we also see at times a decided failure of memory 
of the actual words. If we repeat to them any long sentence, they can repeat 
only the first four or five words correctly, while they have wholly forgotten the 
end of the sentence, or at best they have retained the sense but not the sound of 
the words. We can readily understand how this actual weakness of memory, 
or abnormally easy fatigue of memory, may have an inhibitory influence on the 
understanding of speech. 

The list of disturbances occurring in aphasia is by no means exhausted by the 
examination of the motor power of speech as such and of the understanding of 
words when heard. Word and idea are yet closely associated with two other 
modes of expression, which are brought about not by the ear but by the eye. We 
mean the movements of mimetic expression (or the language of signs in the ordi- 
nary sense of the word) and then the far more important written or printed 
optical signs — letters, script, numbers, etc. Here also we find the close associa- 
tions between signs and ideas on the one hand and signs and sounds on the other. 
These associations may be loosened or wholly lost, and then there follow a series 
of further morbid symptoms which are often to be observed as existing with 
aphasia. 

The disturbances of movements of mimetic expression (" amimia ") have 
not a very great practical significance, but they often show many interesting 
features. We are often surprised to see how incapable aphasic patients, who 
can not speak, are in giving expression to their thoughts, desires, etc.. by signs. 
They sometimes employ signs in a way that is quite contrary to their usual mean- 
ing. Thus we have often seen patients nod their heads when they clearly wished 



THE LOCALIZATION OF CEKEBRAL DISEASES 1081 



to deny something. The understanding of signs made by others may also be 
much diminished. 

Agraphia, the disturbance of the power of expression in writing, is far more 
important than amimia. We can also distinguish here a pure motor (ataxic) 
and an amnesic agraphia. 

By motor (ataxic) agraphia we understand, of course, not the inability to 
write on account of any paralysis of the arm, but the inability to unite the dif- 
ferent letters correctly to make up the written word. The patient is also unable 
to copy a word put before him, but he can often do this well when he can not write 
spontaneously or from dictation. Then there is writing amnesia (amnesic 
agraphia). In such cases also we often see interesting relations of association, 
since the patient may write a wrong word which in sound or idea is somewhat 
like the word desired. The entire manner of writing in such cases is often notice- 
able. The patient holds his pencil or his pen with peculiar awkwardness; he 
writes a very small hand, or the letters gradually grow smaller, etc. 

Alexia has the same relation to agraphia that word deafness has to aphasia. 
Alexia is word blindness — that is, the defective understanding of written speech, 
the inability to read. This disturbance is plainly allied to soul blindness above 
described (page 1076), but alexia may very well exist without special soul blind- 
ness, since only the association between the written signs and the corresponding 
idea has been lost. Patients with pure alexia can neither read nor copy what is 
written, but they are able to write very well spontaneously or from dictation. 
Speaking accurately, we must distinguish between reading aloud and reading to 
one's self. The printed word when seen may excite the idea, although it can not 
be pronounced aloud. On the other hand, many patients can read aloud without 
understanding what is read or pronounced. 

In conclusion we may mention briefly an interesting disturbance which is also 
closely related to aphasia — the disturbance in the power of musical expression 
\amusia~\. In these cases the most varied morbid symptoms may occur, which 
refer both to the perception and to the reproduction of musical tones. The asso- 
ciations between ideas of tone and the printed notes may be loosened or wholly 
lost. The examination of the relations existing between words and tones as they 
exist in singing is also very interesting. We have often seen aphasic patients 
who could not repeat the words of a familiar song, but who could at once utter the 
correct words plainly if they sang it. 

From all that has been said we can see how extremely manifold and in how 
many varying combinations the special symptoms of aphasia may occur. Only 
a careful and tho ough study of each individual case of aphasia will insure an 
exhaustive review of all the disturbances present. 

The Anatomical Changes occurring in Aphasia. — As has already been men- 
tioned, aphasia was the first cerebral symptom which could be referred to disease 
of any definite part of the brain. The whole " topical diagnosis " of diseases of 
the brain has therefore started from aphasia. As early as 1825 Bouillaud affirmed 
that disease of the anterior lobes of the brain is alone capable of producing dis- 
turbances of speech. In 1836 another French physician, Marc Dax, pointed out 
for the first time that only lesions of the left half of the brain cause aphasia ; and 
in 1861 Broca was able at last to declare that the " center for speech " lies in the 
left third frontal convolution (" Broca's convolution "). This law has since been 
confirmed by hundreds of autopsies, but it applies only to true motor aphasia. If 
there is motor aphasia, we may with certainty assume that there is disease of the 
posterior portion of the left third frontal convolution. It is in this region, there- 
fore, that those complicated processes of motor co-ordination which are essential 
to the utterance of a word take place. A second important and positive fact we 
owe to Wernicke : if there is, either with motor aphasia or alone, word deafness — 



1082 



DISEASES OP THE NERVOUS SYSTEM 



that is, a defective understanding of spoken language — we may from this fact 
almost always conclude that there is disease of the left upper (first) temporal 
convolution (and especially its posterior portion). In this part of the brain, then, 
is the connection between the heard word and the corresponding idea. Among 
other localizations we may mention that pronounced motor agraphia probably 
points to a lesion of the foot — that is, of the posterior portion — of the second left 
frontal convolution. Pure alexia (word blindness) has been observed especially 
in focal diseases of the left lower parietal lobe (region of the angular gyrus) and 
the neighboring parts of the occipital lobe. 

The anatomical localizations of the different forms of amnesic aphasia can 
be determined less accurately because in such cases there may be various possible 
interruptions between the various centers of perception and the speech centers 
(" conduction aphasia," " subcortical aphasia "). Since, however, the tracts lead- 
ing to the motor-speech center probably pass through the neighborhood of the 
island of Keil, we may expect that amnesic aphasia would occur most frequently 
in destruction of this region; but, from reasons that are easily understood, foci 
of disease in other situations may also give rise to such " conduction aphasias." 
As soon as amnesic aphasia is associated with defective understanding of speech 
(soul deafness), we may almost always assume a lesion in the vicinity of the 
upper temporal convolution. 

No general rules can be laid down as to the prognosis and course of aphasia, 
inasmuch as everything must of course depend upon the nature of the disease 
which excites the aphasia. In the aphasias due to cerebral haemorrhage or cere- 
bral embolism (vide infra), which are the most common, we very often observe 
that the disturbances are very marked at first, but that they gradually diminish 
or wholly disappear. On the other hand, there are also cases of almost complete 
motor aphasia, which may persist for years until the death of the patient. [When 
aphasia occurs in childhood it usually disappears completely, perhaps because the 
other hemisphere of the brain becomes educated. — K.] 

In regard to treatment we can here mention only one thing, that methodical 
training in the form of actual lessons in speaking or writing may sometimes be 
of some service. In motor aphasia we may give lessons, just as to deaf-mutes, 
by assisting the new practice of the necessary muscular movements by visual 
impressions, while in verbal amnesia methodical training of the memory is 
necessary for a new " impression " of the forgotten word. Of course all such 
training demands much tact and patience on both sides. 

[Dejerine's Views on Aphasia. — The doctrines of Dejerine and his pupils 
have acquired so much importance in the study of aphasic disturbances, and these 
doctrines differ so much from the views expressed above, that it seems advisable 
to give a brief synopsis of them. 

According to Dejerine there are only three centers for images of language : 
Broca's center, for motor images of articulation, at the foot of the left third 
frontal convolution; Wernicke's center, for auditory images of words, in the pos- 
terior part of the first and second left temporal convolutions ; and the center for 
visual images of words in the angular gyrus. These three centers form the 
" zone of language," and surround the extremity of the fissure of Sylvius like a 
horseshoe (see Fig. 173, page 1073). They are connected with one another and 
also with the adjacent sensori-motor (especially that part which contains centers 
for the lips, tongue, and larynx), visual, and auditory centers. 

The zone of language may be affected by disease in two ways: (1) The lesion 
may destroy a part of the zone or its intrinsic fibers ; or (2) it may isolate a part 
of the zone from the adjacent cortex. In the first case — aphasia from lesion of 
the zone of language, true aphasia, or cortical aphasia — internal language as a 
whole and all the forms of language will be affected to a greater or less extent, 



THE LOCALIZATION OF CEEEBRAL DISEASES 1083 



although the dominant clinical phenomena — motor aphasia, word deafness, word 
blindness — will vary with the seat of the lesion. The idea of the word is affected, 
and this gives rise to a considerable degree of mental impairment. 

In true motor aphasia from destruction of Broca's center the patient may 
utter an occasional word {vide supra, page 1079), but he is unable to do more than 
that. He has, moreover, lost the idea of the word so completely that he can 
not even indicate the number of syllables of which it is composed, and he is 
wholly unable to write spontaneously or from dictation, except that he can often 
write his name or some very familiar word. The co-existence of agraphia is 
characteristic of this form of motor aphasia. There is no marked word deafness, 
although the spontaneous evocation of auditory images is affected and the patient 
has difficulty in comprehending rapid speech. Word blindness is less marked, 
and in copying the patient will copy print as script. In true word deafness from 
destruction of Wernicke's center the patient may seem deaf, confused, or even 
demented, although the mental failure is much less than at first it appears. There 
is inability to understand what is said, and the loss of all auditory images de- 
prives the motor center of any regulator, so that the patient uses wrong words, 
or even mere jargon — paraphasia or jargonaphasia. There is usually some word 
blindness and the patient becomes unable to write, or else, on account of the loss 
of the idea of the word, he may write nonsense or jargon — jargonagraphia. 
When he copies he usually makes a servile copy, copying print as print and script 
as script. In true word blindness there is also complete agraphia, and some 
degree of word deafness and paraphasia. In these sensory forms of true aphasia 
there is less likely to be any paralysis, owing to the situation of the affected 
centers. 

When the zone of language is still intact, but when the lesion has simply 
cut off the connections of its centers with other centers, we find the condition 
which Dejerine calls pure aphasia, or sub-cortical aphasia. In these cases inter- 
nal language is unaffected, the idea of the word is retained, and there is never 
agraphia. The symptoms are referable solely to the affected center. With pure 
motor aphasia the patient can write normally and can tell the number of sylla- 
bles in a word. With pure word deafness the only symptoms are inability to 
understand what is said and to write from dictation. With pure word blindness 
there is also right homonymous hemianopsia, and the patient copies in a slavish 
manner, but there is no agraphia; he can write normally, both spontaneously and 
from dictation. In no form of pure aphasia is there any mental impairment. 
Dejerine furthermore, does not believe that there is any special writing center 
at the foot of the second left frontal convolution or anywhere else ; for there is 
agraphia in every case of lesion of the zone of language, and the agraphia is mani- 
fested not only by inability to write with either hand, but by inability to produce 
words intelligently by arranging lettered blocks or by the use of the type- 
writer. — K.] 

4. The Centrum Ovale, Internal Capsule, Central Ganglia, and Region of the 

Corpora Quadrigemina 
Centrum Ovale. — The white substance of the hemispheres is made up, so far 
as we know at present, both of commissural fibers, which connect the various 
cortical centers together, and of fibers which proceed downward from the centers 
of the cortex and connect these centers with peripheral parts of the body (corona 
radiata). As to the symptoms caused by diseases which destroy the commissural 
fibers, there is hardly anything known. We can only surmise that in case of 
disturbances of association, such as we have studied under aphasia and kindred 
disorders, we should consider lesions of commissural fibers, as of those connect- 
ing together the temporal and frontal lobes, the occipital and frontal lobes, etc. 



1084 



DISEASES OF THE NERVOUS SYSTEM 



A break in the continuity of the fibers of the corona radiata must of course result 
in the same symptoms as if the corresponding center were itself destroyed. This 
explains why circumscribed lesions of the centrum ovale, if they involve the 
motor fibers of the corona radiata, which proceed from the central convolutions 
(and only if they do this), cause hemiplegia, or, if very limited, monoplegia. 
In an analogous manner, disease of the white substance of the occipital lobe may 
entail hemianopsia; of the temporal lobe, auditory disturbances, such as word 
deafness. More than once, quite extensive disease of the white substance of the 
frontal lobe on one side has been discovered post mortem, although no symptoms 
whatever had been caused by it. Only when the coronal fibers which proceed from 
the left third frontal convolution are involved in disease is motor or ataxic 
aphasia inevitable. 

Internal Capsule. — The most important facts relating to the functions of the 
internal capsule, as far as at present known, have been already stated. In par- 
ticular, it was pointed out that through the posterior limb of the internal cap- 
sule, in a comparatively narrow space, passes the pyramidal tract on its way from 
the central convolutions to the crura cerebri (see Fig. 95, page 829). Here, 
then, even a very limited focal disease must lead to complete hemiplegia on the 
opposite side of the body. Clinical experience also shows that the largest number 
of cases of persistent hemiplegia are occasioned by disease in this spot. The 
arrangement of the fibers in this region is such that the fibers for the face are 
for the most part anterior, the fibers for the arm next, and the fibers for the leg 
posterior. In a brilliant experimental study Horsley and Beevor have shown that 
in monkeys the different motor portions of the internal capsule can be separately 
irritated in a much more exact fashion. They found in these experiments that 
the motor fibers of the internal capsule showed the following arrangement from 
before backward: opening the eyes, associated movements of the head and eyes 
to one side, tongue, angle of the mouth, shoulder, elbow, wrist, fingers, thumb, 
trunk, hip, ankle, great toe, other toes. 

The sensory tract (compare page 799, and Fig. 95, page 829) lies at the pos- 
terior extremity of the internal capsule, and apparently includes not only the 
fibers for cutaneous sensation, but also for the organs of special sense. Com- 
plete disorganization of this spot ought therefore to cause, in the opposite half 
of the body, not only anaesthesia of the skin, but also simultaneously a corre- 
sponding impairment of smell, taste, and hearing, and hemianopsia — in short, a so- 
called complete cerebral hemianesthesia. Still, in regard to this very point we 
are much in need of further and definite observations. 

Certain practical conclusions in regard to diagnosis can be deduced from the 
preceding facts. A purely motor hemiplegia, unattended by impairment of sen- 
sation, implies a lesion that does not involve the posterior portion of the internal 
capsule; but probably this portion is also affected, when there is not only pa- 
ralysis, but considerable sensory disturbance. The sensory disturbance does not 
invariably extend to all the senses; quite often there is nothing but cutaneous 
anaesthesia. 

Lesions in the neighborhood of the internal capsule may also cause symptoms 
of irritation of the tracts which pass through the internal capsule. Thus unilat- 
eral symptoms of motor irritation in particular have frequently been observed in 
the form of choreic twitchings (so-called post-hemiplegic chorea, vide infra), and 
unilateral symptoms of sensory irritation (pain, paresthesia) may also be caused 
sometimes by lesions in the vicinity of the posterior portion of the internal cap- 
sule (Edinger). 

Central Ganglia; Caudate Nucleus (Corpus Striatum proper), Lenticular 
Nucleus, and Optic Thalamus. — Before the course of the pyramidal tract had 
been accurately determined, ordinary cases of cerebral hemiplegia were almost 



THE LOCALIZATION OF CEREBRAL DISEASES 1085 



universally ascribed to lesions of the central ganglia, and in particular of the 
caudate and lenticular nuclei. At present, however, observations seem to force 
one to the conclusion that a complete hemiplegia can be produced only by a cutting 
off of the pyramidal tract. There are, indeed, numerous cases of hemiplegia pre- 
senting circumscribed disease of the central ganglia ; but they can probably all be 
explained by supposing either that the pyramidal tract, as it lies in the contiguous 
internal capsule, is directly involved in the disease, or that its functions are sus- 
pended by the indirect effects of the neighboring lesion — for instance, by the 
pressure it exercises. Accordingly, we find that circumscribed lesions of the 
central ganglia in the neighborhood of the internal capsule generally produce a 
temporary hemiplegia — that is, the paralysis gradually improves as the indirect 
influence of the focal disease upon the internal capsule ceases. Chronic and in- 
curable hemiplegia, however, if due to a lesion anywhere in this region, always 
implies an actual lesion of the pyramidal tract in the internal capsule. In regard 
to hemiansesthesia, also, the facts seem to be quite analogous. It was formerly 
held that this phenomenon was especially connected with a lesion of the optic 
thalamus, the reason being that the sensitive fibers lie so close to the thalamus 
in the posterior extremity of the internal capsule that they become themselves 
involved. 

About the symptoms which lesions of the central ganglia directly produce 
little is definitely known. The results of both clinical observation and experiment 
are quite contradictory, and in repeated instances quite extensive disorganization 
of these parts has existed without producing any symptoms to speak of during 
life. In particular, it should be borne in mind that softening may occur in the 
lenticular and caudate nuclei, and yet not a trace of hemiplegia be observable. It 
seems probable also that the optic thalamus has nothing to do with voluntary 
motion ; but apparently it has some importance for movements of mimetic expres- 
sion (Bechterew, Nothnagel). In hemiplegics we sometimes see that the lower 
half of the face on one side can not be moved voluntarily, but it is moved very 
actively in emotional expression, such as laughing or crying. In such cases we 
can decide that the thalamus is intact, while in lesion of the thalamus the con- 
trary is observed — the affected half of the face can be moved voluntarily, but 
it remains completely rigid in emotional expression. As to sensory functions, 
there is only one which the optic thalamus is certainly known to possess : the 
central termination of some fibers of the optic nerve lies in its posterior por- 
tion (the so-called pulvinar), while other fibers go to the corpus geniculatum ex- 
ternum. Destruction of the posterior part of the thalamus accordingly produces 
complete hemianopsia (vide page 1075) of the opposite side. The thalamus is also 
very probably connected with other centripetal fibers from the lemniscus, but we 
do not know positively whether these are sensory or co-ordinating fibers, and 
pathology has not yet taught us as to the functions of the thalamus in this 
regard. Focal disease of the thalamus has repeatedly occasioned post-hemiplegic 
symptoms of irritation ("post-hemiplegic chorea," vide supra), as is easily to 
be explained from the propinquity of the pyramidal tract. According to recent 
experiments, the lenticular nucleus contains centers for regulating heat. The 
striking changes in temperature sometimes seen in cerebral affections may often, 
therefore, be brought into possible relation to diseases of the lenticular nucleus, 
but accurate observations are still almost wholly lacking. 

Corpora Quadrigemina and Crura Cerebri. — Diseases of the corpora quadri- 
gemina are infrequent, and usually, when they do occur, they are merely a part 
of more extensive lesions of the brain. They are therefore very rarely considered 
from a diagnostic point of view. 

The anterior tubercles are certainly connected with the fibers of the optic 
nerve. If both of the anterior tubercles be destroyed, total blindness is inevitable, 



10S6 DISEASES OF THE NEKVOUS SYSTEM 



while if only one be disorganized, hemianopsia is to be anticipated. Still, these 
symptoms are, of course, too ambiguous ever to be regarded as pathognomonic of 
localized disease of the anterior corpora quadrigemina. Another point to be con- 
sidered, whenever the corpora quadrigemina are diseased, is the position of the 
nuclei of the nerves which preside over the motions of the eyeball, and in particu- 
lar of the oculo-motor and trochlear nerves. This explains why unilateral, or even 
bilateral, paralysis of the oculomotorius has been repeatedly observed in connec- 
tion with lesions of the corpora quadrigemina, as have also more rarely nystag- 
mus and immobility of the pupil. It is also worthy of note that in diseases in 
the region of the corpora quadrigemina, especially of the posterior corpora, ataxia 
of the body, similar to cerebellar ataxia, has been repeatedly observed (Noth- 
nagel). This ataxia is in all probability due to a disturbance of the superior 
cerebellar peduncle coming from the corpus dentatum of the cerebellum, which 
after decussating goes to the red nucleus (nucleus ruber, Eig. 86, page 798), be- 
neath the corpora quadrigemina, and is further connected with the cerebrum. If 
we have to do, therefore, with an ophthalmoplegia affecting both eyes, but not com- 
pletely symmetrical, and manifesting itself especially by symptoms of paralysis 
of the oculo-motor and trochlear nerves (more rarely the abducens), and if this 
ophthalmoplegia is associated with an uncertain, staggering gait, we must con- 
sider disease of the corpora quadrigemina. Of course a similar association of 
symptoms may also occur in tumors of the cerebellum. The posterior corpora 
quadrigemina and the median geniculate bodies are connected with the acoustic 
nerve, so that in diseases of this region we may expect disturbances of hearing. 

Should the crura cerebri become involved in the disease, the resulting symp- 
toms are often very characteristic of the locality affected ; there is paralysis of one 
side of the body (arm, leg, facial nerve), and at the same time a crossed paralysis 
(that is, one situated upon the opposite side) of the motor oculi. A glance at Eig. 
96 (page 830) will explain this phenomenon. Thus, a circumscribed lesion on the 
right side would destroy the fibers of the third nerve (III) on that side, and 
therefore produce a right-sided paralysis of the oculo-motor nerves, and at the 
same time, if extensive enough, the lesion would involve the pyramidal fibers of 
the right crus, and thus occasion left hemiplegia. That disease of the tegmentum 
would lead to sensory disturbances or sometimes ataxia may be taken for granted. 
Diseases of the tegmental region and its vicinity therefore cause a clinical pic- 
ture which is composed of hemiplegia, tactile hemiansesthesia (or hemiataxia), 
and crossed oculo-motor paralysis of the opposite side. 

5. The Cerebellum 

Quite extensive destruction of the cerebellum may take place without any 
symptoms to indicate it. In such cases, however, the disease is almost invariably 
confined to the hemispheres ; but, if the central portion or vermiform process be 
attacked to any great extent, peculiar symptoms almost always result, pointing in 
many instances with considerable certainty to disease of the cerebellum. In 
some cases, however, disease limited to the cerebellar hemispheres may cause 
pronounced cerebellar symptoms. 

There are two especially characteristic symptoms — a peculiar uncertainty of 
gait (cerebellar ataxia), and troublesome vertigo. 

Cerebellar ataxia affects the trunk and lower extremities. Both standing 
and locomotion are chiefly interfered with. When the patient is lying in bed he 
can move his legs almost as well as ever, and with normal vigor; but as soon as 
he gets up, the characteristic motor disturbances become very evident. Even 
while standing still, the whole body can usually be plainly seen to sway back and 
forth. This becomes more marked if the patient brings his heels together. If he 
stands with his legs widely apart, the trouble is less noticeable. Closing the eyes. 



THE LOCALIZATION OF CEREBRAL DISEASES 1087 



as a rule, does not aggravate the swaying, inasmuch as the cutaneous and mus- 
cular sensibility of the lower limbs remains normal in uncomplicated cerebellar 
disease. When the patient tries to walk, he sways and totters, precisely as if 
he were deeply intoxicated, but usually in a very different way from that seen in 
tabes dorsalis. Instead of the uniform stamping and pitching gait of the latter, 
cerebellar ataxia causes a real staggering of the whole body, so that in severe 
cases the patient loses entirely the ability to walk straight, but seems to fall 
forward, as it were, in a zigzag line, now to the right and now to the left. Some- 
times, but by no means invariably, it is noticed that, in walking, the body sways 
principally in one particular direction, either forward, backward, or to one 
side. Such peculiarities, however, do not enable us, with our present knowledge, 
to determine with certainty just what position in the cerebellum the lesion 
occupies. The most we can do is to surmise, in such a case, that the middle 
peduncles of the cerebellum {vide infra) are involved. It is worthy of note that, 
with few exceptions, the ataxia does not involve the upper extremities. Many a 
patient who can scarcely walk unaided is still able to perform the most delicate 
manipulations with his hands. This shows that it is only in maintaining the 
bodily equilibrium — essential to standing and locomotion — that the function 
of the cerebellum is important. 

As already stated, this cerebellar ataxia is in most cases attended with pro- 
nounced vertigo. There is not, however, a complete correspondence between the 
locomotor disturbance and the dizziness. Exceptionally one symptom may be 
present without the other. The vertigo is usually felt only when the patient 
is erect, standing or moving about, and is very seldom felt when he lies quietly 
in bed. Cerebellar vertigo is usually a true vertigo or turning sensation: the 
patient feels as if he himself or the surrounding objects were revolving. The 
feeling of vertigo may be constantly present or it may come on in severe individ- 
ual paroxysms. The cause of the vertigo is probably to be looked for in a dis- 
turbance of those tracts which go to the cerebellum through the corpus restif orme 
as a continuation of the vestibular nerve. 

Little definite is known about other symptoms of disease in the cerebellum. 
True ataxia of the legs (as in tabes) is also seen at times; but in such cases 
we usually have to do with the distant action of the disease on the tract of the 
lemniscus. The patellar reflex has sometimes been found absent in cerebellar 
disease. This symptom also is probably always dependent upon co-existing dis- 
turbances of the spinal cord. In some cases intention tremor has been found in 
the arms; in others hemiparesis of the extremities on the side of the disease 
(corresponding to the results of Luciani's experiments on animals). The signifi- 
cance of all these symptoms is still doubtful. We will return later to certain spe- 
cial symptoms, especially those occurring in tumors of the cerebellum. 

We must add in conclusion a few words about diseases of the middle cerebellar 
peduncles (crura cerebelli ad pontem). Those peculiar symptoms known as forced 
movements, and forced positions are usually referred to an irritation of these 
peduncles on the ground of physiological experiments. Forced positions are 
when the patient always lies upon one particular side in bed, whether he is per- 
fectly conscious, or in a state of complete unconsciousness. If he is put in any 
other posture, he at once involuntarily reassumes his former position. Not infre- 
quently this forced position of the trunk is accompanied by a corresponding 
forced position of the head and eyeballs, while the extremities are seldom affected- 
Genuine forced movements are seen far less often. They produce either often- 
repeated rotations of the body on its longitudinal axis, or, if the patient be able 
to walk at all, involuntary circular movements ("circus movements ")> etc. Ac- 
cording to the statements of Russell, the forced movements in disease of the right 
middle cerebellar peduncle are in the direction " of a corkscrew screwed into a 



1088 



DISEASES OF THE NEEVOUS SYSTEM 



cork," and, in disease of the left peduncle, the direction " of a corkscrew screwed 
out of a cork." It must be said, however, that the symptoms of forced positions 
and forced movements are on the whole rare and of doubtful value in diagnosis ; 
for in some cases of cerebral disease the same symptoms have been observed with- 
out any discoverable affection of the middle cerebellar peduncle. On the other 
hand, in two cases of tumor of the middle cerebellar peduncle with autopsy we 
failed to find any forced movements. 



Eor convenient reference we subjoin a summary of the most important facts 
bearing- upon the localization of cerebral diseases. 

1. The most frequent cause of ordinary hemiplegia is a lesion of the pyramidal 
tract in the posterior limb of the internal capsule. If the hemiplegia be persist- 
ent, then this tract is actually destroyed; if temporary, the tract has been func- 
tionally deranged for a time by focal disease in neighboring parts of the brain. 

2. Monoplegia cerebral paralysis is usually due to affections of the cortex of 
the brain — that is, the central convolutions and the paracentral lobule. Mono- 
plegia of the face and tongue is the result of lesions in the lower extremity of the 
anterior central convolutions. Monoplegia of the arm is referable principally to 
some lesion of the middle third of the anterior central convolutions. Monoplegia 
of the lower extremity implies some affection of the upper portion of the anterior 
central convolutions and the paracentral lobule. 

3. Hemiplegia or monoplegia, if associated with epileptiform convulsions 
affecting either one half or one particular portion of the body, are almost always 
caused by cortical lesions. These same symptoms of motor irritation without 
accompanying paralysis are likewise to be ascribed to some irritation of the above- 
mentioned regions of the cortex. 

4. Hemiplegia with crossed paralysis of the oculo-motor nerve indicates a 
lesion of the crus cerebri. Co-existing tactile hemianesthesia implies that the 
tegmentum is involved. 

5. Hemiplegia with crossed facial paralysis implies, with great certainty, that 
the lesion is situated in the pons. 

6. Post-hemiplegic chorea {vide infra) seems to occur especially when there 
is focal disease in the neighborhood of the posterior part of the internal capsule. 

7. Hemiansesthesia of the skin and of the organs of special sense, associated 
with hemianopsia, is due chiefly to lesions of the most posterior portion of the 
internal capsule. 

8. Hemianopsia may be due to a lesion of the occipital lobe (cuneus). Prob- 
ably, also, a lesion of the posterior extremity of the internal capsule may cause it, 
in which case it is usually associated with hemiansesthesia. Finally, it may be 
produced by affections of the pulvinar of the optic thalamus, of one lateral genicu- 
late body, of one of the anterior corpora quadrigemina, or of one of the optic 
tracts. 

9. Genuine motor aphasia indicates disease of the foot of the third left frontal 
convolution. 

10. Word deafness (loss of understanding of speech) is due to disease of the 
first left temporal convolution ; word blindness (loss of understanding of writing) 
is due to disease of the left lower parietal lobe (angular gyrus). 

11. Difficulty in articulation implies disease of the medulla, as does also dys- 
phagia. 

12. Staggering gait and vertigo are the most constant symptoms of cerebellar 
disease, but they may also occur in diseases of the corpora quadrigemina and of 
the frontal lobe (vide supra). Forced positions and forced movements perhaps in- 
dicate lesions of the crura cerebelli ad pontem. 



CEEEBEAL HiEMOBBHAGE 



1089 



As an appendix, we may add a very brief review of the course of the most im- 
portant conducting tracts : 

1. Chief Motor Tract. — (a) First central neurone: Ganglion-cells in the 
motor cortex of the brain, axis-cylinder processes through the corona radiata, pos- 
terior limb of the internal capsule, crusta of the crus cerebri, decussation in the 
pyramids, postero-lateral column of the spinal cord, terminal arborization in the 
anterior horns (for the motor cranial nerves previously in their nuclei). (b) 
Second peripheral neurone: Ganglion-cells in the anterior horns (or in the nuclei 
of the motor cranial nerves), axis-cylinder processes in the anterior root and the 
peripheral nerve, terminal arborization in the muscular fibers. 

2. Chief Centripetal (Sensory and Co-ordinating) Tract. — (a) First (periph- 
eral) neurone: Ganglion-cells in the spinal ganglion, axis-cylinder processes 
partly in the peripheral sensory nerve [modified protoplasmic processes], partly 
in the posterior root; terminal arborization, partly in the posterior horns (sen- 
sory fibers), partly, after passing through the posterior columns of the cord, in 
the nuclei of the columns of Goll and Burdach (co-ordinating fibers), (b) Second 
neurone : Ganglion-cells in the posterior horns or in the nuclei of the columns of 
Goll and Burdach, axis-cylinder processes through the antero-lateral columns, 
inter-olivary layer, lemniscus tract of the medulla and pons, tegmentum of the 
crus cerebri, posterior portion of the internal capsule. Terminal arborization 
in part in the optic thalamus, (c) Third neurone: Ganglion-cells in the optic 
thalamus, axis-cylinder processes to the cerebral cortex (central convolutions, 
parietal lobe). 

3. Chief Optic Tract. — Eirst peripheral neurones lie wholly in the retina, and 
the ganglion-cells of the second neurones are also in the retina, axis-cylinder pro- 
cesses through the nerve and optic tract (partial decussation!) to the lateral 
geniculate body, the anterior corpora quadrigemina, and the pulvinar of the 
optic thalamus, where the terminal arborization takes place. Third neurones 
from the cells of the parts mentioned through the posterior portion of the inter- 
nal capsule [and the optic radiations of Gratiolet] to the cortex of the occipital 
lobe. 

4. Chief Acoustic Tract. — The ganglion-cells of the peripheral neurone lie in 
the cochlear ganglion of the cochlea, the axis-cylinder processes in the cochlear 
nerve, termination in the ventral acoustic nucleus. Here the second neurone 
begins, whose axis-cylinder process goes in the trapezoid body and the strise acous- 
ticse (?), and then in the lateral lemniscus to the posterior corpora quadrigemina 
and the median geniculate body. Here probably a third neurone begins, which 
ends mainly in the cortex of the temporal lobe. The acoustic fibers also run partly 
crossed and partly uncrossed, so that each auditory nerve is connected with both 
hemispheres. 



CHAPTEE III 
CEREBRAL HEMORRHAGE 

etiology. — The cause of cerebral hemorrhage should always be "sought in 
some disease of the coats of the minute cerebral arteries. Cerebral hemorrhage 
occurs most frequently, therefore, in persons who suffer from general arterio- 
sclerosis, and especially from arterio-sclerosis of the cerebral arteries ; but other 
forms of disease of the walls of the blood-vessels, fatty and hyaline degeneration, 
and, in particular, syphilitic endarteritis, may give rise to cerebral haemorrhage. 
In 1868 it was first shown by Charcot and Bouchard that in many cases of large 
69 



1090 



DISEASES OF THE KEKVOUS SYSTEM 



cerebral haemorrhage there are miliary aneurisms of the small atheromatous arter- 
ies of the brain substance, some one of which has burst and allowed the blood to 
escape. All later investigators have confirmed their statements about the occur- 
rence and importance of these miliary aneurisms. The aneurisms may attain a 
diameter of a millimetre or more. They usually appear like spindle-shaped dilata- 
tions of the entire circumference of the vessel, although sometimes the bulging is 
confined to one side of it. Inasmuch as the intra-cerebral arteries possess almost 
no true adventitia, it is easy to see that these vessels are especially predisposed to 
aneurismal dilatation (especially in the form of a so-called dissecting aneurism) .. 

Most of the circumstances which come under our consideration as favoring 
the development of cerebral haemorrhage have also a close relation to arterio- 
sclerosis. Age plays a specially important part. Although exceptionally a 
younger individual may be attacked, the majority of sufferers are over fifty years 
old — that is, at the time of life when arterio-sclerosis usually becomes most fully 
developed. Again, cerebral haemorrhage is decidedly more frequent in men than 
in women, which is also true of atheroma. Alcoholism, syphilis, and gout are also 
reckoned among the aetiological factors of both disorders, and in both a hereditary 
predisposition is not very rarely demonstrable. What is called the " apoplectic 
habit " also deserves brief mention. Although there is no variety of constitution 
which exempts its possessor from the possibility of cerebral haemorrhage, yet it 
can not be denied that often the victims of apoplexy do exhibit a certain " habit." 
Such persons are not very tall, but are corpulent, broad-chested, with a short, 
thick neck and round face ; and they have not been disinclined to the pleasures 
of the table and the bottle. Such persons often suffer at the same time from 
emphysema, moderate hypertrophy of the heart, and general arterio-sclerosis, as 
the condition of the radial and temporal arteries may disclose even during life. 

Granting, therefore, that disease of the arteries, and sometimes more particu- 
larly miliary aneurisms resulting from chronic endarteritis of the smaller cere- 
bral arteries, must be regarded as the chief cause of cerebral haemorrhage, then, 
on the other hand, the question suggests itself whether an abnormal elevation of 
the blood-pressure may not have some part in determining the haemorrhage. If 
the coats of the arteries be normal the greatest increase of pressure would not 
be able to cause rupture of the vessels ; but if the wall of the artery is diseased, 
or if aneurisms have already been developed, then there can be no doubt that a 
persistent or even a temporary elevation of the blood-pressure must favor the 
bursting of the vessels. In this sense a cerebral haemorrhage, occurring in pa- 
tients with certain forms of cardiac hypertrophy (contracted kidney, idiopathic 
hypertrophy, etc.), combined with disease of the vessels, may be referred in part 
to the increased arterial tension ; but it is most of all with regard to many excit- 
ing causes, which are immediately followed by a cerebral haemorrhage, that in- 
creased blood-pressure assumes great importance. Here it is temporary. Cere- 
bral haemorrhage may, for example, follow excessive muscular exertion, the inges- 
tion of a large amount of food, indulgence in alcohol, taking a cold bath, violent 
mental excitement, etc. An apparently slight injury is especially to be consid- 
ered. In all such cases, however, the change in the arteries is a necessary pre- 
requisite. 

It should be mentioned, in conclusion, that cerebral haemorrhage is sometimes 
merely the expression of a general haemorrhagic diathesis, as we find it in 
leukaemia, pernicious anaemia, and those affections which are called, in a stricter 
sense, haemorrhagic diseases, such as scurvy and purpura haemorrhagica. The 
grave infectious diseases, including septicaemia, typhus or typhoid fever, and 
small-pox, may occasion haemorrhage into the brain as well as into other organs. 
The haemorrhages are generally, however, from capillary vessels, and are very 
rarely extensive. 



CEREBRAL HEMORRHAGE 



1091 



Pathology. — Arterio-sclerosis and miliary aneurisms do not develop in all the 
cerebral arteries with equal frequency, and accordingly we find certain regions 
particularly liable to cerebral haemorrhage, being very much oftener affected by 
it than others. These regions seem also to be the ones where the arterial blood- 
pressure is relatively the highest." Haemorrhage takes place by far the most 
frequently from the branches of the artery of the fissure of Sylvius. The large 
central ganglia in the neighborhood of the lateral ventricles, the optic thalamus, 
caudate and lenticular nuclei, and also the adjacent white matter of the internal 
capsule and centrum ovale, are therefore usually affected by the haemorrhage. 
Haemorrhages in other portions of the brain are much less frequent — such as 
haemorrhages into the convolutions, the pons, the cerebellum, the crura cerebri, or 
the medulla. If the blood escapes into the neighborhood of a ventricle, it may 
burst into the latter. Likewise, in rare instances, an effusion of blood in the 
cortex may make its way out upon the surface of the brain. 

An extensive collection of blood in one of the hemispheres may exercise so 
decided a pressure upon surrounding parts that the results of increased tension 
upon the affected side are at once recognized when the skull is opened. The dura 
on that side is more tightly stretched, the f alx is crowded over to the opposite side, 
the convolutions on the convexity seem flattened, and the furrows are shallow. 
Exceptionally, when there is a very large effusion reaching nearly to the surface, 
we may even detect fluctuation. 

On cutting through the brain-substance we find the seat of haemorrhage, and 
are enabled to determine its position and extent. Its size, of course, varies con- 
siderably in different cases ; it may be small, or it may occupy a large part of an 
entire hemisphere. The wall of the effused mass is made up of ragged and torn 
cerebral tissue, and the mass itself contains debris of the nervous elements entan- 
gled in the coagulated blood. The blood-clots are almost always very dark-colored 
when fresh. Later on, the mass changes to a chocolate-colored or more brownish- 
yellow pulp, composed of the disintegrated remnants of the nervous substance 
and the clotted blood. The microscope reveals, particularly in the immediately 
surrounding tissues, numerous fatty granular cells. These are white blood- 
corpuscles which have absorbed the fat resulting from the decomposition of the 
myeline substance. There is also always an abundance of haematoidine crystals, 
due to the disintegration of the red blood-globules. At a greater distance from the 
effusion the tissues present a yellowish tinge, from the imbibition of such blood- 
pigment as has reached them in a state of solution ; and there is also usually an 
oedematous softening of the parts not too far removed from the haemorrhagic focus. 

If the patient survive, the mass is gradually absorbed. It slowly diminishes 
in size, and the surrounding parts tend to reassume their normal relations. The 
final result in many cases is a cavity filled with serous fluid and bounded by 
smooth walls. This " apoplectic cyst " remains stationary. In some instances, 
however, and particularly if the effusion be rather small, the walls approach each 
other as more and more of the fluid is absorbed ; there is a great hyperplasia of 
connective tissue; and so, finally, there is nothing left but a so-called apoplectic 
scar, usually of a yellow color, due to vestiges of the blood-pigment. The position 
and dimensions of the permanent lesion determine, of course, the question of sec- 
ondary descending degeneration (vide page 1033), as well as the nature and extent 
of the persistent clinical symptoms. 

Clinical History. — The symptoms of cerebral haemorrhage agree closely with 
the anatomical lesions just described. The vascular disease responsible for the 



[* Mendel has found that the normal blood-pressure in the lenticulo-striate arteries, which are 
most prone to rupture, is much higher than it is in the cortical and many other small arteries of the 
brain.— K.] 



1092 



DISEASES OF THE XEKYOUS SYSTEM 



haemorrhage (arterio-sclerosis, miliary aneurisms) in many cases excites no mor- 
bid symptoms; but, on the other hand, we often find that persons attacked by a 
cerebral haemorrhage have suffered much from vertigo, headache, etc., for more or 
less time before the shock. Such symptoms are undoubtedly due to the disease of 
the cerebral blood-vessels and to the slight disturbances of the circulation thus 
produced. 

As soon as the vessel wall or an aneurism bursts, however, and blood escapes 
into any part of the brain-substance, there is immediately seen a group of grave 
cerebral symptoms, collectively termed an apoplectic attack, or " shock." As the 
blood escapes under a pressure nearly equal to the general arterial pressure, and 
doubtless much greater than that to which the soft substance of the brain is nor- 
mally exposed, the affected portion of the brain is at once subjected to a consid- 
erable increase of tension, which is transmitted for various distances in all direc- 
tions. It need not be said that the destructive influence of the haemorrhage, which 
is probably manifested by a compression of the nervous tissue itself and also 
more especially by a compression of the blood and lymph channels and a conse- 
quent disturbance of the circulation, may vary exceedingly, and that therefore 
the symptoms are by no means equally severe in all cases. The larger the rent 
in the blood-vessel, and the more rapid and abundant the consequent haemorrhage, 
the worse is the apoplectic attack. Bleeding from larger vessels is therefore usu- 
ally attended by graver symptoms than from the minute arterial twigs. An ex- 
tensive cerebral haemorrhage sometimes causes the patient to fall down suddenly 
in complete unconsciousness, while smaller haemorrhages may occasion only a 
temporary attack of vertigo and slight cloudiness of intellect. If the tear in the 
wall of the artery be very small and narrow, permitting the blood to escape but 
slowly, then there may be no sudden attack at all, the phenomena requiring a cer- 
tain length of time for their development. 

There is also an important relation between the location of the haemorrhage 
and the severity of the apoplectic attack. The chief symptom of these cases is 
loss of consciousness (about which we shall soon speak at length) ; and as this 
is certainly due to an interruption of the functional activity of the cerebral 
cortex, it is plain that the nearer the cortex is to the haemorrhagic focus, the 
more apt are the symptoms to be serious. It is confirmatory of this that haemor- 
rhage into the more deeply situated portions of the brain, the crura cerebri 
or the pons, quite often occasions comparatively slight symptoms. But there 
is a fact about the circulation in the brain that often causes the shock from 
haemorrhage into the brain-stem to be greater than the shock following haemor- 
rhage into the cortex or the white substance of the hemispheres. This fact 
is that the brain-stem has comparatively much larger arteries than the other 
parts just mentioned, which contain only minute blood-vessels. Furthermore, as 
Duret and Heubner have shown, the blood-vessels are so distributed that the 
arterial tension in the brain-stem is not a little higher than in the other portions. 
This renders intelligible the clinical phenomenon that haemorrhages in the terri- 
tory of the main arteries, besides being, as we have said, the most frequent of any. 
produce apoplectic symptoms even when the effusion is comparatively small; 
while sometimes haemorrhages of about the same size in the cortex or white sub- 
stance may not be noticed. 

The clinical phenomena of the apoplectic attack will now be considered in 
detail. The onset is sometimes absolutely without warning, but in other cases it 
is preceded for a greater or less length of time by certain prodromata. These are 
either the result of the disturbance of circulation caused by the disease of the 
blood-vessels in the brain, and then, as already stated, they comprise occasional 
headache, vertigo, tinnitus aurium. spots before the eyes, languor, and muscular 
weakness ; or they are caused by minute haemorrhages, which seem not infre- 



CEEEBEAE ILEMOEEHAGE 



1093 



quently to precede a greater one. In such a case, the friends state that of late 
the patient has had one or more slight and brief attacks, characterized by faint- 
ness, temporary trouble in speaking, sudden but temporary weakness of an arm 
or leg, and similar symptoms. The prodromata may extend over several days 
or even weeks and months preceding the severe attack. 

In other cases there are no such premonitory symptoms. The apoplexy occurs 
unexpectedly and suddenly. In the midst of apparently vigorous health the 
patient sinks down " as if he had been struck.'' In still other cases there are 
indeed no prodromata, but the symptoms do not at first appear in all their sever- 
ity, and occupy some hours or even a whole day in their gradual development. 
This is due to a slow and gradually increasing haemorrhage, and is termed a slow 
or delayed apoplectic attack. The patient grows confused, anxious, and delirious 
(a case of our own had pronounced hallucinations of sight) ; the arm and leg on 
one side become paretic, and gradually more and more completely paralyzed; and 
after a few hours complete unconsciousness comes on. 

The attack may be rapidly fatal. In such cases the abnormal pressure prob- 
ably involves the medulla oblongata and paralyzes the cardiac and respiratory 
centers there situated. Usually, however, there is merely a complete loss of con- 
sciousness, more or less rapidly developed. Sometimes the patient has time to 
lie down. He usually sinks back in his chair or falls to the floor, and becomes 
deeply comatose. The face is often noticeably flushed, and the pulse full and 
tense, but not infrequently somewhat slow, because of the increased cerebral 
pressure. The respirations are deep, noisy, stertorous, and likewise often slow. 
The relaxed cheeks and lips are often drawn deeply in at every inspiration, and 
puffed out at every expiration. The temperature is usually subnormal at first, 
later regaining the normal, or even a higher point. In a rapidly fatal case, how- 
ever, the temperature remains depressed till death. It is not very rare in severe 
cases to observe a peculiar position of the head and eyes, both being turned in the 
same direction. This phenomenon is termed by Prevost conjugate deviation 
(deviation conjuguee) of the eyes and head. It is generally temporary, and is 
said by Landouzy to be connected principally with a lesion of the lower parietal 
lobule (see also page 1075). There is no perfectly constant relation between the 
lateral deviation and the half of the brain affected. The most common condition 
is that the eyes are directed toward the affected hemisphere, and so to a certain 
extent " look toward the lesion " and away from the paralyzed side of the body. 
The pupils present no constant peculiarities. Often they are of normal size. In 
other cases they are contracted, dilated, or unequal. Xo definite diagnostic con- 
clusions can be drawn from them. In the worst cases the pupils will not react to 
light ; in other cases they react, but often sluggishly. 

During the deep apoplectic coma the extremities generally lie completely 
motionless and limp. In the worst cases reflex action is wholly suspended; but 
sometimes the vigorous thrust of a pin or the pinching of the skin will excite an 
occasional slow reflex twitch, or a motion as if to ward off the tormentor. 
Whether the apoplexy has caused hemiplegia at all, and if so in what place, can 
not always be easily determined during the initial coma. Still, it is often to be 
observed, even now, that one angle of the mouth hangs down lower than the 
other, and that the corresponding cheek is more puffed out during expiration 
than is the other; that the extremities of one side are much heavier and fall 
much more limply than those on the opposite side of the body, and that the reflex 
action and defensive movements are almost absent upon one side (the paralyzed 
side), while they can be clearly demonstrated on the other. 

In contrast to the usual laxness of the arms and legs during the apoplectic 
coma is the tonic rigidity sometimes seen in the extremities, particularly 
on the side opposite to the haemorrhage. This symptom seems to be especially, 



1094: 



DISEASES OF THE NERVOUS SYSTEM 



although, not exclusively, connected with a bursting of the escaping blood 
into a lateral ventricle. It is rather exceptional for cerebral haemorrhage to 
be attended with general or unilateral epileptiform convulsions— a symptom 
which, as we have seen, is referable to irritation of the motor regions of the 
cortex. 

It should be mentioned that in many cases of cerebral haemorrhage the urine 
passed after the attack has been found to contain small amounts of albumen or 
sugar. This symptom is usually ascribed to compression of the medulla from the 
effusion. There is usually retention of urine; in other cases there is involun- 
tary micturition. 

A certain number of patients never awake from the initial coma. Death may 
not be immediate, but they remain completely unconscious ; the respirations 
become more rapid and irregular (sometimes of the Cheyne-Stokes character), 
and there is a rattling in the throat, because mucus and saliva run down into it ; 
the pulse, which was at first retarded, now becomes accelerated; the face grows 
paler and more and more sunken ; the eyes are deep in their sockets ; the cornea 
becomes opaque; and at last, after the coma has lasted some hours, or even 
one or two days, death occurs, often attended by a considerable rise in tem- 
perature. 

This termination is, however, by no means the usual one. More frequently 
the patient survives the attack. The bleeding ceases, the clot contracts, and 
begins to be disintegrated and absorbed. At the same time the pressure exerted 
upon surrounding parts grows less and less, the more distant parts of the brain 
gradually recover from the shock, and consciousness slowly returns. The patient 
begins to open his eyes when he is spoken to in a loud tone ; he raises his hand to 
his head, sighs, and yawns ; gradually the intellect clears up, he tries to talk, or 
to express himself by signs ; memory returns, and he recognizes those about him 
once more. Exceptionally, recovery is interrupted by a fresh and perhaps a 
fatal relapse. This may result from a renewal of the haemorrhage. Generally, 
however, improvement persists, the patient fully regains his consciousness at the 
end of a few days, and it now becomes possible for the first time to " estimate the 
damage." 

The symptoms thus far described belong to severe apoplectic attacks. There 
are also, as we have said, cases of all degrees of mildness, as regards the first onset. 
In these there is no deep and persistent coma. The patient loses consciousness 
only temporarily, if at all. He is seized with vertigo, or with sudden headache, 
and is for a time stupefied. Nausea and vomiting are of frequent occurrence, 
just as in ordinary syncope. Yet cases presenting these comparatively slight 
early symptoms, and with few even of these, may exhibit the genuine focal symp- 
toms referable to the haemorrhage, such as hemiplegia, in all their severity. These 
latter phenomena must now be considered. 

We term the symptoms of loss of function directly dependent upon the destruc- 
tion of a definite portion of the brain the direct focal symptoms of cerebral haem- 
orrhage. Where the haemorrhage takes place we have seen tjiat a larger or smaller 
extent of the brain-substance is completely destroyed by the sudden and forcible 
escape of the blood. The dimensions of this lesion are represented later by the 
apoplectic scar or cyst, and its position by the nature and extent of the persistent, 
and for the most part irreparable, loss of function (Ausfallserscheinungen). But 
there are, in addition to these direct symptoms, other indirect focal symptoms, 
which outlast the apoplectic shock, and vary with the locality of the haemorrhage. 
These do not, however, correspond to the territory actually destroyed. They are 
due to the influence exerted for a certain length of time by the haemorrhagic focus 
upon the immediate surrounding structures. The pressure of the effusion, the 
disturbance of circulation resulting from it, the collateral oedema, and perhaps 



CEREBRAL HEMORRHAGE 



1095 



also the imbibition of the soluble products of disintegration of the apoplectic 
focus, are the chief factors in exciting these indirect symptoms. They do, indeed, 
outlast the initial shock, but are nevertheless temporary, vanishing sooner or 
later, at the end of several days or weeks, or even months. If the apoplectic shock 
is over and if the symptoms still exhibited have been minutely determined, yet we 
are unable to say, at first, whether the existing focal symptoms are direct or indi- 
rect. We can decide about this only after 
further observation. If the early symptoms 
disappear within the next few days or weeks, 
or after the first two or three months, we 
<3an then affirm, retrospectively, that they 
were indirect. Such as outlast the first six 
months are to be regarded as direct, and as 
not destined to improve much. Erom a 
practical point of view this distinction is of 
extreme importance. We shall revert to the 
subject when considering the course of cere- 
bral apoplexy. 

A minute description of all the focal 
symptoms which might occur after cerebral 
haemorrhage, and of the light thus thrown 
upon the location of the haemorrhage, need 
not be attempted here, for it would neces- 
sitate a repetition of all the facts enumer- 
ated in the preceding chapter. It is only 
requisite to describe, in detail, the chief 
and by far the most frequent results of a 
-cerebral haemorrhage — ordinary cerebral 
hemiplegia (see Eig. 175). 

It has been mentioned that most of 
these haemorrhages occur near the lateral 
ventricles. Hence, in a majority of in- 
stances, the motor pyramidal tract, as it tra- 
verses the internal capsule, is either direct- 
ly destroyed or at least indirectly affected. 
Consequently, most patients who survive the 
apoplectic shock present a paralysis of that 
half of the body which is opposite the seat 
of haemorrhage. On minute examination 
we usually find, in the first place, that even 
in the distribution of the facial nerves there 
is a distinct difference between the two 
sides, the lower division of the facial 
(which supplies the muscles of the cheek, 
nose, and mouth) being evidently para- 
lyzed on one side, while its upper division (going to the eyes and forehead) 
is entirely, or almost entirely, intact. The forehead can be wrinkled on one 
side as well as on the other, or only a little less on the paralyzed side than 
on the sound side ; but if the patient tries to dilate his nostrils, or alter the 
shape of his mouth, or whistle, or blow, or talk, etc., the paralysis becomes evi- 
dent. Often, indeed, while the face is quiet, it can be noticed that one naso- 
labial fold is obliterated, or that one corner of the mouth droops. It is an in- 
teresting fact that the paresis of the lower division of the facial is much more 
noticeable during voluntary efforts, as in showing the teeth, than when the patient 




Fig. 175.— Patient with right hemiplegia. 
(Personal observation.) 



1096 



DISEASES OE THE NERVOUS SYSTEM 



smiles involuntarily. A patient will sometimes try in vain to draw back the cor- 
ner of his mouth, then begin to laugh at his own awkwardness, and thereupon 
open his mouth in an almost perfectly normal manner. We have seen above, in 
the chapter on cerebral localization, that this condition can probably be explained 
by the relation of the optic thalamus to the movements of mimetic expression. 
The difference in the behavior of the upper and the lower part of the face in cere- 
bral hemiplegia is probably connected with the fact that the muscles supplied by 
the upper division (frontalis, corrugator supercilii, and to a certain extent the 
orbicularis) are very seldom exercised upon one side alone, but always bilaterally. 
Perhaps both sides receive nervous fibers from each cerebral hemisphere, so that, 
if a single center be intact, it alone answers for the muscles on both sides.* In the 
distribution of the lower division of the facial, also, ordinary cases of cerebral 
hemiplegia present almost always a more or less marked paresis, and only excep- 
tionally a complete paralysis. 

There is quite often a slight impairment of the hypoglossus in addition to the 
paresis of the facial nerve. If the patient puts out his tongue, its tip deviates 
toward the paralyzed side. This is a result of paresis of one of the genio-hyo- 
glossi. When both these muscles contract, they may be said to push the tongue 
forward. If this thrust be more vigorous on one (the healthy) side, the tongue is 
deflected toward the other (paralyzed) side. In ordinary cerebral hemiplegia this 
is almost always the sole way in which the movements of the tongue can be seen 
to be impaired. Sometimes, however, the slight paresis of half of the tongue, 
combined with the facial paresis, entails a noticeable difficulty in articulation. 
This, to be sure, is only exceptionally great, and is often appreciated by the 
patient alone, who is conscious that an effort is required in order to speak. 

The soft palate is rarely much affected. It may, however, hang rather lower 
down on the paralyzed than on the affected side, and move less. The uvula is 
inclined sometimes toward the healthy and sometimes toward the paralyzed side. 
There are no special disturbances of function as a result of these changes. 

The trapezius is the only muscle of the trunk which is ordinarily much 
affected in cerebral hemiplegia. As a result of the paresis of this muscle, the 
shoulder sags and it can not be raised as high as on the normal side. If the pa- 
tient tries to take a very deep breath, it is in some cases possible to see that the 
paralyzed side lags behind a little in respiration, which is due to a paresis of the 
respiratory muscles on that side. It is perhaps due to this that the pulmonary 
diseases which attack hemiplegic patients frequently develop in the lung on the 
affected side, where respiration is deficient. 

The most important element in the hemiplegia is the paralysis of the extrem- 
ities. Immediately after the haemorrhage it is often so complete that even the 
slightest voluntary motion in the affected arm and leg is impossible. Other cases, 
however, exhibit only a more or less severe paresis (hemiparesis) from the first; 
or the complete paralysis at any rate is confined to certain groups of muscles, the 
others still retaining vestiges of their normal contractility. Even when there is 
total hemiplegia at first some of the muscles almost always regain a certain 
amount of their old power later on (vide infra). 

The behavior of the reflexes is comparatively constant in nearly all cases of 
cerebral hemiplegia. In general the rule is that the tendon reflexes are increased 
on the paralyzed side, but that the skin reflexes are diminished. The increase of 

* There is a remarkable general rule which should be mentioned here, and which is perhaps to be 
explained in the same way, namely, that those muscles which are usually called into play in pairs are 
never completely paralyzed in cerebral hemiplegia. Furthermore, it is impossible for us to contract 
most of these singly, on one side alone, or at least not without special practice ; this applies, for 
instance, to the corrugator supercilii, the frontalis, the motores oculi, and the muscles of mastication 
and respiration. 



CEREBRAL HAEMORRHAGE 



1097 



the tendon reflexes is an almost constant symptom. Only when the symptoms of 
the initial shock are very severe, there may at first be no tendon reflexes whatever. 
In all cases of any duration they are, with few exceptions, exaggerated, and usu- 
ally very much so. In the arm we find very lively periosteal reflexes on tapping 
the lower end of the radius and the ulna (see page 840), also on striking the ten- 
dons of the biceps and triceps, the clavicle, etc. In the leg the increase of the 
patellar reflex is most noticeable ; but there is often a lively Achilles reflex also, 
an increase of the adductor reflexes, etc. This increase of the tendon reflexes is 
by no means limited to the affected side ; it can almost always be detected on the 
sound side also, although to a lesser degree. Many have expressed the opinion 
that the increased tendon reflex upon the paralyzed side is a result of the sec- 
ondary degeneration of the pyramidal tracts in the spinal cord. In our judgment 
this view is entirely unfounded, inasmuch as the exaggeration of the tendon reflex 
often appears within a few days, or even a few hours, after the apoplectic attack — 
that is, before a secondary degeneration in the spinal cord is to be thought of. We 
would rather seek to explain the phenomenon as being due to the suspension of 
certain reflex inhibitory influences because of the cerebral lesion. 

There is very often found, particularly in cases of long standing affected with 
well-marked contractures, an increase of " direct mechanical excitability " in the 
paralyzed muscles, such that a tap upon them causes them to contract vigorously. 
We are of the opinion that a part of these contractions are of reflex origin and are 
due to the mechanical irritation of the fascia of the muscles (fascial reflex). 
There is also the direct mechanical irritation of the nerves of the muscles. 

The skin reflexes in hemiplegia behave in precisely the opposite way from the 
tendon reflexes, being almost invariably decidedly diminished on the paralyzed 
side. In the paralyzed arm it is usually impossible to excite any skin reflex what- 
ever; and in the corresponding leg there is either no, or at any rate a greatly 
diminished reflex. The difference in certain other skin reflexes, especially the 
abdominal and cremaster reflexes (page 839) is still more evident than in the 
plantar reflex. [The plantar reflex, however, is often manifested by extension of 
the great toe — the Babinski reflex. — K.] These reflexes are almost always much 
diminished or wholly absent on the paralyzed side, while they can be elicited on 
the sound side in normal strength, a distinction which is not infrequently of 
service in determining the seat of the hemiplegia when the patient is stupid or 
even quite unconscious. There is often a marked difference in the conjunctival 
reflex also. On the paralyzed side we can touch the eyeball with the finger or the 
head of a pin without causing an immediate reflex closure of the eye, as is the 
case on the healthy side. It is not easy to explain the striking behavior of all the 
skin reflexes in cerebral hemiplegia, especially the peculiar contrast between them 
and the tendon reflexes. It is ordinarily assumed that certain inhibitory influ- 
ences for the tendon reflexes are lost through the cerebral disease, while the 
inhibition of the skin reflexes is, on the contrary, put into a state of irritation. 
This explanation is evidently forced and unsatisfactory, and thus the suspicion is 
not wholly unwarranted that these skin reflexes, contrary to the physiological 
theories thus far generally accepted, have their reflex arcs not in the spinal cord, 
but much higher up in the brain. The absence of certain skin reflexes in cerebral 
hemiplegia is accordingly due to a direct injury of the reflex path. Of course it 
must be emphasized that further studies upon this important point are extremely 
necessary. 

Sensation is but little impaired in most cases of cerebral hemiplegia, but on 
careful examination we often find a decided blunting of sensibility for simple 
contact, although the sensibility to pain and temperature and the muscular sense 
are retained. Slight paresthesia is not infrequently complained of on the affected 
side, especially at first. Pain in the paralyzed parts is not uncommon. It is often 



1098 



DISEASES OF THE NERVOUS SYSTEM! 



to be referred to special peripheral conditions (contractures, etc.)? but sometimes 
there is apparently an irritation of the central sensory tracts (Edinger). Any 
marked disturbance of sensation indicates, as has been seen (compare page 1084), 
that the posterior extremity of the internal capsule is involved. Such cases are 
rare. In them we may observe a complete cerebral hemianassthesia combined with 
the hemiplegia. According to Gowers, a temporary hemianopsia is often present 
directly after the occurrence of a cerebral haemorrhage. We have seen the initial 
hemianopsia combined "with associated paralysis of the ocular muscles. It is also 
not uncommon to find hemiplegia associated with permanent hemianopsia ; but as 
yet little is known about the pathological anatomy of such cases. The most likely 
thing would seem to be some lesion of the fibers of the optic nerve in the internal 
capsule or in the pulvinar of the optic thalamus. The muscular sense is not usu- 
ally affected in hemiplegia. [The stereognostic sense (vide page 795) is not in- 
frequently affected. — K.] 

Turning now to the further course of hemiplegia, we find a new group of im- 
portant symptoms. First of all should be considered the changes in the paralyzed 
muscles. If the hemiplegia be incomplete, even from the start, almost the normal 
degree of motility may in a comparatively brief period be regained by the affected 
side. At most there will persist a certain slight amount of weakness and stiffness : 
and even this will gradually diminish. From what has been already said, it is 
evident that in these cases the initial paresis is an indirect focal symptom, and 
accordingly vanishes as soon as the effusion ceases to affect the tissues not im- 
mediately involved. 

Even where there is a complete hemiplegia it is exceptional for this con- 
dition to remain unabated throughout the entire region affected. After a few 
weeks, or even a few days, one part and another of the paralyzed half of the 
body begin to recover their former motility. The improvement goes on slowly, 
and in the most favorable cases the paralysis may for the most part have vanished 
at the end of some months. Usually, however, the improvement advances only to 
a certain point, and the condition then attained remains stationary. We now 
find the ordinary characteristic typical " hemiplegic," who can be recognized at the 
first glance by the practiced eye. The most noteworthy phenomenon in such cases 
is this, that, in spite of many individual differences in the final recovery of cer- 
tain movements and also in the permanence of the paralysis of other groups of 
muscles, there is still a very striking regularity and uniformity. There is one 
chief fact which is very noteworthy, that almost invariably the leg regains greater 
power of movement than the arm. In regard to the condition of the individual 
groups of muscles, moreover, we almost always find the same manifestations. As 
has been shown chiefly through the interesting investigations of Wernicke and 
L. Mann, the permanent paralysis in cerebral hemiplegia, or the return of motion, 
never relates to individual muscles, but always to whole groups of muscles whose 
functions are closely connected. In the upper extremity there is usually perma- 
nent paralysis of all the muscles that rotate the arm outward (supinators of the 
forearm, outward rotation of the upper arm by the infra-spinatus and teres minor, 
and fixation and outward rotation of the shoulder-girdle by the lower portion of 
the trapezius and the rhomboidei), and of those that raise the upper arm (deltoid, 
serratus), and also paralysis of the movements at the elbow, especially of exten- 
sion, of opening the hand (extensors of the fingers, fixation of the wrist by the 
flexors), and of opposition of the thumb (opponens, abductor brevis). On the 
other hand, inward rotation of the arm and closure of the hand are, as a rule, pre- 
served. The patient can therefore not take hold of an object on account of the 
difficulty of opening the hand, but he can hold firmly what he has once grasped. 
Fine movements of the hand, however, are much impaired on account of the dis- 
turbances in the movement of the thumb. In the leg the flexors of the lower leg 



CEEEBEAL ILEMOBKHAGE 



1099 



and the dorsal extensors of the foot usually remain permanently paretic, and 
also the abductors and inward rotators of the hip, while the ilio-psoas, the quadri- 
ceps extensor, and the plantar flexors of the foot often regain their power of mo- 
tion. The return of mobility in the ilio-psoas and quadriceps is therefore of 
great practical significance, because by it the patient is enabled to walk again. 
Of course the patient needs the help of a cane, and the gait remains slow and la- 
bored, but the advantage of independent locomotion is extremely great. The gait 
of the hemiplegic is very characteristic and is always of the same type. The 
affected leg has the toe turned slightly outward, it is moved forward slowly, drag- 
ging on the ground, in a slight curve whose convexity is outward. We can not 
state with certainty the reason for these facts just mentioned — that both the im- 
provement and the permanent paralysis almost always involve regularly the same 
definite groups of muscles. The muscles which regain the power of motion are 
probably those which can be most easily innervated from the healthy hemisphere 
on the same side of the body. 

It is improbable, although of course not impossible, that fibers when once 
destroyed can undergo regeneration ; but the fact above mentioned is of the great- 
est practical consequence, that hemiplegic symptoms can not improve materially 
after the first six months. 

The permanently paralyzed muscles become very often contractured later on. 
The appearances produced exhibit considerable uniformity. The arm, which 
suffers more from paralysis than the leg, is also usually more contracted. The 
fingers are almost invariably flexed; the forearm contracted in a position of 
pronation, and usually flexed rather than extended ; and the upper arm adducted 
(the pectoralis major being chiefly affected). These contractures correspond ex- 
actly to the natural positions which the paralyzed arm almost always assumes if 
left to itself, either from gravity or as a result of any remaining power of move- 
ment. The contractures are almost always found in the same groups of muscles 
which suffer relatively the least loss of power in hemiplegia (vide supra). Since 
the position once acquired from the paralysis of the antagonistic muscles can not 
be altered, so-called passive contractures appear in the permanently shortened 
muscles. The correctness of this theory is favored by the fact that the deformity 
can to a certain extent be prevented by the persistent use of passive motion, which 
renders any permanent shortening of the muscle impossible. Nevertheless, Char- 
cot and his pupils, including Bouchard, hold an entirely different opinion — 
namely, that the contractures are due to the secondary degeneration of the 
pyramidal tract. In defense of their position no fact can be adduced, save that 
fatal cases exhibiting hemiplegic contractures do invariably present the secondary 
degeneration mentioned ; but of course this is no proof that the two things have 
any causative relation to each other. A contracture occurs only in connection 
with persistent paralysis ; a persistent paralysis is never seen unless the pyramidal 
tract be destroyed ; and if it be destroyed, a secondary degeneration must result. 
The contractures and the secondary degeneration are therefore two sequelae, inde- 
pendent of each other. That the degeneration should " irritate " the fibers, 
and thus excite muscular contractions, is extremely improbable ; for, according to 
all analogy, fibers which are undergoing degeneration can not be stimulated, and 
can not therefore transmit any sort of stimulus to the paralyzed muscles. 

If the contractures become marked in the lower limb, they may involve either 
the extensors or flexors, which depends in the main upon accidents of position, 
etc. At the ankle we almost always find a contracture of the muscles of the calf, 
because the dorsal extensors of the foot are paralyzed and the foot falls into a 
position of plantar flexion from its own weight. The fact that the muscular tonus 
is increased on the paralyzed side (analogous to the increase of the tendon re- 
flexes) is a circumstance which is not wholly without influence on the strength 



1100 



DISEASES OE THE NERVOUS SYSTEM 



of the contracture. We may mention here the fact brought forward by Hitzig 
that many contractures are slight in the morning, when the patient wakes from 
sleep, and become more marked after he has begun to move. 

Among other symptoms we will mention first the interesting associated move- 
ments, which are of frequent occurrence in hemiplegics. The chief explanation 
of them is that the patient can no longer innervate the different paretic groups 
of muscles with ease. In order to do so, it is always necessary to make a forcible 
associated movement of the leg, when the patient is endeavoring with all his 
energy to move his arm, and vice versa. If the patient tries to raise the arm at 
the shoulder, he flexes his forearm at the same time. The common associated 
movement in the foot (dorsal extension from contraction of the tibialis anticus) 
on flexing the hip and knee, which was first described by the author, is especially 
striking. Not infrequently the patient is quite unable to extend the foot dorsally 
as an isolated movement, but, if he draws the whole leg up to the trunk, there is 
then always a simultaneous marked dorsal extension of the foot. Associated 
movements also occur on the sound side on movements of the affected side, and it 
is said that the opposite condition has also been observed. 

Another peculiar phenomenon must be mentioned here. It is what Weir 
Mitchell has termed post-hemiplegic chorea. Some time after the paralysis begins 
the parts affected by it exhibit involuntary movements, reminding one of chorea 
or athetosis (vide page 836). Sometimes these movements are continuous, some- 
times they occur only as associated movements in connection with voluntary 
motions of the paralyzed, or even of the sound, side. Hemiplegia due to cerebral 
hsemorrhage very seldom exhibits this phenomenon. It is said to occur chiefly 
in focal disease of the posterior extremity of the internal capsule, and of the 
optic thalamus (irritation of the adjacent pyramidal tract?)- It is much com- 
moner in cerebral infantile paralysis (vide infra). 

It is interesting to observe the trophic and vaso-motor changes in the paralyzed 
parts. At first the skin may be somewhat redder and warmer on the paralyzed 
than on the sound side. Nothnagel has shown that, even in the distribution of 
the cervical sympathetic, symptoms of vaso-motor paralysis occur. They are partly 
temporary and partly persistent, and comprise increase of temperature and color 
in the paralyzed side of the face, swelling of the eyelids, and contraction of the 
pupil; but they are usually slight. We very frequently find, especially on the 
back of the hands, more or less puffmess, which is likewise usually regarded as of 
vaso-motor origin. It should, however, be considered that the natural movements 
of any part of the body greatly promote the nervous and lymphatic circulation, 
and that the quietude of paralysis may therefore have much to do with the oedema. 
In hemiplegia of some duration the extremities upon the paralyzed side are always 
cooler than normal, and the hand in particular is very often deeply cyanotic. 
The skin sometimes becomes harsh and fissured, and often is thickened. The in- 
ternal surface of the hand, in case of contracture, is frequently quite damp with 
perspiration. 

Among the specific trophic symptoms of hemiplegia Charcot includes " acute 
malignant decubitus." This sometimes develops with extreme rapidity within a 
few days after the shock, and usually occupies the buttock on the affected side. 
There appears a circumscribed redness with the formation of vesicles, which is 
soon succeeded by a deep-reaching necrosis of the soft parts. We have ourselves 
never met with this in a case which has been properly nursed, and we can not 
therefore help thinking that its development is not wholly due to trophic disturb- 
ance, but to pressure and to the penetration of septic matter below the skin. Of 
course, patients long confined to bed with hemiplegia are as liable to bedsores as 
are any others similarly situated. 

If the hemiplegia has existed for some time, we almost always find the para- 



CEREBRAL HEMORRHAGE 



1101 



lyzed muscles more or less atrophied in comparison with those on the sound side. 
On microscopic examination we also find an evident atrophy of the individual 
fibers, but this atrophy, as a rule, is not so extreme as in peripheral or polio- 
myelitic paralyses (see page 834). Furthermore, the atrophy is always "simple," 
not " degenerative," and accordingly the f aradic and galvanic excitability of the 
paralyzed muscles is completely preserved, even if the muscles are very much 
atrophied. The electrical excitability does not even show a slight quantitative 
diminution, as careful examinations have taught us. In some cases, even in 
ordinary hemiplegia, the atrophy of certain muscles (for example, the interossei, 
the thenar muscles, the deltoid, etc.) may come on unusually early and become 
extremely marked, so that we may speak of a " cerebral muscular atrophy." In 
such cases certain trophic influences actually seem to be especially manifest. 
The joints of the paralytic extremities, and in particular the knee and shoulder, 
may exceptionally become inflamed. The arthritis is sometimes acute, and some- 
times more of a chronic variety. Its cause is not evident. Charcot thinks that 
it is probably a neurotrophic symptom, and he is of the same mind with regard to 
the rarely seen swellings of the peripheral nerve-trunks of the paralyzed side 
(" hypertrophic neuritis "). 

Mental symptoms are rare, except the initial loss of consciousness. There is 
sometimes, however, a persistent general uneasiness of mind, accompanied by 
great excitability and wakefulness. In a large number of cases of persistent 
hemiplegia there finally come on, in the course of years, constantly increasing 
indications of mental weakness. The patient grows dull and forgetful. Very 
often he exhibits a peculiar tendency to weeping, bursting into tears at the slight- 
est provocation; but frequently he is subject to quick alternations of feeling, 
weeping and laughing in the same minute. The patient sometimes becomes 
eventually confused, excited, etc. All such pronounced conditions are usually 
dependent upon the general cerebral atrophy that comes from arterio-sclerosis. 

The general nutrition is often good for a long time. Sometimes there is even 
a decided tendency to corpulence. In other cases, and especially in the bedridden, 
marasmus gradually comes on and hastens the fatal termination, particularly if 
there be some intercurrent trouble, such as a bedsore or bronchitis. 

We have detailed the peculiarities of hemiplegia somewhat minutely, because 
the statements will apply in the main to all cases of cerebral hemiplegia, no mat- 
ter in what place the pyramidal tract is interrupted or by what sort of a lesion. 
It is needless to enter into the diverse symptoms which are caused by diversity 
in the exact location of the haemorrhage. The hemiplegia itself is the same, 
whether the effusion be in the cortex, internal capsule, crus cerebri, or pons. It 
is easy to infer from the preceding chapter what the accessory symptoms are 
which would enable us to localize the trouble. We need mention here only the 
frequent combination of right hemiplegia and aphasia. This occurs when there 
is a large effusion in the left hemisphere, extending from the internal capsule to 
the neighborhood of the third frontal, or possibly the uppermost temporal con- 
volution (compare page 1077 et seq.). 

Diagnosis. — The diagnosis of cerebral haemorrhage rests on the sudden onset 
of the apoplectic symptoms, and on the later symptoms (if there be any) of im- 
pairment of the cerebral functions. The diagnosis can scarcely ever be made 
with absolute certainty, for cerebral embolism may exhibit almost identical phe- 
nomena : the differential diagnosis between the two will be given in the following 
chapter. Occasionally there may be danger of mistaking other cerebral affections 
for a haemorrhage, such as meningitis and tumors. The same may be said of a 
suddenly developed uraemia, and of constitutional sepsis. In these cases the rapid 
onset of grave cerebral symptoms of a general nature, such as unconsciousness, 
simulates the apoplectic coma. 



1102 



DISEASES OF THE NERVOUS SYSTEM 



Prognosis. — The first question is, whether the patient will survive the initial 
shock. The answer depends upon the severity of the early symptoms. The 
deeper and more persistent the unconsciousness, the more deficient the respiration 
and pulse, the less the prospect of recovery ; hut we can never decide absolutely. 
[A steady rise of temperature or a very high temperature is also of bad omen. 
— K.] If the patient have withstood the first onset and be hemiplegic, then the 
possibility of improvement hinges on the question whether the paralysis is a direct 
or an indirect focal symptom. Inasmuch as there are no means of knowing about 
this at first, we must speak very guardedly. [The early appearance of ankle 
clonus or greatly exaggerated patellar reflex is apt to portend permanent paraly- 
sis with contractures. — K.] It should never be forgotten that the haemorrhage 
may recur. The predisposing disease of the blood-vessels renders individuals 
who have had one stroke liable to be visited, sooner or later, by another. 

Treatment. — The treatment of the apoplectic shock demands, first of all, rest 
in bed, with the head and shoulders elevated. To avoid bedsores it is very impor- 
tant to maintain cleanliness, and to watch attentively that portion of the skin 
which is pressed against the bed by the weight of the body. An ice-bag should 
be put upon the head, and particularly over that side on which the haemorrhage 
is supposed to be. Bleeding was formerly universally practiced, but of late its 
usefulness is doubted. It is at most indicated only when the deep congestion of 
the face, the violent pulsation of the carotids, and the full, slow pulse show in- 
creased arterial tension. In such a case, if the patient seem otherwise robust, we 
may bleed at the commencement of an attack, in the hope of checking the flow of 
blood by lowering the intra-arterial pressure. In similar conditions experience 
shows that the local abstraction of blood from the temples is sometimes advan- 
tageous. The bowels should be well emptied by enemata, and later on by drastic 
purgatives. If the respiration and pulse fail, we may try stimulants (ether, cam- 
phor) . 

[Horsley and Spencer have found, by experiments on animals, that if the in- 
ternal carotid be tied the bleeding from the divided lenticulo-striate artery is 
checked. Horsley therefore suggests that in the very earliest stage of cerebral 
haemorrhage ligature or compression of the internal carotid may check the bleed- 
ing, and prevent the formation of a large clot and extensive destruction of the 
brain. This procedure has been tried with some benefit in one or two cases of 
ingravescent haemorrhage. 

Where there is much difficulty in respiration during the period of coma, relief 
may sometimes be obtained by turning the patient upon the side. — K.] 

When the patient is safely over the shock, our resources for aiding him in the 
further stages of his trouble are very limited. As long as headache and symptoms 
of fever persist, the application of ice to the head should be kept up, and other 
disturbances should be treated symptomatically. For uneasiness and wakeful- 
ness, small doses of morphine or chloral are given. Treatment of the hemiplegia 
must be deferred for the first three or four weeks, until all the initial symptoms of 
irritation are over. Then electricity plays the chief role. Local galvanization 
should be tried, the current being made to pass transversely through the head, 
with as much regard as possible to the position of the hemorrhagic focus; the 
current should be feeble, and the application should occupy two or three minutes. 
With this may be combined galvanization of the sympathetic nerve on the side of 
the haemorrhage ; nor should galvanization (stroking with the cathode) and fara- 
dization of the paralyzed muscles and nerves be neglected. If favorable changes 
take place, it is, however, uncertain how much should be ascribed to treatment; 
since, as has already been stated, there is often improvement without treatment. 

Passive movements and massage of the paralyzed limbs are very important as 
a prophylaxis against contractures. They should be commenced promptly, and 



CEEEBEAL EMBOLISM AND THEOMBOSIS 



1103 



be continued methodically. Massage, and later on systematic and appropriate 
gymnastic exercises, may contribute much to the restoration of voluntary motions. 
The same object is also promoted by rubbing with spirits of camphor, chloroform 
liniment, etc. 

Internally, potassic iodide is frequently given, out of regard for its " absorb- 
ent " properties. We may also try the effect of strychnine ; it is most adapted for 
cases of some duration. 

As to baths, they should not be too warm— that is, not over 90°-93° (26°-27° 
E.). Moderately warm baths, medicated with common salt if it seems desirable, 
and employed three or four times a week, seem to be beneficial. If it be thought 
best to send the patient to a regular bathing-place, Wildbad, Eagatz, Teplitz, 
Wiesbaden, Oeynhausen, ISTauheim, etc., may be chosen. At the first-mentioned 
places too hot baths should be avoided. 

Hemiplegic paralysis often lasts so long that the physician must repeatedly 
change the details of treatment, so as to support the courage and patience of the 
sufferer. Particular care should be given to regimen, in order that any recur- 
rence of the haemorrhage may, if possible, be avoided. The diet should be simple ; 
any large amount of alcohol should be forbidden ; and there should be no severe- 
bodily exertion or mental excitement. 



CHAPTEE IV 

CEREBRAL EMBOLISM AND THROMBOSIS (ENCEPHALO-MALACIA) 

(Softening of the Brain from Embolism or Thrombosis) 

^Etiology and Pathology. — Occlusion of the cerebral arteries is one of the 
most frequent injuries inflicted by embolism. Usually the emboli originate in the 
left side of the heart, from thrombi in the left auricle, or from the thrombotic 
deposits which form in chronic endocarditis (mitral or aortic disease) upon the 
valves of the left ventricle. Chronic arterio-sclerosis may also lead to thrombosis 
in the larger arteries, particularly the aorta; and in case the cerebral arteries 
themselves are extensively atheromatous, the larger vessels at the base of the 
brain may furnish material for embolism of the smaller cerebral arteries. 

Thrombosis of the arteries of the brain is always due to primary disease of the 
blood-vessels, the most common cause being the chronic arterio-sclerosis just men- 
tioned. Wherever the atheroma has altered the normal structure of the intima, 
deposits of fibrine may take place. Their development is further promoted by 
the subnormal elasticity of the arteries, and by the occasional narrowing of their 
lumen; for thus the flow of blood is rendered slow, if not even completely 
checked. It is easy to understand that thrombosis and embolism may each give 
rise to the other. From every thrombus an embolus may be detached ; and every 
firmly lodged embolus may form a nucleus for thrombosis. 

Next to arterio-sclerosis, the most frequent cause of a cerebral thrombus is 
syphilitic endarteritis. In the chapter on cerebral syphilis this subject will be 
minutely considered. Whether thrombi ever form here independently of disease 
of the vessels is doubtful. An apparently spontaneous thrombosis is now and 
then seen in patients who are cachectic or severely ill (cancer, grave typhoid 
fever, etc.). Such cases are explained either by the existing cardiac weakness, 
or perhaps by an abnormal tendency of the blood to coagulate. 

In whatever part of the arterial system complete occlusion has been produced 
by an embolus or thrombus, the results depend upon the possibility or impossi- 



1104 



DISEASES OF THE NERVOUS SYSTEM 



bility of blood reaching by collateral channels the region thus deprived of its 
ordinary supply. If the collateral circulation prove efficient, no harm is done ; if 
not, the tissues must perish and undergo " softening." It is thus a matter of the 
greatest practical import that the perforating arteries of the brain-stem, and par- 
ticularly the branches of the middle cerebral artery in the fissure of Sylvius, 
which supply the great central ganglia and internal capsule, are all " terminal," 
in Cohnheim's sense — that is, they form few anastomoses with neighboring ves- 
sels. Now, the middle cerebral artery and its branches are known from experience 
to be peculiarly liable to embolism, above other cerebral arteries. Hence we see 
why the region they supply suffers so severely and so very frequently from emboli. 
It is noteworthy that the left middle cerebral artery is more frequently plugged 
by emboli than is the right. In the centrum ovale and cortex there is more op- 
portunity for collateral compensation than in the central ganglia; but even here 
the supply of blood often proves insufficient, as is shown by the not infrequent 
occurrence of spots of softening in the cortex and the white substance of the cere- 
brum. On the other hand, embolic foci are much rarer in the crura cerebri, pons, 
and cerebellum. 

The various steps in the process which begins with embolic or thrombotic 
occlusion and ends in softening of the brain-substance are essentially the same as 
occur in other organs (compare chapter on pulmonary embolism, page 273). The 
tissues which are deprived of their arterial blood perish, become disintegrated, 
and are transformed into a soft homogeneous mass. Into the empty portion of the 
artery, beyond the embolus, blood flows in the reversed direction from the veins, 
and, if the anatomical relations permit, from the minute arteries in the neighbor- 
hood; but the supply is not sufficient to nourish the tissues. The walls of the 
blood-vessels become abnormally permeable and delicate, so that some red glob- 
ules invade the disintegrating region by diapedesis, and others in the way of 
minute but genuine ecchymoses. Actual infarctions are, however, never formed 
in the brain, perhaps because, as Weigert suggests, the nervous structures swell so 
much as to exclude any large amount of blood ; but the little punctif orm ecchy- 
moses are in many instances so abundant that the whole softened spot seems dis- 
tinctly reddish or yellowish. This red or yellow softening is also due in part to 
the tissues being stained by the dissolved pigment of disintegrated blood-glob- 
ules. If the discoloration be not very striking, then we speak of a white soft- 
ening. 

Fresh foci of softening are seen through the microscope to be composed of 
drops of myeline, bits of swollen nerve-fibers, numerous fatty granular cells, and 
free fat globules. The time required for these changes is one or two days. If 
within that period a compensatory collateral circulation is set up, the nervous 
structures may be restored and resume their functional activity. If not, the tis- 
sues perish and become disintegrated. The white blood-corpuscles and leucocytes 
(and possibly also the endothelial cells of the blood-vessels, and the neuroglia and 
ganglion-cells) absorb the fatty detritus thus made, and come to form the fatty 
granular cells above mentioned. If the patient live, the dead and disintegrated 
tissue is gradually absorbed, and it may even finally be replaced by a cyst not 
differing in appearance from those which occur after cerebral haemorrhage. A 
minute focus of softening may also be replaced at times by indurated cicatricial 
tissue. If portions of the surface of the brain become softened, quite a deep de- 
pression often results. This is filled up in part with serous fluid and in part by 
hyperplasia of the pia mater. Sometimes the convolutions are still recognizable 
in places ; but they are atrophied, of a yellowish color, and of a greatly increased 
consistency, due to the growth of cicatricial tissue. 

Clinical History. — The occurrence of cerebral embolism is attended with 
almost precisely the same sort of shock as is cerebral haemorrhage. We do not 



CEREBRAL EMBOLISM AND THROMBOSIS 



1105 



need to enter into the particulars again here, but will refer to the preceding chap- 
ter (vide page 1091). In embolism, also, the intensity of the shock varies from 
transitory confusion of intellect or slight vertigo to the deepest persistent coma. 
One chief factor in determining the nature of the case is the size of the occluded 
artery; another is its position, according as the embolism has taken place in 
the hemispheres or toward the base of the brain. In general, however, the shock 
of embolism, especially the loss of consciousness, is not often so severe and long 
•continued as that of haemorrhage ; and embolism does not so frequently give rise 
to symptoms of cerebral compression, including slowing of the pulse. The tem- 
perature does not usually show the decline which is seen in fresh cerebral haem- 
orrhage, but moderate fever sets in as a rule in the course of a few days. On the 
other hand, epileptiform convulsions are seen more often in embolism than in 
haemorrhage. Embolism again may have a rather slow onset, where there is at 
first a small embolus and this becomes the nucleus of a gradually formed 
thrombus. 

It is not easy to explain why there should be a shock at all in case of embolism. 
Perhaps the main reason is the diminution of pressure which the embolism occa- 
sions in the region directly affected and in its neighborhood. The portion of 
the artery beyond the plug becoming empty not only causes a draught upon 
the blood and lymph, but subjects all the soft surrounding structures to a dim- 
inution of tension and to a certain amount of strain (Wernicke). It is not 
impossible, however, that the disturbance of circulation occasioned in the sur- 
rounding blood-vessels, including the capillaries of the cortex, by sudden em- 
bolism of a good-sized artery is of itself enough to account for the symptoms 
of shock. 

With regard, also, to the persistent symptoms of embolism we may be equally 
brief, inasmuch as they very closely resemble those which follow a cerebral haem- 
orrhage. As has been said, it is only when a compensatory collateral circulation 
is developed within the first forty-eight hours that the early symptoms of focal 
disturbance can entirely vanish. After this period, the tissues which have been 
deprived of their normal blood-supply must undergo necrosis; although there is 
still room for hope that some of the symptoms will prove indirect, and therefore 
capable of improvement, so that embolic hemiplegia, like that from haemorrhage, 
may improve decidedly in the course of the first few weeks. 

Inasmuch as the middle cerebral artery is by far the most frequent seat of 
cerebral embolism, and inasmuch as this artery supplies the internal capsule as 
well as the great central ganglia, the most frequent focal symptom of embolism 
of the brain is ordinary cerebral hemiplegia, all the features of which have been 
depicted in the preceding chapter. Aphasia is associated with it with comparative 
frequency, for, as already mentioned, the left middle cerebral artery is especially 
apt to suffer. Less frequent is paralysis of a single member, due to cortical embo- 
lism, or an occipital lesion with hemianopsia. 

Where softening is the result of thrombosis, the symptoms are but seldom 
abrupt in their onset. Usually the focal symptoms and the more general ones 
(such as unconsciousness) are developed rather gradually. This is most often 
seen in so-called senile softening of the brain, a disorder almost always caused by 
sclerosis of the cerebral arteries. The various symptoms generally come on under 
cover of repeated relapses and fresh aggravations of the disease. A severe initial 
shock seldom occurs; but almost invariably there is a gradual and progressive 
dementia. 

The further course and the final termination of cerebral softening vary as do 
those of cerebral haemorrhage. Embolism of a larger artery may cause speedy 
death. If, however, the first shock passes away, the impairment of function 
which may be left behind may last for years without seriously affecting the gen- 
70 



1106 DISEASES OE THE NERVOUS SYSTEM 



eral health. There is always danger of a recurrence when the source of the em- 
bolism continues unchanged, as in cardiac disease or atheroma. 

Diagnosis. — Both the onset and the persistent focal symptoms are so much 
alike in haemorrhage and embolism that in many cases it is utterly impossible to 
decide which caused the apoplexy and hemiplegia. The following are factors in 
making a differential diagnosis, if one can be made : 1. It is very important to find 
whether there be any source for an embolus. Thus, if the patient have valvular 
cardiac disease (particularly mitral), embolism is more probable than haemor- 
rhage. 2. A young person is, on the whole, more apt to have embolism than haem- 
orrhage. At a later period of life one is about as probable as the other. 3. When 
the shock is severe and persistent, with red face, strong pulsation of the carotids, 
and signs of cerebral compression (slow pulse), we should think of haemorrhage 
rather than embolism, in which latter the initial symptoms are sometimes com- 
paratively slight (vide supra). 4. Einally, it is sometimes possible to obtain sup- 
port for a diagnosis of cerebral embolism by demonstrating embolism elsewhere, 
as in the fundus oculi, by means of the ophthalmoscope. 

In rare instances, also, tumors of the brain, into the substance of which haem- 
orrhage takes place, may induce symptoms closely simulating a primary apoplec- 
tic shock, as may also abscesses which have been previously latent, and then sud- 
denly burst into a ventricle. In such cases a correct diagnosis is seldom possible. 

Softening due to a thrombus is the most readily diagnosticated in those cases 
where there is cerebral syphilis (q. v.). Senile softening is inferred from the age 
of the patient, the signs of general arterio-sclerosis, the abrupt, advances of the 
disease from mildness toward severity, and the developing dementia. 

Eor the prognosis and treatment of cerebral embolism we may refer simply to 
what was said in the preceding chapter. 



CHAPTER V 

INFLAMMATION" OF THE BRAIN 

(Acute and Chronic Encephalitis) 

1. Abscess of the Brain (Suppurative Encephalitis) 

etiology. — In most cases of cerebral abscess it is possible to demonstrate 
with certainty that infectious material capable of exciting suppuration has pene- 
trated to the encephalon. This is particularly true of those not very rare ab- 
scesses which follow injuries of the scalp, ' cranium, or brain (traumatic abscess 
of the brain). Here the wound is probably almost always an open one, affording 
free ingress to the infection. In the rare cases of traumatic cerebral abscess, 
apparently without any open wound, small injuries of the skin have probably been 
overlooked. It is not essential that the bones should be' injured, however, for 
experience shows that, even where the soft parts alone are wounded, suppuration 
may extend to the brain. The manner in which this extension takes place deter- 
mines the question whether a suppurative meningitis (q. v.) or an abscess shall 
be developed. ISTot infrequently we find the two combined. Another source of 
traumatic cerebral abscess is foreign bodies which penetrate into the brain (for 
instance, through the orbit), and thus carry septic matter into the very substance 
of the organ. 

Besides traumatic causes, any existing suppuration in neighboring parts may, 
by direct extension, occasion cerebral abscess. The same processes are prominent 



INFLAMMATION OF THE BKAIN 



1107 



in this connection which we have already found to excite purulent meningitis 
(vide page 1055) — particularly suppuration in the middle ear and in the petrous 
bone (chronic purulent otitis media, caries of the petrous bone). As a rule, the 
suppuration attacks the brain by contiguity, after the disease of the bone extends 
to the dura, and this becomes infected. In rare cases extra-dural abscesses are 
also formed. If the thin roof of the tympanic cavity is broken through, the ab- 
scess usually forms in the temporal lobe, while suppuration in the mastoid usually 
leads to cerebellar abscess. The excitants of suppuration may also reach the brain 
along the lymph-sheaths of the acoustic and facial nerves or by means of the peri- 
vascular lymph-sheaths and veins. About one third of all abscesses of the brain 
are due to purulent ear disease. The danger of the development of a cerebral 
abscess arises especially when the discharge of pus is checked by the growth of 
granulations, by the formation of cholesteatoma, etc., and also in acute exacerba- 
tions of chronic purulent otitis. Abscesses of the frontal lobe, following suppura- 
tive processes in the nasal cavity and the ethmoid, are much less common. 

In yet a third class of cases the morbific agents are conveyed from foci of 
disease situated in distant parts of the body. These are metastatic or embolic 
abscesses. They occur, for instance, in pyaemia and ulcerative endocarditis. 
Abscesses of this sort, however, are usually small, and seldom are conspicuous in 
modifying the grave general disease. Of more importance are cerebral abscesses 
connected with certain suppurative affections of the lungs and pleura. These are 
not so very rare. They are oftenest associated with fetid bronchitis, pulmonary 
gangrene, and empyema. Purulent meningitis (q. v.) may occur in the same way. 
There can be no doubt that virus is in some way conveyed to the brain, but just 
how is not yet known. 

In some few cases of cerebral abscess no certain aetiology can be made out. 
To these the term idiopathic is applied. We met with several of them just at the 
time of an epidemic of cerebro-spinal meningitis ; and it therefore seems reason- 
able to suspect that possibly many apparently spontaneous cerebral abscesses are 
referable to the same poison as is epidemic meningitis. In other cases we have 
to do with other forms of infection. 

From the variety of exciting causes, it is evident that in cerebral abscess 
the special variety of the purulent infection is not always the same. We find 
streptococci or staphylococci most frequently in the pus of an abscess, or under 
some circumstances the pneumonia diplococci. 

Pathology. — The pathological anatomy of abscess of the brain is precisely the 
same as that of abscesses in other organs. The size varies from minute foci 
hardly as large as a lentil to extensive cavities occupying nearly the whole of 
one lobe. The traumatic and otitic brain abscesses are usually single, but meta- 
static abscesses are not infrequently found in considerable numbers. The pus is 
usually greenish yellow. It may be odorless or offensive. Sometimes remnants of 
the destroyed (" melted ") nervous tissue and red blood-globules are mixed with 
it. The walls of the abscess often bulge out irregularly. The cerebral paren- 
chyma around the abscess for a greater or less distance exhibits white softening. 
This softening is due partly to the pressure and partly to the spread of the in- 
flammation. An abundance of granular cells is generally to be found in the tis- 
sues near the abscess. 

If the abscess be very large and reach nearly to the surface of the brain, it may 
sometimes be recognized externally by a distinct bulging and perceptible fluctua- 
tion. The convolutions on the surface of the affected hemisphere are almost al- 
ways flattened. If the abscess extends completely to the surface of the brain, pu- 
rulent meningitis is excited. The complication of cerebral abscess with purulent 
phlebitis and sinus thrombosis has also been quite frequently observed. Abscesses 
which are centrally situated not infrequently burst into a lateral ventricle. An 



1108 



DISEASES OF THE NERVOUS SYSTEM 



abscess of long standing may finally become encapsulated — that is, become encased 
in a smooth, firm layer of connective tissue, which prevents further extension of 
the process. The pus inside gradually becomes thick and cheesy. Apparently, 
however, it is very seldom entirely absorbed, and a new acute outbreak of inflam- 
mation, excited, for example, by an injury, is always among the possibilities. 

Clinical History. — Small abscesses, and even large ones, may for a long time 
have scarcely any symptoms. This is particularly true of apparently idiopathic 
abscesses, and of those which develop very slowly and insidiously after appar- 
ently insignificant injuries of the head or in connection with chronic inflamma- 
tion of the middle ear, etc. There is sometimes a long " period of latency " or a 
longer period of indefinite mild precursory symptoms (occasional headache, ver- 
tigo, general malaise, a slight elevation of temperature, etc.) preceding the onset 
of severe cerebral symptoms. 

In abscesses following more extensive injuries, the symptoms are more vio- 
lent from the start; this is also true of many abscesses which develop acutely 
and enlarge rapidly. The symptoms can hardly be distinguished from acute 
meningitis. The patient is dull, or grows delirious; he has violent headache, 
vomiting, symptoms of motor irritation (general or limited convulsions), and 
fever. Sometimes the temperature repeatedly rises to a high point. Definite 
focal symptoms (hemiplegia or monoplegia, partial cortical epilepsy, aphasic 
disturbances, hemianopsia, etc.) may manifest themselves according to the spe- 
cial situation of the abscess. The loss of consciousness becomes more and more 
complete; and in a comparatively brief time (one or two weeks) there may be 
profound coma and death. Rarely the violent symptoms abate, and the acute 
passes into a chronic stage. 

The symptoms of cerebral abscess, when it pursues a chronic course, may be 
divided into (1) the general symptoms and (2) the focal symptoms, resulting from 
the special position of the abscess. There is no other localized cerebral disorder 
in which the focal symptoms are so often absent, either for a long time or even 
throughout the illness. This is partly because the abscesses are often situated in 
parts of the brain, injury to which does not occasion any demonstrable focal 
symptoms. Such localities are the white matter of the frontal lobe, the hemi- 
spheres of the cerebellum, etc. A second reason is that an abscess is not very 
apt to excite indirect focal symptoms by its influence upon the parts around it. 

Among the general symptoms, the most important is a persistent, deeply situ- 
ated, dull headache. For a long time it may be the only symptom, especially 
when the abscess is gradually developed after an injury to the head or after aural 
disease of long standing. The pain is referred mainly to the seat of the abscess ; 
but the exceptions to this rule are not infrequent. The skull is sometimes espe- 
cially sensitive to percussion in the vicinity of the abscess; but we should not 
lay too much stress upon this symptom. Another frequent symptom besides 
headache is vertigo; and there may also be vomiting, either after meals or 
entirely independently of food. Another valuable symptom in diagnosis is the 
irregular fever, sometimes slight, and sometimes exhibiting great elevations with 
intervals between them; but in many cases also, particularly where the abscess 
is encapsulated, there may be no fever whatever. The pulse is often slow. An 
important diagnostic point is that choked disk and optic neuritis may occur in 
abscess of the brain, but they develop far less frequently and only exceptionally 
do they reach so high a degree as in tumors of the brain (q. v.). 

The general health may be but slightly disturbed. Usually, however, there is 
decided indisposition. The patient is pale, has no appetite, loses flesh, and 
sometimes shows slight mental changes (a melancholy condition, temporary con- 
fusion, etc.). 

As to the focal symptoms, little need here be added to what is contained in 



INFLAMMATION OF THE BRAIN 



1109 



Chapter II of this section. Abscesses involving the motor region of the cortex 
have been repeatedly found to cause limited epileptiform attacks and monoplegic 
paralysis. It is particularly characteristic that, as the abscess grows, one 
symptom of paralysis is added to another, and that often the advance of the 
paralysis is ushered in by epileptiform convulsions. Abscesses in the occipital 
lobe have repeatedly been observed to cause hemianopsia, and abscesses in the 
temporal lobe word deafness ; and these facts have been used in making a diag- 
nosis of the location of abscesses. Abscesses in the cerebellum may remain unsus- 
pected for a long while; but in other cases characteristic cerebellar symptoms 
(staggering gait, vertigo) may be evident as well as severe general symptoms. 

The duration of chronic cerebral abscess varies greatly. In most cases it lasts 
for months ; and sometimes it has certainly lasted for years. Particularly when 
the abscess gives rise to no symptoms, or merely to slight and indefinite ones 
referable to the head, it may last a very long time. It is quite often the case that 
there are separate attacks of the severe symptoms, such as headache, vomiting, 
and fever, and that in the intervals of variable duration between these paroxysms 
the patient feels pretty well. 

The final termination of cerebral abscess, unless there is surgical interven- 
tion, is almost always fatal. Recovery is not impossible, but it has been seen with 
certainty in only a very few instances. Death either comes on gradually, when, 
as the abscess grows larger, all the symptoms become correspondingly aggra- 
vated; or it may happen quite suddenly. Sometimes it is brought about by the 
abscess bursting into a lateral ventricle, or by the supervention of meningitis. 
Often a cerebral abscess terminates in a sudden and unexpected death, where 
no immediate cause for the event can be found. 

Diagnosis. — Although it is often possible to make a correct diagnosis of cere- 
bral abscess, yet there is usually a good deal of difficulty in arriving at such a 
conclusion, and entire certainty is seldom attainable. The most important points 
in diagnosis are : (1) The demonstration of some cause, such as trauma, chronic 
otitis, fetid pulmonary diseases, or empyema. (2) The presence of general cere- 
bral symptoms, such as headache, vertigo, and vomiting; and the fact that these 
are sometimes better and sometimes worse. To aid in excluding tumor, we have 
(3) the febrile symptoms frequently caused by abscess, but rare in case of tumor; 
and (4) the rarity of optic neuritis, which is very frequently occasioned by 
tumors. The focal symptoms, if there be any, are not characteristic. They 
grow worse by fits and starts in tumor just as in abscess. One fact, however, is 
of value, namely, that while tumors (vide infra) frequently cause disturbances in 
the area of distribution of the nerves at the base of the brain (such as paralysis 
of the oculo-motor), an abscess does this only exceptionally. It is often quite 
impossible to make a differential diagnosis between acute abscess and purulent 
meningitis, unless focal symptoms are developed, which indicate the existence of 
an abscess. 

The timely recognition of an abscess of the brain following purulent otitis is 
of the greatest practical importance. It is important to know that cerebral 
symptoms (headache, vomiting, vertigo, stupor, etc.) may also occur from reten- 
tion of pus in the middle ear, and that they may disappear completely after 
evacuation of the pus by paracentesis of the membrana tympani. If we find no 
retention of pus in the ear, however, we must suspect an abscess of the brain, 
if any persistent cerebral symptoms arise. Since such abscesses of the brain are 
most frequently situated, as we have said, in the temporal lobe or in the cere- 
bellum, we should pay special attention to the localizing symptoms of these por- 
tions of the brain. Abscesses in the left temporal lobe may be diagnosticated with 
the greatest relative certainty by the discovery of aphasic disturbances, word 
deafness, verbal amnesia, optic aphasia, etc. (Oppenheim). Deep-seated ab- 



1110 



DISEASES OE THE NERVOUS SYSTEM 



scesses may also cause heniiparesis, hemianopsia, ataxia, and, by pressure on the 
base of the brain, paresis of the oculo-motor or abducens. Otitic abscesses of the 
cerebellum cause occipital pain, slight stiffness of the neck, vertigo, and an un- 
certain gait ; but not infrequently definite cerebellar symptoms are absent. The 
general cerebral symptoms (headache, vomiting, disturbances of the sensorium, 
etc.) are the same in otitic abscesses of the brain as in other varieties of abscess. 
We may also consider the local tenderness of the skull on percussion, usually 
above the upper border of the ear. In other cases, however, the diagnosis of otitic 
abscess of the brain is very difficult, especially if we can find no pronounced focal 
symptoms. We often can not avoid confounding it with extra-dural abscess, 
purulent meningitis, sinus thrombosis, etc. The presence of meningitis can 
sometimes be established by lumbar puncture. 

Treatment. — The only possible way in which to cure an abscess is by opera- 
tion; the skull is trephined and the abscess laid open. The earlier and the more 
accurately the diagnosis of abscess can be made, the more favorable is the out- 
look for the patient. With the present -antiseptic modes of procedure, the dangers 
of an operation are slight, and the series of successful results that have already 
been obtained urgently demand further surgical intervention. Many a life can 
be saved by timely surgical interference, especially in abscesses of the brain 
following chronic ear disease. For particulars we must refer to special works 
on surgery. 

If operation be not justifiable, nothing but purely symptomatic treatment is 
left us. Ice to the head, narcotics, potassic bromide, electricity, and sometimes 
also the local abstraction of blood, are the main remedies beyond general hygienic 
measures. 

2. Acute and Chronic Non-suppurative Encephalitis 

While the spinal cord is quite frequently affected by idiopathic circumscribed 
inflammation (transverse myelitis), analogous cerebral disease is much more 
exceptional. The scanty information which we possess upon the subject is as 
follows : 

1. Idiopathic (Inflammatory) Softening of the Brain. — In rare instances 
there are found in the brain quite extensive foci of softening, the pathological 
anatomy of which is almost identical with that of embolic softening, and yet the 
afferent blood-vessels do not furnish any explanation of the condition. They have 
accordingly been termed " foci of inflammatory softening." The mode of their 
production is unknown. The symptoms resemble closely those of softening from 
thrombosis. 

2. Curable Form of Encephalitis. — In certain cases pronounced symptoms of 
focal disease exist for a time, and suggest a tumor or the like; but after some 
months, or even a still longer time, the symptoms gradually abate, and finally 
there is complete recovery. Such cases are usually explained by assuming that 
there has been a localized encephalitic process, capable of a restoration to the 
normal state. The nature of the symptoms, as we have observed them, would 
seem to imply that the lesion is generally in the neighborhood of the cortex, 
for there is usually paresis of some part of the body, often associated with 
certain symptoms of irritation and impairment of speech. Possibly the recovery 
of these cases' may be assisted by electricity and potassic iodide. It is always 
hazardous, however, to class such affections as " encephalitis," since we can 
hardly ever exclude absolutely other affections (especially syphilis). 

3. Diffuse Cerebral Sclerosis-. — Diffuse sclerosis of the brain is a peculiar dis- 
ease, which is usually classed as a chronic inflammation. The whole brain may 
"be involved, or the disease may be confined chiefly to a large part of one hemi- 
sphere. There is a very marked increase in the consistency of the brain-sub- 



INFLAMMATION OF THE BEAIN 



1111 




stance, so that it cuts like a tough piece of leather. The microscope reveals in 
many cases, but not in all, diffuse hyperplasia of the neuroglia. In a case which 
we recently examined there was a decided atrophy of the'nervous fibers lying in 
the white substance of the brain.— The disease is rare, and its characteristic 
symptoms can not yet be stated absolutely. They are developed slowly. The 
most constant among them seem to be hemiplegia or paraplegia without much 
change in sensation; symptoms of motor irritation, such as epileptiform convul- 
sions (sometimes general and sometimes uni- 
lateral), tremor, or single twitchings, which 
may be rhythmical or like those of chorea; 
^nd, lastly, dementia. When both hemispheres 
are involved, there are usually marked spastic 
symptoms in the lower limbs. 

The disease has been observed especially in 
children and also in elderly people. Alcohol- 
ism and hereditary syphilis seem to be among 
the causes, but nothing definite is known 
upon this point. Transitional forms between 
diffuse sclerosis and pseudo-sclerosis apparent- 
ly occur (vide page 959). Treatment can be 
only symptomatic. 

4. The Acute Encephalitis of Children. 
Cerebral Paralysis of Children. (Spastic 
Infantile Hemiplegia of Benedikt.) — Chil- 
dren not infrequently suffer from a definite 
form of hemiplegia, which deserves a brief 
special description. 

The patient is usually between one and 
four years of age. The symptoms almost al- 
ways begin acutely. Having been previously 
Wealthy, the child is suddenly attacked with 
malaise and fever. Very often there is nausea 
and vomiting, speedily or at once followed 
hy grave cerebral symptoms. There is stupor, 
and convulsions are particularly frequent. 
This condition may last but one or two days ; 
or it may continue, perhaps with unabated 
severity, for two or three weeks. Then the 
acute symptoms abate, and the child recovers 
comparatively fast; but it is noticed by the 
parents to be paralyzed; and this paralysis 
seldom entirely disappears, although it may 

diminish. Sometimes the paralysis follows the convulsions, without any other 
definite encephalitic symptoms. 

If such children come under observation after the paralysis has lasted some 
time, as is usually the case, their condition is generally as follows : The cranial 
nerves, as a rule, are but little affected. The main change is in the extremities of 
one side; and the arm is almost always worse than the leg. The affected parts 
hetray an arrest of development, more or less impairment of motion, in many 
-cases a marked exaggeration of the tendon reflexes, and almost invariably con- 
tractures of more or less severity (compare Fig. 176). The muscles, although 
.generally somewhat atrophied, never exhibit the reaction of degeneration. Sen- 
sation, as a rule, is unimpaired; but on careful examination we sometimes find 
in the paralyzed arm a slight diminution of the sensibility to touch, and especially 




Fig. 176. — Cerebral infantile paralysis. 
Right hemiplegia. (Personal observa- 
tion.) 



1112 



DISEASES OF THE NERVOUS SYSTEM 



a loss of the ability to recognize objects by the aid of the sense of feeling when 
the eyes are closed (see page 795). Permanent hemianopsia may also be asso- 
ciated with the hemiplegia. Symptoms of motor irritation are found upon ih& 
affected side with striking frequency; the commonest are athetoid movements 
(hemiathetosis, hemichorea) ; and associated movements are also not infrequent.. 
The constant movements of the fingers resulting from the athetosis sometimes 
render the articulations so lax that it is possible to make the fingers assume an 
angle of ninety degrees or even less with the back of the hand, at the metacarpo- 
phalangeal joint. The child may keep making motions with its paretic arm while 
walking. It is not very rare for epilepsy to develop later. There are con- 
vulsive attacks, which usually begin on the paralyzed side, but which may later 
affect the whole body. With right hemiplegia we sometimes see co-existing dis- 
turbances and a defective development of speech. The intellectual development 
of many such children is tolerably normal. Others, however, are more or less 
demented, or betray defective moral sense. 

The whole course of the disease suggests very strongly an acute encephalitis. 
The process is probably in most cases limited more or less completely to the- 
motor region of the cortex, and hence it has been called " polio-encephalitis." * It 
reminds one forcibly of the acute poliomyelitis of children, with a difference 
merely in the localization of the disturbance. It is not impossible that the two 
diseases have a very similar, if not identical, aetiology. They can hardly be differ- 
entiated in their initial stage ; but when further developed they can not be con- 
founded, because the cerebral disease causes unilateral paralysis, leaves the elec- 
trical reactions unimpaired, and frequently causes exaggeration of the tendon 
reflex. It deserves mention that precisely similar phenomena may be presented- 
by children during recovery from measles, scarlet fever, pneumonia, and other 
acute infectious diseases. 

The pathological conditions of the early stage have not yet been studied. 
Long after the process has run its course, the affected portion of the cerebrum 
presents marked atrophy with cicatricial contraction. If the cortex has been 
affected we find a cicatricial depression, a loss of substance, a so-called poren- 
cephaly. At these places the pia is thickened. Sometimes limited cystic forma- 
tions are found. The pyramidal tract exhibits a secondary descending degen- 
eration. It is thus evident that the process is, from an anatomical point of view,, 
precisely like the atrophy of the anterior cornua occasioned by poliomyelitis. 

Of course not all the hemiplegias arising in childhood are due to an encepha- 
litis, for in not a few cases infantile hemiplegia may be due to embolic softening, 
and perhaps sometimes to haemorrhage. In some cases it is often hard to decide 
whether we should regard a cerebral infantile paralysis as the result of a pre- 
vious encephalitis or of some other form of cerebral disease; but it seems to us 
highly probable that a large part at least of the very peculiar infantile hemi- 
plegias must have their special cause, which we have assumed to be encephalitis. 
The chief thing to be considered in the diagnosis is the peculiar onset of the 
disease with fever, convulsions, etc., in a child who was previously perfectly 
healthy. This distinguishes encephalitic paralysis from hemiplegia existing 
since birth (congenital defect, injury at birth). [There is really little patho- 
logical evidence of acute polioencephalitis in children. Sachs and Osier, from 
the study of a large number of cases, find that the cause of the paralysis is almost 
always haemorrhage or embolic softening. — K.] 

The treatment at first is to be governed by the same rules as in the initial 
period of acute poliomyelitis (q. v.). The hemiplegic symptoms which persist 



[* This name, however, has been previously applied by Wernicke to that form of external ophthal- 
moplegia due to changes in the nerve nuclei in the pons (vide page 1045). — K.] 



INSOLATION 



1113 



after the first few months will never improve much. The most we can do will be 
by means of electricity, massage, and cold baths with friction (" cold rubbing")- 
For the epileptic attacks large doses of bromide of potassium are decidedly bene- 
ficial. This may be combined with chloral, belladonna, etc. 

5. Acute Hemorrhagic Encephalitis in Adults. — Cases of acute hemor- 
rhagic encephalitis certainly occur in adults. They have been observed either 
as a sequel of other acute diseases (especially influenza) or as a primary acute 
disease. In such cases very severe cerebral symptoms (headache, loss of con- 
sciousness, hemiplegia) come on quite suddenly and lead to a speedy death with 
high fever. The autopsy shows several haemorrhagic-encephalitic foci, usually 
confined to one hemisphere. The brain substance is yellow and softened, very 
cedematous, and studded with numberless little capillary haemorrhages. Milder 
curable cases of acute encephalitis also seem to occur in adults. 



CHAPTER VI 

INSOLATION. SUNSTROKE. HEAT PROSTRATION. THERMIC FEVER 

[Etiology and Pathology. — Under exposure to undue heat, either in the 
direct rays of the sun, or, during hot weather, in engine-rooms, laundries, and 
the like, marked effects may be produced on the human organism, manifesting 
themselves in a widely different manner in different cases. The liability to these 
effects is much greater with us than in most portions of Europe or in Great Bri- 
tain, and is enhanced by a moist atmosphere which tends to prevent evaporation 
from the surface of the body. Attacks may come on at night and under cover as 
well as by day. While excessive heat is the sole and sufficient exciting cause of 
the changes and symptoms to be described, exhaustion due to muscular exertion 
or other cause plays a very important secondary role. A vigorous person, how- 
ever, of regular and temperate habits, can stand much greater heat and exertion 
than an individual who is debilitated or addicted to the use of stimulants. The 
frequency of attacks after a full meal has been noted. Those newly arrived in 
the country are, other things being equal, more likely to succumb than natives or 
those who have become accustomed to the climate. That high temperature due 
to solar or artificial heat, or a combination of the two, is the prime causative con- 
dition, has been clearly shown by experiments on animals. There is practically 
nothing to add to the researches of H. C. Wood. 

Pathological Anatomy. — In cases of sudden death from shock there are no 
constant and peculiar lesions. The blood is dark, imperfectly coagulated, and 
collected in the veins; ecchymoses are frequently found. 

After death, due chiefly to abnormally high temperature — that is to say, in 
cases of thermic fever — the heart, and especially the left ventricle, is firmly con- 
tracted from post-mortem coagulation of its myosine; the lungs are apt to be 
much engorged with dark fluid blood, and they may be the seat of haemorrhage ; ex- 
travasation of blood under the skin is more or less marked, and haemorrhage into 
and about the cervical sympathetic ganglia has also been observed. The mem- 
branes of the brain and cord are often greatly congested, and there may be evi- 
dences of beginning meningitis. The blood-corpuscles are crenated and show 
a diminished tendency to the formation of rouleaux. Rigor mortis is marked 
and early in the voluntary muscles as well as in the heart, and is attributable to 
the same ca^ise. Parenchymatous degeneration of the organs is sometimes 
found. 



1114 



DISEASES OF THE NERVOUS SYSTEM 



Symptoms and Course. — The onset of the attack is usually sudden, though 
there may be slight premonitions, such as dizziness, pain, or uncomfortable sensa- 
tions in the head. 

It will, perhaps, add to clearness to distinguish three leading forms of attack, 
it being understood that nature does not always classify cases as sharply as is 
done here. The first of these comprises cases of heat prostration, denoted by 
faintness, syncope, nausea, and sometimes vomiting, with marked muscular and 
general weakness. The surface of the body is cool, the pulse rapid and feeble. 
The great majority of these cases are mild, and the symptoms pass away more or 
less quickly on placing the patient in the recumbent posture in a relatively cool 
and quiet place with free ventilation. After a few hours the patient can be re- 
moved to his home, and in a day or two he has recovered perfectly, except for some 
sensitiveness to heat or the sun's rays. There may be transient insensibility, or, 
on the other hand, the case may terminate fatally very soon from general exhaus- 
tion and cardiac failure. 

The second form includes cases with respiratory as well as circulatory failure, 
due especially to the exhaustion of the nerve centers presiding over these func- 
tions. Under this head comes cases of true sunstroke — patients suddenly losing 
consciousness while exposed to the sun. The skin is cold and the pulse is feeble ; 
death may quickly ensue or recovery may follow, especially if prompt and suit- 
able treatment be instituted. The after-effects of the attack may be very slow to 
pass away, and may never disappear entirely. 

The most striking characteristic of the third form is the great increase in the 
temperature- — a symptom which has given rise to the term thermic fever. In this 
form premonitions are more common than in the others. The thermometer may 
register 110° or even more; the skin is burning hot and generally dry; the pulse 
is slow and full, or quick and jerking; the respiration is quickened, sighing, or 
even stertorous; the pupils at first are usually contracted; there may be great 
restlessness ; coma and convulsions sometimes occur ; vomiting is common ; and, 
toward the close of life, the sphincters are sometimes relaxed. A fatal result is 
due to apnoea and asthenia combined. What was said with regard to recovery 
from the second form holds good also for the third. 

Diagnosis. — This is seldom difficult. The circumstances under which the 
attack comes on are generally patent; and the hyperpyrexia, if present, is dis- 
tinctive. Acute alcoholism and meningitis are the chief affections which might 
lead to error. 

Prognosis. — The mortality rate of the severer forms of the disease is very 
high, but the prognosis depends much on the possibilities of securing prompt and 
skillful treatment. Under this many a case recovers from a seemingly desperate 
condition. The tediousness and imperfection of recovery have been already 
alluded to. For long periods in some cases the mental and physical powers are 
much impaired, and great care has to be exercised as regards exertion, high tem- 
perature, and the sun's rays. Insanity is sometimes a sequel. 

Treatment. — In the first place, much may be done by preventive measures to 
obviate the necessity for any treatment. A regular and temperate life will do 
much ; and special precautions of an obvious nature should be taken during hot 
weather by those whose occupations involve a liability to exhaustion and exposure 
to unusual heat. It would be well if it were generally known that there is com- 
paratively little danger of sunstroke so long as perspiration is free. Many an 
attack might be averted by noting the activity of the skin and seeking rest and 
shelter as sweating diminishes. A considerable responsibility rests upon militia 
surgeons and others in similar positions during hot weather. 

Mild cases of heat prostration seldom require other measures than those 
already indicated in describing the symptoms. If there be nausea, and it seem de- 



TUMOKS OF THE BRAIN 



1115 



sirable to give stimulants, they are better given under the skin or by the rectum. 
The clothing should be loosened; the cold douche and other refrigerating meas- 
ures are not indicated unless there is fever, and they should then be used with 
caution. 

For true sunstroke, treatment should be active and energetic, the indications 
being to reduce the temperature of the overheated centers and to stimulate their 
activity. If a cool or shady spot be near at hand, the patient should be removed to 
it and largely stripped of clothing; if not, no time should be lost before resort- 
ing to the cold douche on the head and body while stimulants are administered 
by enema or subcutaneously. External stimulation by mustard or flagellation, 
and purgative enemata, are said to be sometimes useful. The use of cold exter- 
nally should not be prolonged in these cases unless there is fever. Nervous ex- 
haustion is the prominent symptom, and all depressing measures are out of 
place. 

The case is widely different with the third form of the attack. Here the imme- 
diate danger is from the hyperpyrexia, which must be combated by rubbing the 
patient with ice, placing him in a tub of water with lumps of ice, or similar meas- 
ures, until the temperature in the rectum is reduced nearly but not quite to the 
normal point. In the application of the refrigerating measures the head must not 
be neglected. The sole indication at firs^ is the reduction of the temperature. 
Antipyrine subcutaneously has been given in a few cases in the Boston City Hos- 
pital, and also in Brooklyn, with good results, After a reduction of the tempera- 
ture, any symptoms of collapse or exhaustion demand stimulants. 

With regard to the employment of bloodletting there is considerable differ- 
ence of opinion. That cases occur in which this procedure is indicated is un- 
doubtedly true, but they are exceptional; they are characterized by the evi- 
dences of great cerebral congestion without hyperpyrexia. 

The subsequent management of convalescents from any form of sunstroke is 
often very important. Prolonged rest, and sometimes change of climate, may be 
demanded. A symptomatic and common-sense treatment is in place. It has 
seemed to the editor that quinine, especially in solution with a moderate excess of 
sulphuric acid, is distinctly useful in those suffering from mild or moderate after- 
effects of undue heat.] 



CHAPTER VII 
TUMORS OF THE BRAIN 

etiology. — The precise causes which lead to the development of tumors in the 
brain are no more definitely known than in regard to other organs. The new 
growths are usually formed insidiously and gradually without ascertainable cause 
in persons previously healthy. We are therefore disposed at the present 
time to assume that there is some abnormal embryonic predisposition of the tis- 
sues which acts as the special cause of the subsequent new growth. A circum- 
stance which deserves mention is that sometimes the first symptoms come on 
immediately or a short time after some injury to the head. Especially in cases 
of sarcoma arising from the periosteum, the meninges, etc., is a traumatic ori- 
gin (that is, the " setting free " of a predisposition to tumor by the injury) very 
probable, although, of course, hardly ever quite certain. Glioma is also re- 
ferred at times to a traumatic cause. 

Most cerebral tumors are found in persons in youth or middle life. Certain 
forms of tumor, however, particularly solitary tubercles, are comparatively fre- 



1116 



DISEASES OF THE NERVOUS SYSTEM 



quent in children. Sex seems to exert a decided influence : men are much of tener 
affected than women. 

Varieties of Cerebral Tumor.*— The most important forms of tumor seen in 
the brain are as follows : 

1. Glioma. — Glioma is a kind of tumor peculiar to the central nervous system, 
but seen much of tener in the brain than in the spinal cord (vide page 1024). 
Apparently the new growth always originates in the neuroglia, which is the con- 
nective-tissue framework of the true nervous matter. As seen under the micro- 
scope, a glioma is made up of fibers and cells, the latter being like the normal 
cells of the neuroglia, while the fibers seem to consist mainly of the numerous 
cell-processes. Whether the ganglion-cells also take an active part in the new 
growth has not yet been proved. It is characteristic of gliomata that they are 
seldom sharply defined, but shade off gradually into the healthy tissue. The 
affected portion of the brain is usually enlarged, but yet maintains pretty nearly 
its original shape. On cross-section, the parts that have undergone " gliomatous 
degeneration " present a yellowish or reddish-gray surface. It is usually rather 
soft, and almost always is very vascular. This great vascularity is not without 
clinical importance, for variations in the fullness of the blood-vessels, and, above 
all, sudden haemorrhages into the interior of the new growth, which not infre- 
quently occur, may produce marked symptoms. 

Gliomata are most frequent in the white substance of the cerebral hemi- 
spheres, but they are also found in the central ganglia, cerebellum, and else- 
where. They are usually single, seldom multiple. 

2. Sarcoma. — It is very seldom that any form of sarcoma originates in the 
brain-substance. It usually begins in the connective tissue of neighboring parts, 
in the dura mater, the periosteum of the cranium, or the cranium itself (osteo- 
sarcoma). The sarcoma is found most frequently at the base of the skull, in the 
form of a circumscribed tumor of varying consistency, and by pressing upon 
neighboring parts, or by involving them in the diseased process, it may cause 
the gravest disturbances. Histologically, we have here such varieties as round- 
celled or spindle-celled sarcoma, fibro-sarcoma, etc. 

3. Gumma and Solitary Tubercle. — Both gumma and solitary tubercle are 
very prone to attack the brain. We shall revert to gumma in the chapter on 
cerebral syphilis. Solitary tubercles may grow to the size of a cherry or larger. 
They may be single or multiple, and may occupy any part of the brain. They 
are found most frequently in the cortex, and in the cerebellum and pons. 

Solitary tubercles and. gummata, upon cross-section, have a yellowish, cheesy 
appearance, and are usually distinctly defined. Histologically, they are composed 
of granulation tissue. It was formerly no easy matter to distinguish gumma 
from tubercle in all cases; but now certainty is attainable by determining the 
presence of tubercle bacilli in the latter. 

4. Carcinoma. — Carcinoma completes the list of such cerebral tumors as have 
much clinical importance.- It is almost always secondary in the brain. It has 
been our experience that secondary cancer of the brain is associated principally 
with primary cancer of the breast, or of the lungs and pleura ; which fact bears a 
remarkable analogy to the occurrence of secondary cerebral abscess after primary 
empyema, pulmonary gangrene, etc. g± 

5. Among the rarer varieties of tumor is psammoma^whioh. usually starts 
from the meninges, is hard, generally comparatively small, and therefore often 
harmless, and contains calcareous matter, so that it grates under the knife. 



* From a clinical standpoint, the term "cerebral tumor" usually is meant to include also such 
tumors as originate in the neighborhood of the brain (as in the base of the skull), if they finally 
involve the brain itself. 



TUMORS OF THE BRAIN 



1117 



The calcareous deposits are found in the form of roundish objects, which are 
composed of flat cells which lie over one another like the coats of an onion. 
Psammoma is probably of endothelial origin. Cholesteatoma, which has a sheen 
like mother-of-pearl, has also been observed in rare instances, and also angio- 
sarcoma, angioma, etc. The not very rare growths arising from the hypophysis 
cerebri (" struma of the pituitary gland ") remind us of adenomata in their 
structure. 

6. In addition to the true tumors we may mention the cysts of the brain. 
They develop in very rare cases without known cause (perhaps as a sequel to 
cranial injuries?), they may grow to the size of an apple, and may cause pre- 
cisely the same clinical symptoms as a tumor of the brain. 

The General Symptoms of Cerebral Tumors. — As is the case with all focal 
diseases of the brain, some of the symptoms of cerebral tumors are connected with 
the special localization of the new growth. There are definite focal symptoms, 
varying with the part destroyed, or at any rate functionally impaired, and it is 
from these symptoms alone that we are enabled to determine the position of the 
tumor. But, in addition to these focal symptoms, there are certain general symp- 
toms common to almost all cerebral tumors of any size. They are in large part 
referable to the general compression of the brain due to the enlargement of the 
new growth. In the first place, numerous clinical facts indicate that whenever 
there is a tumor of any great size, a large part of the entire encephalon is sub- 
jected to pressure; and, secondly, the anatomical appearances of almost every 
brain affected by a large-sized tumor lead to the same conclusion. The convolu- 
tions are flattened and obliterated, the dura mater is crowded against the crani- 
um, and perhaps thinned or even perforated because of the persistent pressure, or, 
on the other hand, thickened as a result of chronic inflammation. Now and 
then the effects of pressure are visible even in the bones of the skull : they are 
worn thin, or even perforated, or their sutures are loosened. Another result of 
the general intracranial tension, through its effect upon the venous trunks of 
the brain, is serous effusion into the ventricles (internal hydrocephalus), which 
occurs very frequently. The largest effusions are caused by tumors in the pos- 
terior cerebral fossa, which directly compress the vense Galeni. 

The symptoms of cerebral tumors, referable to the effects of general compres- 
sion, are as follows : 

1. Headache is one of the earliest and most constant symptoms. It is usually 
persistent, although subject to temporary exacerbations and intermissions. The 
patient describes it as dull, deeply seated, and stupefying. Although it affects the 
whole head, it is sometimes (not invariably) referred mainly to the neighborhood 
of the tumor. It is particularly true of persistent occipital headache that it indi- 
cates a new growth in the posterior fossa. Sometimes also it is possible, by tap- 
ping upon the skull, to find an especially tender region. Considerable caution, 
however, should be used in drawing diagnostic conclusions from such observa- 
tions. The headache usually lasts to the close of the disease, and, even after the 
patient has become completely comatose, the persistence of the pain is still evi- 
dent from his low groans and the way in which his hand seeks his head. 

2. Next in frequency to headache are disturbances of the sensorium and intel- 
ligence. Even the facial expression may be somewhat characteristic, being pe- 
culiarly languid, apathetic, and dull. The patient talks slowly, often having to 
think a long time before knowing what to say. Memory becomes impaired, 
especially with regard to the most recent events. The interest of the patient in 
those about him, and the things he used to care for, grows less and less. He has 
a sleepy, dazed look, and grows careless and untidy. There is sometimes pro- 
nounced somnolence. Of course, individual cases present various deviations from 
this outline ; but in general, all cases are a good deal alike, although the degree of 



1118 DISEASES OF THE NEEVOUS SYSTEM 



mental disturbance may vary from the slighter forms of stupor to the highest de- 
grees of mental weakness. We occasionally see other forms of mental disturb- 
ance in tumors of the brain, such as melancholy, hallucinatory confusion, states of 
excitement, abnormal attempts at wit (Witzelsucht), etc. In such cases, however, 
local disturbances (especially in the frontal lobe) are probably to be taken into 
account. 

If unusual fullness of the blood-vessels, a haemorrhage into the new growth, or 
some similar cause, induces a sudden temporary increase of tension, there may be 
such marked symptoms as syncope or an apoplectiform shock. 

3. Other general cerebral symptoms are vertigo, slowing of the pulse, and 
vomiting. If, however, vertigo be a very prominent symptom, it implies that the 
cerebellum is especially encroached upon by the tumor. The retardation of the 
pulse is a frequent symptom, and not without diagnostic value. It has already 
been mentioned as one result of general compression of the brain, in connection 
with cerebral haemorrhage. The rate may be put at about 50 to 60, or even lower. 
The pulse is also sometimes slightly irregular. Cerebral vomiting may be one of 
the earliest and most troublesome symptoms. It frequently occurs independently 
of the ingestion of food, especially in the morning, and is not infrequently asso- 
ciated with dizziness. 

4. Epileptiform convulsions are sometimes excited by cerebral tumors, al- 
though many patients are free from them. Such attacks in all probability origi- 
nate invariably in the cortex of the cerebrum, and it is therefore natural that 
they should be seen most frequently (as they are) in connection with tumors in 
the cerebral hemispheres. This rule, however, is not without exceptions. If the 
convulsions are not general, but are unilateral or confined to distinct portions of 
the body, they are to be regarded rather as focal than as general symptoms, and 
they may be utilized to determine the position of the lesion (vide page 1073). A 
certain amount of information in the same direction may also be obtained from 
those attacks which begin unilaterally or in one particular limb, and then quickly 
involve the entire body. 

5. Optic neuritis (" choked disk ") is one of the most important and common 
general objective symptoms of cerebral tumor, occurring in about eighty per cent, 
of all cerebral tumors. We should therefore never omit to make an ophthal- 
moscopic examination of the fundus oculi in a case of chronic cerebral disease. 
Some differences of opinion yet exist in regard to the special pathology of optic 
neuritis ; but we may regard it as extremely probable that the main factor in its 
production is the purely mechanical one of general compression of the brain. 
This opinion is supported especially by the fact that even a marked choked disk 
may disappear completely in a short time, if a lessening of the intracranial 
pressure be brought about by trephining the skull and causing an abundant dis- 
charge of cerebrospinal fluid. The original view of Yon Graefe was that the 
increased intracranial pressure obstructs the venous return through the vena 
centralis retinae into the cavernous sinus. The opinion which prevails at present 
is that advanced by Schmidt and Manz — namely, that the increased tension forces 
the cerebro-spinal fluid into the lymph-sheath of the optic nerve (Schwalbe), and 
that the " hydrops vagince nervi optici " thus produced compresses the nerve 
and the blood-vessels which traverse it. [Leber and Deutschmann have shown 
pretty conclusively that the increased pressure is not the chief cause of optic 
neuritis. It favors its production, but probably there must be the presence of 
some irritant as well, in order to produce the inflammation. — K.] At any rate, 
optic neuritis is not a focal symptom. The tumor occasioning it may have any 
position, if only it gives rise to general compression of the brain. 

Disturbances of vision may be entailed by optic neuritis, but they are not a 
necessary consequence of neuritis; the patient may have amblyopia, defects in 



TUMORS OF THE BRAIN 



1119 



the field of vision, or even total blindness. Only in a few instances has amblyopia 
been one of the earliest symptoms of cerebral tumor, so that the patient has 
applied first of all to an oculist. Usually the sight is preserved for quite a long 
time, in spite of the abundant objective evidences of optic neuritis. The latter 
consist of swelling of the disk, marked distention and tortuosity of the veins, 
possibly haemorrhages (from passive congestion), and cloudiness of the disk, 
although the retina still exhibits its normal transparency. It is not until the 
long-continued congestion impairs nutrition to such an extent as to cause atrophy 
of the optic nerve that vision is much impaired. 

6. General loss of flesh and strength may sometimes appear comparatively 
early in cases of tumor of the brain. It is due in large part to the small amount 
of food taken, vomiting, and wakefulness ; but it is not impossible that the grave 
cerebral disorder itself exerts a direct and unfavorable influence upon all the 
processes of nutrition. There is in most cases, also, a tendency to obstinate con- 
stipation. 

7. In conclusion we may mention that, on examination of the spinal cord of 
persons who have died of cerebral tumor, degenerative changes have been found 
in the posterior columns and posterior roots (Dinkier, Mayer, and many others), 
besides the ordinary secondary descending degenerations. These changes are 
probably a consequence of the increased cerebral pressure and the stasis of cere- 
brospinal fluid thus occasioned, and thus they may be classed among the " gen- 
eral symptoms " of tumor. As a rule they have no clinical significance ; but an 
otherwise inexplicable loss of patellar reflex may perhaps often be referred to 
these secondary changes in the spinal cord. 

Tumors in the Different Parts of the Brain and their Focal Symptoms.— The 
symptoms above discussed indicate the existence of a tumor, but not its particular 
location. Other phenomena are necessary to enable us to localize the disease, 
but it is not exceptional to have none but the general symptoms. Tumors in the 
white matter of the frontal lobe, or tumors of the corpus striatum or optic thala- 
mus, as well as others, may run their course without any focal symptoms; but 
most cases afford evidence which points with more or less certainty to the exact 
position of the tumor. Almost all of these focal symptoms have already been 
fully discussed in Chapter II of this section, and their interpretation follows the 
rules for all focal lesions of the brain. We may therefore be brief here. It is 
necessary only to emphasize the fact that with regard to cerebral tumors, as well 
as other lesions, focal symptoms should be divided into the direct and the indirect. 
Direct focal symptoms are the immediate result of the destruction of nervous tis- 
sue by the new growth, while the indirect symptoms are excited by the pressure ex- 
erted by the tumor upon the parts closely surrounding it. This pressure varies 
with the amount of blood in the vessels of the new growth, and therefore the indi- 
rect symptoms may undergo temporary exacerbations and remissions. An inter- 
mediate position is occupied by those focal symptoms which occur in many cases 
as the result of certain anatomical changes secondary to the new growth. Not 
infrequently there is white softening of the substance of the brain around the 
tumor proper. Probably this condition is generally the result of a compression 
of the minute blood-vessels surrounding the new growth, but sometimes it is the 
sequel of an obliterative endarteritis (Friedlander). The latter cause is espe- 
cially operative when the tumor is a gumma or a solitary tubercle. In vascular 
new growths also, especially in gliomata, haemorrhages may occur which may 
often exert a destructive influence over a greater territory than the new growth 
itself. 

1. Tumors of the Cerebral Hemispheres. — Tumors in the vicinity of the 
central motor convolutions are especially important, because they give the best 
opportunity for an accurate topical diagnosis and surgical treatment. The 



1120 



DISEASES OE THE NERVOUS SYSTEM 



first focal symptoms are usually attacks of partial epilepsy, such as have already 
been described in detail (page 1073)". Monoplegia gradually sets in, which may 
gradually develop to complete hemiplegia. At first there is, for example, a 
brachio-facial or a crural monoplegia, and later the paralysis attacks the leg 
or the arm on the same side. The precise peculiarities of cortical spasms and 
paralyses have been described above (see page 1072). On careful examination, 
disturbances of the tactile and stereognostic senses can often be discovered in 
the paralyzed limbs. Ataxia and, with tumors of the left hemisphere, disturb- 
ances of speech may also occur. Tumors which involve the temporal lobes cause 
soul deafness or amnesic (sensory) aphasia. Tumors of the occipital lobe may 
be recognized by the occurrence of disturbances of vision (soul blindness, hemian- 
opsia). In tumors of the frontal lobe Bruns and others have repeatedly observed 
a striking disturbance of the gait (a staggering gait, a tendency to fall to one 
side or backward, similar to cerebellar ataxia). This is probably connected 
with a disturbance of the motor centers for the muscles of the trunk, which are 
situated in the frontal lobe. Tumors of the brain not very infrequently arise in 
the corpus callosum, but these can hardly ever be diagnosticated with certainty. 
Characteristic focal symptoms are lacking; there are usually only the general 
symptoms of a tumor and especially deep disturbances of consciousness (stupor, 
somnolence, loss of intelligence, etc.). 

2. Tumors at the Base of the Brain. — The base of the brain is a favorite 
seat of new growths. The symptoms are in a majority of cases quite character- 
istic. Some of the tumors spring from the base of the skull; among these are 
many sarcomata and syphilitic growths ("gummatous periostitis")- Other tu- 
mors originate in the meninges, especially the dura; and still others from the 
brain itself. Of these last, it is remarkable that some spring from the pituitary 
gland. The exact starting point is very seldom of much clinical importance, for 
all the parts mentioned are in such close proximity to one another that there is 
no great difference in the symptoms produced. We can decide merely that there 
is a tumor in this or that place at the base of the brain. 

Tumors at the base of the brain owe their characteristic clinical stamp to the 
frequency with which the cranial nerves at the base are involved. The anatom- 
ical relations are such that these nervous trunks are often compressed by the new 
growth or actually incorporated in it. Of the symptoms thus occasioned, the 
most frequent is paralysis of the motores oculi (oculo-motor and abducens). This 
is at first usually unilateral, but it may later affect both sides. If one of the optic 
tracts be involved, hemianopsia may result, and pressure upon one optic nerve may 
produce unilateral choked disk with unilateral disturbance of vision. Tumors of 
the pituitary gland are especially prone to cause symptoms referable to the optic 
nerve at an early period (compare also page 902). Lesions of the trigeminus 
not infrequently cause disturbances of sensation in the face, and occasionally 
also paralysis of the muscles of mastication. The trunk of the facial often 
suffers. The facial paralysis thus occasioned throws considerable light upon the 
diagnosis, for the frontal muscle and the orbicularis oculi are involved (compare 
page 862), and there is usually to be found in the paralyzed muscles the reaction 
of degeneration, showing that the paralysis is peripheral. We have therefore 
reason to assume that the lesion is situated at the base of the cranium, rather than 
in the brain itself. Tumors arising from the posterior fossa at the base of the 
brain cause pressure paralysis of the lower cranial nerves (hypoglossus, accessory) 
and sometimes pronounced bulbar symptoms (disturbances of swallowing and ar- 
ticulation) from pressure on the medulla. As might naturally be expected, vari- 
ous degrees and forms of paralysis in the extremities are often found in combina- 
tion with all the above-mentioned disturbances of the cranial nerves. Such condi- 
tions are most frequent when the cms cerebri, with its pyramidal tract, is affected. 



TUMORS OF THE BRAIN 



1121 



There is no need of enumerating all the possible varieties of symptoms. We 
must consider them all carefully in each individual case, and then, by bearing 
in mind the anatomy of the parts, we shall, in a majority of instances, be enabled 
to determine with some approach to accuracy the place at the base of the brain 
where the new growth must be. Sometimes we may be led into error by tumors 
which, though situated in the brain-substance and at a comparative distance, yet 
by their pressure give rise to indirect symptoms referable to the cranial nerves 
at the base. 

3. Tumors in the Neighborhood of the Third Ventricle. — Tumors sometimes 
develop, which are situated in a central position in the interior of the brain, 
especially in the neighborhood of the third ventricle, and therefore give rise to 
few well-marked focal symptoms. Besides the general symptoms of tumor (amau- 
rosis from optic neuritis, stupor, headache, vomiting) there is general weakness 
of the extremities, often associated with spastic rigidity, which is usually only 
a little more developed on one side than on the other. As a rule, therefore, it is 
hard to make an accurate topical diagnosis. 

4. Tumors of the Cerebellum. — Cerebellar tumors are comparatively frequent, 
and they can usually be diagnosticated with considerable certainty. The charac- 
teristic focal symptoms of all cerebellar diseases have already been fully de- 
scribed above (see page 1086). We will recall here in particular the feeling of 
vertigo and the staggering gait. But cerebellar tumors generally occasion also 
very strongly pronounced general symptoms — namely, headache, mainly occipital ; 
sometimes a spasmodic and persistent stiffness of the neck ; vomiting ; and visual 
disturbances, due mainly to the frequent existence of optic neuritis. Analogous 
to this last symptom would seem to be disturbances in other nerves of special 
sense. Thus, when the general intracranial pressure is elevated, the acoustic 
and olfactory nerves seem liable to passive congestion. Tumors in the posterior 
fossa have several times been found to occasion bilateral anosmia and deafness ; 
and they should always be considered when such a condition is found. Cere- 
bellar tumors not infrequently as they continue to grow exert pressure upon 
the pons and medulla, and thus special clinical symptoms may arise : symptoms 
of paralysis or irritation on the part of the posterior cranial nerves, nystagmus, 
hemiparesis, hemiataxia, etc. 

5. Tumors in the pons, the crura cerebri, and the medulla are to be judged 
according to the general rules for the localization of cerebral diseases. 

We may also observe, by way of an appendix, that repeated attempts have been 
made of late to make use of percussion of the skull as an aid in the diagnosis 
of the seat of a cerebral tumor. Over a tumor which is not too deeply seated 
the bones of the skull are said to give sometimes on percussion a note which is 
not wholly dull but rather tympanitic. A sort of " cracked-pot " resonance has 
also been observed. Percussion of the skull, however, can hardly claim great 
practical significance, since the interpretation of the results is too uncertain. 
[A few attempts have also been made to employ the Rontgen rays to reveal the 
situation of the tumor, but the results thus far have not been very definite. 

In view of the increasing importance of the focal diagnosis of tumors of the 
brain, it has seemed advisable to insert the following brief summary of the focal 
symptoms of tumors in different parts of the brain : 

Prefrontal Region. — Marked mental impairment (abnormal attempts at wit 
[Witzelsucht] ?) ; symptoms of invasion of the central region (Jacksonian epi- 
lepsy, aphasia) ; staggering gait ; disturbances of smell. 

Central Region. — Jacksonian epilepsy; monoplegia; tactile hyposesthesia and 
loss of stereognostic sense; motor aphasia. 

Posterior Parietal Region. — Word-blindness; disturbance of muscular sense ( ?) ; 
homonymous hemianopsia. 
71 



1122 



DISEASES OE THE NERVOUS SYSTEM 



Occipital Region. — Homonymous hemianopsia; soul-blindness. 

Temporo-Sphenoidal Region. — Often a latent region. Word-deafness, if the 
left side be affected; disturbances of taste, smell, and hearing. 

Corpus Callosum. — Often a latent region. Progressive hemiplegia, often bi- 
lateral from invasion; mental disturbances. 

Optico-striate Region. — Hemiplegia; contracture. In posterior part, hemi- 
ansesthesia, homonymous hemianopsia, post-hemiplegic chorea, athetosis. 

Crus Cerebri. — Crossed paralyses of the oculo-motor nerve and limbs. 

Corpora Quadrigemina. — Oculo-motor paralyses; reeling gait; blindness (?);. 
deafness ( ?). 

Pons and Medulla. — Crossed paralyses of face and limbs, or tongue and limbs. 
Other cranial nerve lesions. 

Cerebellum. — Marked cerebellar ataxia; marked vertigo and vomiting. 

Base, Anterior Fossa. — Mental impairment; disturbances of smell and vision;, 
exophthalmus. 

Base, Middle Fossa. — Disturbance of vision; oculo-motor disturbances; hemi- 
plegia. 

Base, Posterior Fossa. — Trigeminal neuralgia; neuro-paralytic ophthalmia; 
paralyses of face and tongue; disturbance of hearing; crossed paralyses. 

Hypophysis. — Disturbance of vision, especially bitemporal hemianopsia; ocu- 
lo-motor disturbances; acromegaly. 

It also is of importance, in cases which may come to operation, to determine 
whether the growth be cortical or subcortical. Seguin has given certain rules 
which, however, are not absolute. " In favor of a strictly cortical or epicortical 
lesion are these symptoms, none of them having specific or independent value: 
localized clonic spasm; epileptic attacks beginning by local spasm, followed by 
paralysis ; early appearance of local cranial pain and tenderness ; increased local 
cranial temperature. In favor of subcortical location of a tumor : local or hemi- 
paresis followed by spasm; predominance of tonic spasm; absence, small degree, 
or very late appearance of local headache and of tenderness on percussion; nor- 
mal cranial temperature." — K.] 

General Course of Cerebral Tumors. — The symptoms of these growths almost 
always cover a long period of time. Exceptionally a tumor remains latent till a 
haemorrhage or some similar event takes place in it, giving rise to sudden and 
grave symptoms, and possibly to an equally sudden termination. The rule is, 
however, for the phenomena to develop gradually. According to the location of 
a new growth, either the general or the focal symptoms may come first into 
prominence. They generally occur in the order named. Eirst of all is an ill- 
defined, deeply seated headache, and by degrees all the other general and focal 
symptoms follow after. The symptoms may vary repeatedly and greatly in 
severity, a fact due mainly to the varying pressure of the tumor on neighboring 
parts. Eepeated mention has already been made of the sudden exacerbations 
which may come on, especially in case of the vascular gliomata. 

The entire duration of the disease is usually at least some months, and may be 
one or two years or more. The termination is almost invariably unfavorable. 
Death may be rather sudden, or it may not come till after a long period of wretch- 
edness. Fortunately, however, the lameness, blindness, and marasmus are fre- 
quently made less terrible to the patient because of his mental debility. Eecovery 
is possible only when the growth is syphilitic. It is indeed possible that solitary- 
tubercles may also end favorably, but the matter is still in doubt. 

Diagnosis. — The main points in support of a diagnosis of cerebral tumor would 
be the gradual onset and continuous slow increase of the general symptoms above 
detailed — namely, headache, vertigo, vomiting, convulsions, dementia, etc. The 
most constant of these symptoms is the headache. They all indicate the develop- 



TUMORS OE THE BEATS" 



1123 



ment of some chronic brain trouble., a tumor being the most probable if there be 
no definite aetiology to suggest some other process, such as traumatism resulting 
in abscess, or syphilis. Much stress may also be laid on the optic neuritis, since 
this, as we hare said, is much less often seen in other chronic brain diseases 
(abscess or softening) than in tumor. 

The general symptoms indicate that a tumor of the brain exists ; but, in order 
to learn the position of that tumor, we have to rely mainly upon the focal symp- 
toms. Their gradual development and the way in which one new symptom is 
slowly added to another, also give further ground for the opinion that some 
continuously progressive disease exists, and most probably a cerebral tumor. Of 
diseases with a similar course, abscess is recognized especially by the slighter 
symptoms of general intracranial pressure and by the absence of optic neuritis, 
frequently by febrile symptoms, and by its aetiology (trauma, purulent otitis). 
Inflammatory and thrombotic softening, if they come on slowly, usually produce 
less general disturbance than do tumors; they hardly ever cause optic neuritis, 
and (unless of syphilitic origin) are much rarer before middle age than tumors 
of the brain. Sclerosis sometimes simulates cerebral tumor; but here also there 
is no choked disk; the disease lasts much longer (five or ten years, or more), 
and, inasmuch as the sclerosis is usually multiple, there is frequently too great 
a complexity of symptoms to warrant the assumption of one solitary lesion. 
[We must, however, bear in mind that, in about one seventh of the cases, tumors 
also are multiple. — KJ 

Certain rare cases of chronic circumscribed meningitis can not be differen- 
tiated from a tumor. They generally occur at the base, lead to a considerable 
thickening of the tissues, and they may simulate all the symptoms of a new 
growth in this region. Occasionally, also, chronic hydrocephalus is confounded 
with tumor of the brain. "We met with a case of dropsy of the fourth ventricle 
which presented during life a perfect picture of tumor of the cerebellum. 

As to the nature of a new growth, we can not go beyond surmises. If the 
focal symptoms indicate that the tumor is in the substance of the brain itself, our 
first thought would be of a glioma, because it is by far the commonest sort of 
growth in that situation; and, as has been stated, certain peculiarities in the 
course of the disease (especially if new symptoms add themselves abruptly) would 
make glioma probable. If, on the other hand, the tumor be at the base, it is 
most apt to be sarcoma, which is the most frequent form of new growths here. 
When symptoms referable to the optic nerve occur noticeably early, a tumor of 
the pituitary gland is to be thought of. In all cases, and especially in tumors at 
the base of the brain, we should bear in mind the possibility of syphilis. The 
previous history and the entire body of the patient should be closely searched 
with this point in mind ; its therapeutic importance need not be dwelt on. 

One special form of tumor deserves a brief mention here — namely, large 
cerebral tubercles. The growth may be single or solitary, or it may be multiple. 
It is seen chiefly in childhood, and any chronic cerebral disorder in a child should 
suggest the possibility of such a growth. It is rendered all the more probable by 
the co-existence of the signs of tuberculosis elsewhere, as in the lymph-glands, 
lungs, or bones. The symptoms are analogous to those produced by other tumors. 
Among the most frequent phenomena are headache and convulsions. The latter 
are often unilateral. There may also be all sorts of focal symptoms, according to 
the locality of the lesion. 

Prognosis. — Except gum mat a, all tumors of the brain have a very unfavor- 
able prognosis. It is said that in very rare instances tubercular growths have 
been arrested or cured: but in practice we can never rely upon any such result. 
In all other cases recovery is next to impossible. The time intervening between 
the appearance of the first symptoms and death varies greatly, as has been said. 



1124 



DISEASES OE THE NERVOUS SYSTEM 



We should therefore be very cautious in predicting the duration of the illness. It 
seldom, however, exceeds one or two years, and sudden death without any warn- 
ing may occur at any time. 

[Tubercular growths are occasionally found at autopsies, which have become 
encapsulated, and have apparently existed for years without causing symptoms. 
In some cases, especially with tubercular growths in children, the symptoms 
diminish and the patient may live for years, suffering only from the blindness, 
etc., caused by the growth. Other cases may present only mild symptoms, and 
the patient may lead a fairly comfortable life for years. — K.] 

Treatment. — Inasmuch as the nature of the tumor can not be determined with 
absolute certainty in any instance, antisyphilitic treatment should always be 
tried. Eorty to seventy-five grains of mercurial ointment (grm. 3-5) should be 
used by inunction, and thirty to seventy-five grains (grm. 2-5) of potassic iodide 
should be given internally each day. If the new growth be syphilitic, much bene- 
fit may be obtained in this way. It -must be confessed that the treatment is gener- 
ally of little avail, because the tumors are not of a syphilitic character ; although 
it may be that iodide of potassium sometimes has a temporary good effect 
upon other forms. A long-continued course of arsenic has also been recom- 
mended, in order to check the growth of the tumor. This remedy should be used 
especially in those cases where there is a suspicion of sarcoma or solitary 
tubercle. 

Of late years many attempts have been made to remove tumors of the brain 
by surgical measures. In this respect the special favorable conditions of the 
individual case are chiefly to be considered. If we are able to make an approx- 
imately certain diagnosis of a tumor on the surface of the brain, especially in 
the motor cortex, surgical interference is warranted, and in some cases it has 
been attended with decided success, either permanently or at least for a time. 
Since there is no outlook for the patient's recovery without an operation, we 
should make an attempt at operation in every case where the tumor can appar- 
ently be diagnosticated with certainty and localized in the motor region of the 
cortex. We should, of course, never undertake an operation with too great ex- 
pectations, since errors in diagnosis and unforeseen complications and incidents 
only too often arise. When there are marked general symptoms of pressure 
(headache, somnolence, optic neuritis) it may be well worth while, as a practical 
measure, to advise simple opening of the skull without further interference. 
In some cases the lessening of intracranial pressure that ensues has a very favor- 
able effect, at least upon these general pressure symptoms of tumor. 

Beyond what has just been indicated, treatment must be symptomatic. The 
headache is combated with ice-bags, narcotics, antipyrine, etc.; the convulsions 
require bromide of potassium or the inhalation of chloroform; the vomiting is 
lessened by rest in bed, opium, and bits of ice. The general care and nursing 
of the patient are very important, so that bedsores and the like may be avoided 
if possible. 

APPENDIX 

HYDATIDS OF THE BRAIN 

It was stated on page 510 that the cysticercus cellulose, which originates 
from the taenia solium, may occur in great numbers in the brain. The cysticerci 
most frequently occupy the pia mater, but generally project downward into the 
cortex of the brain. The meninges not infrequently exhibit signs of chronic 
inflammation, and may present hemorrhages, which are not always minute. If 
there are numerous cysticerci in the neighborhood of the ventricles, a varying 
degree of internal hydrocephalus usually develops. The individual cysticerci are 



CEREBKAL SYPHILIS 



1125 



usually enveloped in a capsule of connective tissue, but they may be entirely de- 
void of such a covering. 

JSTo characteristic clinical sketch of hydatids in the brain can be drawn, be- 
cause the symptomatology of each case differs according to the number and posi- 
tion of the parasites. Sometimes cysticerci produce absolutely no symptoms, and 
are discovered incidentally at the autopsy. In other instances they cause a long 
and tedious illness. Epileptiform convulsions seem to be the most frequent symp- 
tom, and these must be due to the position of the cysticerci in the cortex of the 
brain. They may, like true epileptic attacks, come on only at certain times when 
the general condition is otherwise good ; or permanent general cerebral symptoms 
may also appear, such as persistent headache, vertigo, and mental disorder. In 
a case recently under our observation the symptoms consisted solely of parox- 
ysmal headache and uncontrollable vomiting. The diagnosis of suspected tumor 
was made. The autopsy showed a cysticercus the size of a cherry in the fourth 
ventricle with secondary hydrocephalus. Other cases have shown merely mental 
disturbances (confusion), staggering gait, vertigo, etc., so that the disease has 
been repeatedly confounded with hysteria. Special focal symptoms are only 
rarely present with cysticerci of the brain. It is a fact of great practical signifi- 
cance that death may not infrequently come on suddenly and unexpectedly in 
cysticerci of the brain. We have seen several such cases in persons who pre- 
viously had not complained of feeling at all ill, or wno had complained merely 
of slight headache, etc. In such cases the cysticerci are usually in the third or 
fourth ventricle, and probably cause sudden pressure upon the medulla. 

The diagnosis can never be made with absolute certainty. The presence of 
cysticerci in the brain may be suspected when the above-mentioned severe symp- 
toms occur in a butcher or other person who is from his calling especially exposed 
to infection, or who is known to have had or still to have a tapeworm, or in whom 
cysticerci have been demonstrated in some other part of the body, such as the skin. 

We know of no remedy capable of destroying the cysticerci. Treatment, there- 
fore, can be only symptomatic. [In a few cases, chiefly in Australia, the cysticerci 
have been successfully removed hy surgical interference. — K.] 



CHAPTER VIII 
CEREBKAL SYPHILIS 

^Etiology. — The importance of syphilis as an ^etiological factor in many 
chronic diseases of the nervous centers has been repeatedly adverted to in pre- 
ceding chapters ; but, as we have already stated, the influence of syphilis upon the 
genesis of these diseases is shown in two essentially different ways. In one case 
there is a probable toxic, so-called post-syphilitic degenerative process of certain 
tracts of fibers and ganglion-cells (tabes, general paralysis) ; in the other case 
there is the formation of true tertiary syphilitic (" gummatous ") new growths. 
Only this latter form of syphilitic cerebral disease will be spoken of here. 

As a rule, genuine cerebral syphilis develops in the later stages of the whole 
syphilitic process, but sometimes cerebral symptoms come on by the end of the 
first year from the date of the initial lesion. Usually the interval is several 
years, and it may be ten or even twenty years after the beginning of the disease, 
before the first signs of the cerebral trouble develop. We therefore class cere- 
bral syphilis generally among the " tertiary symptoms " of syphilis. 

Liability to the disease does not seem to be influenced essentially by age or 



1126 



DISEASES OF THE NERVOUS SYSTEM 



sex, except so far as pertains to the general distribution of syphilis. Even 
hereditary syphilis has been proved to cause diseases of the nervous system. But 
it can not be denied that a predisposition to cerebral syphilitic disease is often 
engendered by those influences which are apt to promote cerebral disease in gen- 
eral. Just as the position of syphilitic cutaneous lesions is often determined by 
external irritation at some one place on the skin, so the disease seems more liable 
to attack a brain which is exposed to certain unfavorable conditions than one 
which is perfectly normal and vigorous. Such conditions are inherited tendency 
to nervous diseases, various injurious mental influences, poisons, in a broad sense, 
and traumatism. It need hardly be said that even a previously sound brain does 
not enjoy immunity from the affection. 

Pathology. — As far as has yet been ascertained, there are two chief forms 
assumed by syphilis in the brain: (1) a circumscribed, broad, flat syphilitic new 
growth like a tumor (gumma, syphiloma), and (2) a disease of the arteries of the 
brain, which is usually quite extensive. There is no essential difference underly- 
ing these two varieties. They may also occur in combination with each other. 
The disease of the blood-vessels is really a syphilitic new growth affecting the 
walls of the arteries. 

The syphilitic new growths are yellowish or grayish-red, and frequently 
cheesy in the center. Their most frequent seat is the dura mater or the sub- 
arachnoid space whence they spread to the brain-substance or the neighboring 
vessels and nerves ; but exceptionally they may originate in the substance of the 
brain itself. Histologically they are made up of granulation tissue of varying 
degrees of vascularity, presenting yellow spots usually visible to the naked 
eye. These spots are of firmer consistency than the rest of the growth, and have 
undergone coagulation-necrosis (have become cheesy). In the brain substance 
itself circumscribed, wedge-like gummata may sometimes develop, which closely 
resemble solitary tubercles ; but the extensive, flat syphilitic new growths arising 
from the meninges (meningitis gummosa) are of much greater clinical impor- 
tance. These are found most frequently at the base of the brain, especially devel- 
oping from the region of the chiasma, or, more rarely, on the lateral portions of 
the brain (fissure of Sylvius) or on the convexity. In these more extensive new 
formations of tissue we usually find all the different stages of the process to- 
gether, fresh granulation tissue, cheesy places, and finally the transition into 
contracting cicatricial connective tissue (scar formation). 

The syphilitic disease of the arteries was first fully appreciated by Heubner, 
who has described it accurately. It is usually most pronounced in the arteries of 
the base of the brain, and especially in the middle cerebral artery and its branches. 
Even the unaided eye detects a grayish opacity in the arteries. They feel firm 
and stiff, and on cross-section their walls are found to be thickened, either uni- 
formly or in some places more than in others. This causes no inconsiderable nar- 
rowing of the lumen, or even its obliteration, particularly if the last gap be closed 
by the formation of a thrombus. The microscope shows that the new growth 
originates chiefly in the intima of the vessel, where there is a hyperplasia of the 
endothelium, and a gradual transformation of it into a firm connective tissue. 
But the adventitia also undergoes a gradual thickening of considerable extent. 
Syphilitic endarteritis presents no distinctive histological characteristics. Entire 
certainty that the inflammation is syphilitic can be attained only by discov- 
ering other evidences of syphilis, either in the brain or elsewhere, or from the 
personal history and the previous course of the disease. 

The great clinical importance of syphilitic endarteritis is due to its cutting off 
the normal supply of blood from the regions supplied by the diseased arteries. If 
the occlusion be complete, cerebral softening is inevitable, as in ordinary embo- 
lism and thrombosis of cerebral arteries; and, inasmuch as the middle cerebral 



CEREBRAL SYPHILIS 



1127 



artery is particularly liable to the disease, syphilitic softening is most often found 
in the region supplied by this vessel. 

Clinical History. — The variety of the pathological processes and of their loca- 
tion produces a corresponding variety in the symptoms of cerebral syphilis ; but 
certain types, already described in the main by Heubner, may be distinguished, 
and in many cases these present a picture which is very characteristic of 
cerebral syphilis. 

1. Basal Gummatous Meningitis. Basal Cerebral Syphilis. — The development 
of a flat syphilitic new growth spread over the base of the brain, whose anatom- 
ical relations have been briefly described above, causes a form of disease which in 
many respects agrees with that of tumors of the base of the brain (vide supra, 
page 1120), but which also often shows certain characteristic peculiarities. The 
first symptoms consist of persistent headache, sometimes growing worse at night, 
vertigo, vomiting, and a certain mental dullness, which rarely, however, reaches 
such a high degree of stupor as is so often see in genuine tumors of the brain. 
States of marked maniacal excitement also occur at times. The patient often 
has an intense and striking polydipsia and polyuria. To these symptoms are soon 
added others, which are due to the invasion of the different basal cranial nerves 
by the morbid process. The optic nerve and the motor nerves of the eye (espe- 
cially the oculo-motor) are almost always among the first to be affected. Disturb- 
ances of vision (limitation of the visual field, in some cases hemianopsia, blind- 
ness of one or both eyes), changes in the pupils, disturbances of motion of the 
eyeballs or eyelids, may now become manifest in various ways. Optic neuritis 
or choked disk may occur, but in general the ophthalmoscopic changes are de- 
cidedly less frequent in cerebral syphilis than in genuine tumors of the brain. 
It is a very characteristic circumstance that all the different symptoms on the 
part of the cranial nerves (especially the changes in the visual field, as Oppen- 
heim has shown) may show great variations, which are undoubtedly connected 
with changes in the pressure from cicatricial contraction, etc. Of the other 
-cranial nerves, the facial, acoustic, olfactory, and trigeminus are most readily 
affected, but we should always make a very complete examination in every way 
in order to estimate correctly the extent of the process. 

The further course of the disease may vary very much. In fresh cases, which 
are recognized and treated in time, there may be decided improvement, and even 
complete recovery or at least an arrest of the morbid process ; but, on the other 
hand, the symptoms may increase. If there is also syphilis of the arteries (vide 
infra), there may be a slowly developing hemiplegia, hemiplegia following apo- 
plexy, epileptic states, bulbar symptoms, etc. — in short, a complicated form of 
cerebral disease, which is no longer capable of any material change. 

2. Gummatous Meningitis and the Formation of Syphiloma on the Convexity 
of the Brain and in the Vicinity of the Fissure of Sylvius. — In this somewhat 
less frequent localization of the syphilitic new growth prodromata similar to those 
just enumerated precede the severer symptoms. Then appear violent partial or 
general epileptiform convulsions. These often come on very suddenly, and they 
may recur at considerable intervals or in quick succession. There are usually still 
other symptoms of cortical disturbance, especially paresis of one limb or even of 
one half the body ; very frequently slight disturbances of speech (stumbling over 
syllables), referable to the cortex, and indications of mental impairment. Optic 
neuritis as a rule is not present. Many of these cases reach a fatal termination 
comparatively early. The epileptiform convulsions become more and more fre- 
quent, and unconsciousness increases to deep coma ending in death. But in cases 
of precisely this type prompt and energetic treatment may accomplish a great deal. 

3. Cerebral Syphilis Involving the Cerebral Arteries Chiefly. — A third com- 
mon and important variety of cerebral syphilis is characterized chiefly by syphi- 



1128 



DISEASES OF THE NEKVOUS SYSTEM 



litic arteritis. Not infrequently there is a prodromal stage, which is sometimes 
only slight; then, as a result of the occlusion of some vessel, which often occurs 
quite suddenly, there is a pronounced apoplectic attack, followed in most cases 
by hemiplegia. The intensity of the initial shock may vary greatly; sometimes 
there is only a slight dizziness, sometimes there is a coma that lasts for days. 
Sometimes the shock is succeeded by a peculiar condition of mental confusion 
and dullness, which may persist for weeks. In severe cases, death is speedy, 
and is usually ushered in by a great rise of temperature. Other patients improve 
more or less rapidly, especially under proper treatment. 

Apoplectic attacks of this sort may recur after temporary improvement has 
taken place, and may be associated with all sorts of nervous symptoms. 

4. Complicated Cases of Cerebrospinal Syphilis. — Combination of Gumma- 
tous Syphilis and Syphilitic Degeneration of the Nerves (Tabes, General Paraly- 
sis). — Besides the three types of cerebral syphilis already described there are also 
many cases which belong in part to one of the types mentioned, but which, on 
the other hand, exhibit much more complicated symptoms on account of the far 
greater extent of the anatomical changes. In the first place we will mention the 
combination of cerebral and spinal symptoms. The latter are often due to gum- 
matous spinal meningitis also, which is very often situated in the cervical region 
of the cord, and which may lead to paraplegia, brachial paresis, symptoms of 
unilateral lesion (vide page 1036), shooting root pains, vesical disturbances, etc. 
With these symptoms, all of whose varying details it is impossible to speak of here, 
are not infrequently associated cerebral symptoms, which, for their part, corre- 
spond to the conditions above described. A considerable number of cases which 
have been studied anatomically of late are also of especial interest. In these 
cases the symptoms of gummatous syphilis were associated with genuine tabes, 
or in other cases cerebral symptoms ensued, which were of the type of general 
paralysis (weakness of memory, a peculiar disturbance of speech, twitching 
of the facial muscles, paralytic attacks, etc.). In such cases the multiplicity 
of possible details is inexhaustible ; but the characteristic peculiarity of the 
type lies in this regular irregularity, which often admits a positive recognition 
of syphilis of the nervous system and is also capable of a clinical and anatomical 
interpretation, with proper consideration of the nature of the disease. 

Diagnosis. — The most important diagnostic criteria have already been men- 
tioned in the description of the symptoms. Here, too, the diagnosis is first 
topical and then serological and anatomical. The distinction between syphilis 
and genuine tumors is the most difficult. Absence of optic neuritis, a marked 
variability in the severity of the symptoms, and multiplicity of symptoms, espe- 
cially the combination of symptoms demanding different localizations, are in favor 
of syphilis. The discovery of a previous syphilitic infection is, of course, always 
important. We can not here describe in detail the methods of determining 
this fact. The history of the patient, as well as previous specific affections — 
such as, in women, miscarriages, abortions, etc. — and the objective signs on 
other parts of the body, are the two sources of information. There may be 
scars on the skin or mucous membranes, enlarged glands, ulcers, tibial periostitis, 
or changes in the testicles. Age is also important: thus an apoplectic attack 
in a young person would suggest syphilis, because the other causes of such an 
attack operate chiefly upon the aged. The results of treatment often throw 
considerable light upon the diagnosis. As there is nothing to lose and much 
perhaps to gain, we should always give specific remedies in doubtful cases. If 
they prove successful, the diagnosis of syphilis receives strong confirmation. 

Prognosis and Treatment. — There are few severe and dangerous diseases 
in which timely and appropriate treatment is attended with so much success as 
that achieved in many cases of cerebral syphilis. In order, however, both to 



PKOGKESSIVE GENERAL PARALYSIS OF THE INSANE 1129 



understand the favorable results and not to be misled by the failures, we need 
to gain a clear idea of the way in which antisyphilitic remedies can be of benefit. 
They can accomplish this only by causing the dissipation and absorption of the 
new growth — that is, the gumma or the swelling of the intima. If this be 
effected, the surrounding parts are of course relieved from pressure, and the 
circulation becomes unimpeded. If the tissues still retain functional power, 
they resume their duties and all symptoms of disease vanish. But when the 
tissues have already been considerably impaired by the compression, or by the 
scanty blood-supply, the results are quite different. Even then the degenerated 
nerve trunks at the base of the brain may gradually become regenerated ; but such 
parts of the true cerebral parenchyma as have undergone softening have lost 
their functional capacity forever. In such cases, antisyphilitic treatment is 
unavailing. 

It is therefore obvious that the first essential of success is to begin treatment 
as early as possible. The sooner a correct diagnosis is reached, the sooner will 
existing symptoms be relieved, and further danger be averted. The method of 
treatment which will probably accomplish all that can be accomplished, and in 
the shortest possible time, is energetic mercurial inunction. At least a drachm 
(grammes 3-5) of mercurial ointment must be rubbed in every day at first, accord- 
ing to the ordinary method. We should not venture to restrict the diet unless the 
patient be well nourished and "full blooded." If he be anaemic and feeble, a 
generous regimen is demanded. Usually the internal administration of iodide 
of potassium is combined with the inunctions ; we should give thirty to forty-five 
grains (grammes 2-3), or, in severer cases, even a drachm or a drachm and a half 
(grammes 4-6), daily [In this country iodide of potassium is given much more 
freely. In cases where syphilis is suspected, we may safely begin with doses of 
thirty grains (grammes 2) three times a day. If the symptoms be urgent, the dose 
should be rapidly increased until the patient takes three or even four drachms 
(grammes 10-15) three times a day. If the patient have syphilis, the danger of 
iodism seems less. The drug must be given in large amounts of water, and it 
is better borne if given in Vichy or Giesshubler water. Sometimes the stomach 
will not tolerate the extreme doses.— K.] The same remedy should also be given 
afterward, for a long time, in smaller doses. When there is no benefit at all 
after twenty or thirty inunctions, there is little prospect of any appreciable 
improvement. In favorable cases, the mercury often begins to produce some 
effect after the fifth or sixth inunction; and it may cause astonishingly rapid 
improvement. Potassic iodide alone is sufficient for the milder cases only, where 
there is merely headache, trigeminal neuralgia, or paralysis confined to the 
motores oculi. In many cases it may be desirable from other reasons to carry 
out the treatment at some health-resort rather than at home (Aix, Tolz, Hall in 
Upper Austria, Wiesbaden, etc.). These resorts are also suitable for after-treat- 
ment or for repeated courses of treatment, but the treatment by drugs is always 
much more important than the baths. 



CHAPTER IX 

PROGRESSIVE GENERAL PARALYSIS OF THE INSANE 

(Paralytic Dementia. Paretic Dementia. General Paresis) 

Preliminary Remarks. — Although the description of mental diseases is not 
a part of the plan of this book, we must nevertheless make an exception of one 
disease of the sort, namely, the so-called progressive general paralysis of the 



1130 



DISEASES OF THE NERVOUS SYSTEM 



insane, or paralytic dementia, which in medical parlance is often abbreviated 
into " general paralysis." We consider it advisable to make this exception, be- 
cause a great part at least of the symptoms of general paralysis are purely of a 
physical nature, and also because a knowledge of this disease, which is so com- 
mon and so fatal in its results, is of the greatest importance for the general prac- 
titioner. 

We must thank the French alienists Boyle (1822) and Calmeil (1826) for the 
first clinical descriptions of general paralysis, by which it was more sharply 
differentiated than previously from the diseases which resemble it. A more 
accurate knowledge of the different symptoms, and the anatomical changes to 
which the morbid symptoms must be referred, has, however, only of late years 
been rendered possible by the introduction of better methods of investigation. 
Accordingly, we must now say that general paralysis is a disease which may 
attack the most diverse portions of the whole central nervous system * — the brain 
and spinal cord — at the same time or successively, although we can, of course, 
make out certain rules as to the predisposition of individual portions to disease, 
and as to the order of the symptoms. General paralysis begins most frequently in 
those regions of the cerebrum which have an immediate relation to the regular 
course of the psychical and certain psycho-motor processes. Mental and motor 
symptoms accordingly form the introductory features of the disease in most 
cases. More extensive regions of the central nervous system are gradually in- 
volved in the morbid process, which goes hand in hand with a progressive degen- 
eration of all the higher intellectual faculties, while at the same time many physi- 
cal disturbances dependent upon nervous changes constantly increase. 

etiology. — General paralysis is a common disease, and apparently demands a 
heavier quota from the better and more highly educated classes than from the 
lower classes. We may assume that, on the average, one tenth of all patients 
committed to the insane asylums are general paralytics. In most patients the 
beginning of the disease falls in the period between the thirtieth and fiftieth year. 
The disease is much rarer in advanced life. In young people under twenty it has 
hardly ever been observed. [Over one hundred cases of juvenile general paralysis 
have been reported, almost always in victims of hereditary syphilis. — K.] There 
is no doubt that the male sex is much more frequently affected than the female, 
but the number of cases of general paralysis among women is not very small. 

What is the special cause of general paralysis? A generally acceptable an- 
swer can not be given; but the theory is constantly gaining ground, and we 
agree to it, from our own experience, that by far the most important causal factor 
is a previous syphilitic infection. Such an infection can be made out in at 
least seventy-five per cent, of all cases. In this regard precisely the same 
conditions exist, and, of course, the same difficulties in the interpretation of 
this relation are to be considered, as we have previously mentioned in the 
account of the dependence of tabes dorsalis on syphilis (see page 961), a circum- 
stance which again is not without significance, since the most intimate points of 
connection are to be found between tabes and general paralysis (vide infra). If 
we consider that general paralysis depends upon a previous 1 syphilis, we have 
an easy explanation of most of the other peculiarities in the onset of the disease, 
especially the above-mentioned influence of age and sex, the decidedly common 
occurrence of the disease in persons in certain callings — such as artists and offi- 
cers — the frequency of the disease in large cities in distinction from its rarer 
occurrence in the country, etc. 



* At present hardly anything is known in regard to a primary implication of the peripheral nerves 
in the general process. The principle of such an implication would be very readily understood in 
view of the almost regular occurrence of degeneration of the peripheral nerves in tabes. 



PROGRESSIVE GENERAL PARALYSIS OF THE INSANE 1131 



Besides the serological factors named, which, in our opinion, are the most 
important, all other " causes " of general paralysis may well be regarded as merely 
predisposing. Mental over-exertion has the greatest significance, especially if it 
be associated with psychical irritation. In merchants, civil officers, etc., who 
suffer from general paralysis, such a previous over-exertion can often be made out. 
In some cases injury to the head or insolation is claimed to be the cause. Heredi- 
tary predisposition to nervous diseases plays perhaps a certain part in the origin 
of general paralysis, but by no means a very large one. 

Clinical History. — General paralysis usually begins so slowly and gradually 
that a definite period for its beginning can hardly ever be given. In addition, it 
is often clear, at a time when the disease is already fully developed, that certain 
early symptoms, whose nature was at first not correctly recognized, ought to have 
been regarded as the initial symptoms. 

The first symptoms of the disease in the psychical domain usually consist of 
the gradual appearance of a change in the whole nature and in the mental indi- 
viduality of the patient ; wherein, however, the mental disturbance usually shows 
from the start the character of weakness — that is, of a lessened capability of 
mental exertion. The patient's ordinary mental work no longer goes on as easily 
as before. His memory is uncertain, and there are marked forgetfulness and 
inattentiveness, which were previously quite impossible for him to exhibit. The 
patient is often disorderly in his dress, and violates the ordinary social rules of 
decency and morality. Since his judgment as to the value and significance of 
things is uncertain, he commits purposeless actions, wastes money, commits 
crimes, is dissolute, etc. In these respects, too, the increasing mental dullness 
often appears, since the patient becomes incapable of any higher intellectual, aes- 
thetic enjoyment, and since the sway of nobler feeling finally becomes feeble, 
and unable to exert any lasting influence upon his actions. Besides all these signs 
of beginning mental weakness, we often notice, on the other hand, an abnormal 
irritability. The patient easily becomes agitated, or gets angry; but these moods 
rapidly pass away without leaving a lasting impression. We easily understand 
how this change in the whole personality of the patient must distress and alarm 
his family, since the relatives at first can not understand at all why the patient is 
now " so different from what he was." 

In the first period of the disease a subjective feeling of illness is frequently 
present. The patient himself notices that his mental capacity, especially his 
memory, is diminished, and he very often becomes extremely anxious on this 
account. It frequently happens that certain subjective sensations are also no- 
ticed, a feeling of confusion in the head, pressure in the head, dizziness, rheuma- 
toid pains, etc. The sleep is disturbed, as a rule, and also the appetite and the 
digestion. If such a patient comes to the physician with his complaints, it un- 
fortunately only too often happens that he is in the beginning regarded as 
" neurasthenic," and is treated accordingly. 

Careful observation, however, may usually even now discover the disease with 
certainty. The beginning mental disturbance is usually more apparent to the 
family than to the physician, who has not known the patient before and who sees 
him only cursorily, but it is apt to become manifest on a somewhat more 
searching examination of the patient. We generally succeed best by making 
the patient reckon; he often makes the greatest mistakes in simple examples in 
multiplication; especially does he fail in mental arithmetic, etc. 

Certain motor symptoms, however, which usually come on in the early stages 
of the disease, are of the greatest diagnostic significance, especially peculiar dis- 
turbances of speech and handwriting. The paralytic disturbance of speech shows 
itself first in the form of stumbling over syllables (SiJbernstolpern) , or literal 
ataxia. The individual sound (in distinction from bulbar paralysis) can be pro- 



1132 



DISEASES OE THE NEKVOUS SYSTEM 



nounced quite correctly, but the combination of different sounds in the whole 
word causes increasing difficulties. It is a good plan, in order to recognize the 
first beginnings of this symptom, to have the patient pronounce a few difficult 
words, such as " third riding artillery brigade," " representative government," 
" initiative," " electricity," etc. We often hear " artralleriry " instead of 
" artillery," and like blunders. In the later stages of the disease the speech is 
sometimes almost wholly incomprehensible. We also observe other more compli- 
cated aphasic disturbances, such as paraphasia, persistent repetition of the same 
word, etc. In such cases the patients are sometimes no longer able to read any 
sentence correctly. They at times put in entirely different words, so as to make 
utter nonsense; but they do not notice it themselves. The abnormal associated 
movements of the facial muscles on speaking are also often to be observed, and are 
very characteristic. The voice of general paralytics often loses its power of 
modulation and becomes weak and rough — symptoms which depend upon a de- 
fective innervation of the vocal cords. The change in the handwriting, to be 
observed in general paralytics, is even more characteristic than the disturbance 
of speech (see Fig. 177). This is at first purely of a motor nature; the letters are 



Fig. 177.— Examples of handwriting in general paralysis. Attempts made by patients in the Danvers 
Insane Hospital to write li Grod save the Commonwealth of Massachusetts/ 1 Besides the motor dis- 
turbance, the frequent omission of certain letters will be noticed, e. g., " Masschuetts 11 for " Massachu- 
setts. 11 In 3 and 4 the handwriting is almost wholly illegible. 

uncertain, irregular, and tremulous. A psychical factor, however, also shows 
itself; single letters are omitted, the dot on the i and the marks of punctuation 
are forgotten, the patient ceases to keep on the lines, or leave a free margin, etc. 
As the disease advances, the disturbance in the handwriting gradually increases, 
so that the writing may finally become wholly illegible, and may consist merely 
of senseless scratches. 

Besides the changes in the speech and the handwriting, which we have just 







PEOGEESSIVE GENEEAL PAEALYSIS OF THE INSANE 1133 



briefly described, other physical disturbances are often quite early symptoms, and 
prove in how many parts of the nervous system at once the disease may begin its 
work of destruction. The condition of the pupils especially is of importance in 
diagnosis. They are often unequal, and also show a reflex immobility (see page 
972) in a large number of cases, especially in those in which other tabetic symp- 
toms develop (vide infra). Transitory ocular paralyses are at times early symp- 
toms. Not infrequently we find quite early changes in the tendon reflexes, very 
often a decided increase of the patellar reflex, or, in other cases, absence of the 
patellar reflex, which latter has a much more positive value in diagnosis — it is 
almost invariably a tabetic symptom (vide infra). 

The association of reflex immobility of the pupils with an increase of the 
patellar reflex is not uncommon. In the distribution of the sensory nerves we 
may mention as repeatedly observed symptoms, neuralgia, attacks of migraine, 
and finally optic atrophy, the latter usually as one symptom of a co-existing 
tabes. 

We can not give a generally applicable account of the further course of general 
paralysis, since it may differ decidedly in this respect. In what follows we can 
point out only the main features of the different types of the disease, and, in 
particular, we will sketch very briefly the groups of mental symptoms. 

We often say that those cases belong to the " classical form " of general paraly- 
sis where an initial " stage of depression " with a melancholy tendency is followed 
by a second stage of " maniacal exaltation." This is the stage where the de- 
lusions, which are already quite pronounced, assume more and more the character 
of " grand ideas," and thus exhibit the " delusions of grandeur " which have for a 
long time been generally regarded as ominous. The first signs are often found in 
the patient's statements that he is now much better, that he is " very well," that 
he feels " very strong," etc. These delusions, however, often assume gradually a 
more exaggerated form; the patient considers himself enormously rich, he owns 
thousands of palaces, millions of dollars, has made the greatest inventions, con- 
siders himself the Emperor Napoleon, Christ, a " higher God," etc. Any judg- 
ment as to the absurdity of these ideas, and as to the sad contrast between his 
claims and the reality, has already become impossible to him; but, of course, there 
are even now occasional remissions in this condition, when the patient is clearei 
and recognizes temporarily the morbid character of his delusions. 

We must not think, however, by any means, that the delusion of grandeur is 
necessarily an invariable symptom in general paralysis. In many cases (the so- 
called " depressive " form of general paralysis) the initial melancholic-hypochon- 
driacal condition continues. The delusions that appear possess the same color- 
ing; the patient claims that he can no longer eat, that he is poisoned, that he 
has lost his head or an arm, that he is very small (" delire micro maniaque "), etc. 
Sometimes acute and severe conditions of anxiety come on. In other cases, again 
(the agitated or maniacal form of general paralysis), there are states of violent 
excitement, In which the patient raves loudly, cries, and tries to destroy whatever 
falls in his way. Such states sometimes alternate with delusions of grandeur. 
Finally, we see cases of patients — and this is the most frequent form — who, in 
their mental relations, present simply the symptoms of a mental enfeeblement 
gradually increasing to complete dementia, without ever showing, in any notn^e 
form, states of excitement, the development of delusions, etc. 

While the intellectual life progresses to utter ruin in the ways just stated, 
the physical disturbances of the disease, as a rule, gradually advance from bad 
to worse. In many cases ataxia of the extremities develops, and also loss of 
sensibility and vesical disturbances — in short, the symptoms of tabes. In these 
cases the tendon reflexes are almost always lost, and the pupils are often immobi 1 e. 
In other rarer cases, however, there is actual paralysis, first in the lower and then 



1134 



DISEASES OF THE NERVOUS SYSTEM 



in the upper extremities. In these cases the tendon reflexes are often increased, 
so that the picture of " spastic paralysis " develops. Again, in other cases bulbar 
symptoms appear, such as disturbances in swallowing or masticatory paralysis, 
and also ocular paralyses, usually as a part of the tabetic symptom-complex, etc. 

Peculiar attacks, which are among the commonest and most characteristic 
symptoms of general paralysis, are, however, of special interest, and sometimes 
even of marked importance in diagnosis. These " paralytic attacks " in their 
milder degrees sometimes appear even in comparatively early stages of the dis- 
ease. Then they usually consist of attacks of vertigo, an obscuring of conscious- 
ness, or even a loss of consciousness, coming on quite suddenly, and lasting from 
a few minutes to half an hour or more, and they are not infrequently associated 
with mild hemiplegic or monoplegic symptoms. We very often see, besides the 
vertigo, a temporary feeling of weakness in the right arm, associated with a 
marked aphasic disturbance of speech. To this there is often added some slight 
twitching in the affected extremities or in the face. In the further course of the 
disease the attacks usually increase, and are termed apoplectiform or epileptiform 
paralytic attacks, according as the conditions of paralysis or spasm predominate. 
The epileptiform attacks may often be repeated with great frequency — thirty or 
forty attacks a day or more — during which time the patient remains in an uncon- 
scious state. If the patients gradually return to consciousness, sometimes only 
after a week or two, we very often see, as a result of such severe attacks, a 
permanent impairment of the general condition, an increase of the dementia, etc. 

The other organs, apart from the nervous system, are only secondarily impli- 
cated in the morbid process. It may be mentioned briefly here that formerly, for 
a long time, stress was laid upon certain changes in the pulse, the pulsus tardus 
especially being thought to be characteristic ; but the numerous investigations of 
the pulse have so far not given us any significant or sure results. 

The temperature as a rule is approximately normal, or often somewhat sub- 
normal, but very marked changes in the temperature occur in connection with 
the paralytic attacks — sometimes elevations and sometimes very deep declines. 

The whole duration of the disease is in some cases only a few months (the 
" galloping " form of general paralysis), usually it is two or three years, and some- 
times much more. The most rapidly fatal form is that in which there is very 
soon a marked emaciation and a rapid loss of strength as a result of the sleepless- 
ness, the constant unrest, and the refusal of food. In other cases death ensues 
from the gradual and general loss of strength, or in a paralytic attack ; or, finally, 
as is frequently the case, from the onset of secondary conditions, such as severe 
bedsores, pyelo-cystitis, tuberculosis, intestinal diseases, etc. 

Pathological Anatomy and Nature of the Disease. — Considering the great 
difficulty of an accurate microscopic examination of the brain, it is not strange 
that our knowledge of the pathological anatomy of general paralysis is still very 
defective. If we except occasional immaterial changes in the skull, such as 
hyperostoses and the like, or in the meninges, such as hsematoma of the dura or 
secondary thickening of the pia over atrophied portions of the brain,* the first 
striking and at any rate most important anomaly seems to be 'the atrophy of the 
brain which affects chiefly the anterior half, especially the frontal lobes. In this 
region the convolutions are very much diminished, and the fissures are wide; 
the weight of the anterior portion of the brain may be reduced to one fourth or 
one third of the normal. If we examine the convolutions microscopically we find 
that the diminution of the whole organ depends chiefly upon a loss of nervous 
elements. The cortex usually shows the greatest changes. In fresh cases we 



* [An adhesion of the pia mater to the brain substance is very characteristic. This adhesion may be 
so firm that bits of the cortex are torn away on endeavoring to separate the pia from the brain. — K.] 



PEOGEESSIVE GENERAL PARALYSIS OF THE INSANE 1135 



sometimes see the signs of a mild " inflammation " — that is, we find vascular dila- 
tation and little disseminated foci of round cells about the vessels, but the changes 
in the nervous elements themselves are far more important, and consist essen- 
tially of a degenerative atrophy. We must mention especially that in the cortex 
of the frontal lobes, especially marked in the straight convolution and in the 
island of Eeil, and also in other portions, we can make out with certainty, by the 
aid of good methods of examination, a very considerable loss of the fine medullary 
nerve-fibers, mainly those which run parallel with the surface, and hence are 
termed " association-fibers " (Tuczek) ; but signs of degeneration and atrophy are 
very often to be seen in the ganglion-cells themselves. The destruction of the 
nervous elements is regarded by many investigators as secondary, since they lay 
the chief stress upon the marked changes in the interstitial tissue, numerous 
spider-cells, or thickening of the vascular walls, which are almost always to be 
found in old cases, and hence they speak of an interstitial encephalitis (Mendel). 
We ourselves, with Tuczek, Wernicke, and others, are much more inclined to the 
theory that we have to do mainly with a primary process of degenerative atrophy 
of the nerve-fibers and nerve-cells, to which the increase of the connective tissue 
is only a secondary addition. 

The anatomical affection in general paralysis, moreover, is by no means limited 
to the cerebral cortex. We can often make out the loss of fibers in the deeper 
parts also, in the white substance, and the central ganglia. The co-existing 
changes in the spinal cord, first accurately described by Westphal, and since then 
recognized as almost constant, are of especial interest. They usually consist of 
fascicular systemic degeneration of the lateral columns (the pyramidal tract), or 
the posterior columns. A large part of the physical disturbances of general para- 
lytics, such as tabetic symptoms or spastic paralysis (vide supra), are certainly 
due not to the cerebral disease, but to these accompanying changes in the spinal 
cord. 

Accordingly, we believe that, on the basis of our present knowledge, we can 
best conceive the nature of general paralysis in the following way : By the action 
of certain injurious influences, which usually seem to stand in some connection 
with syphilis (see page 961), there is a gradually progressive destruction of nerve- 
tissue in the most diverse portions of the nervous system. The clinical symptoms 
must naturally differ according to the significance and function of the affected 
fibers or cells. As a rule, certain cortical regions of the cerebrum are first dis- 
eased. The disturbances of speech are probably dependent upon the loss of fibers 
in the left island of Reil, the disturbances of intelligence upon the destruction of 
fibers in the cortex. We may also make out corresponding anatomical changes, 
either cerebral or spinal, as an explanation of the later motor, tabetic, and 
other symptoms ; but in many cases the order in which the different sections are 
affected varies considerably. We have seen in a previous section (see page 976) 
that the whole process may begin with a spinal disease, especially tabes dorsalis, 
to which the paralysis is " added " later ; but we must understand that the two 
conditions are wholly analogous to and co-ordinate with each other. Both are 
parts of the same degenerative process, which can accomplish its work of de- 
struction in the most diverse regions of the nervous system. 

No coarse anatomical lesions can be made out, as a rule, to explain the para- 
lytic attacks, but it is very probable that they depend, at least in great part, upon 
the changes in the motor central convolutions. 

Diagnosis. — Since the diagnosis of beginning general paralysis is of the great- 
est practical importance, we will once more mention briefly all those symptoms 
which are especially to be considered in diagnosis : Striking alteration in the 
nature and the behavior, rapid and motiveless change in the disposition, dis- 
turbances of memory, loss of intelligence (failures in reckoning, etc.), the char- 



1136 



DISEASES OF THE NERVOUS SYSTEM 



acteristic changes in the speech and handwriting, and finally the co-existing 
somatic symptoms: inequality of the pupils, immobility of the pupils, loss, or, 
more rarely, increase of the tendon reflexes, and mild paralytic attacks, such as 
vertigo, disturbance of speech, temporary disturbance of motion in one arm, etc. 

We would also mention, as especially common and disastrous mistakes, that 
the symptoms of general paralysis are often misunderstood at first, and are re- 
garded as the signs of immorality, the failure of the sense of duty, etc. It also 
frequently happens that general paralysis is at first regarded as simple neuras- 
thenia or hypochondriasis, and treated accordingly. 

As a rule, general paralysis can be certainly distinguished from other organic 
nervous diseases by careful attention; but of course we must add that in some 
cases cerebral tumors, gummatous processes, and especially certain cases of multi- 
ple sclerosis, may show a type of disease very like general paralysis. We should 
also remember that gummatous syphilis may be combined with genuine par- 
alytic symptoms (vide page 1128). 

Prognosis. — The prognosis of general paralysis, like that of all chronic degen- 
erative conditions of the central nervous system, is wholly unfavorable. At pres- 
ent we know of only a small and decreasing number of (doubtful) recoveries, but 
there are many cases where there is a temporary improvement in the condition, a 
" remission," sometimes of a considerable degree and lasting a long time. The 
earlier the patient comes under proper care and treatment the sooner may we hope 
for such a favorable turn. Of course, as we have said, relapses of the disease al- 
most always come on later. Those cases especially are to be regarded as un- 
favorable in which frequent paralytic attacks come on early, in which other 
physical symptoms, especially of a spinal nature, soon set in, and in which the 
whole nutrition of the body rapidly suffers. 

Treatment. — As soon as the disease is recognized, the first and imperatively 
necessary injunction must be to remove the patient from all physical and intel- 
lectual exertion as well as from all mental excitement. The patient must there- 
fore, if possible, withdraw from business, which up to that time he may have tried 
to carry on. His methods of life and his diet must be regulated, and every excess 
must be forbidden. For the cases which even at first are associated with states 
of great mental excitement, the commitment to a proper asylum is often most 
urgently to be recommended, while for cases that during their course show simple 
mental weakness, care at home is often sufficient. Only by a timely recognition 
of the disease and by adopting the appropriate measures can the patient's relatives 
be spared the many disagreeable experiences which would otherwise undoubtedly 
ensue. 

In regard to the treatment of the disease itself, we should advise inunction 
with mercurial ointment, especially if we can discover a previous syphilitic infec- 
tion. As a rule, we ought not to expect much success from this any more than 
in tabes (see page 978), but we may perhaps check the advance of the disease. 
We should therefore try the antisyphilitic treatment chiefly in the initial stages 
of the disease, and also in the cases where the suspicion that there is also gum- 
matous syphilis is justified. We may combine the internal use of iodide of 
potassium with the inunction. 

Furthermore, we should try tepid baths, with cool sponging, and also a cautious 
application of electricity (galvanization of the head and spinal cord), and pre- 
scribe internal remedies, especially ergotine. We need not go more fully here into 
the numerous symptomatic details. 



CHEONIC HYDKOCEPHALUS 



1137 



CHAPTEK X 
CHRONIC HYDROCEPHALUS 

Etiology and Pathology. — Eepeated mention has been made in preceding 
chapters of the occurrence of dropsy in the ventricles as a sequel to other cerebral 
diseases, such as meningitis and tumors. Besides this " secondary hydro- 
cephalus," a collection of fluid in the ventricles may be a symptom of an appar- 
ently idiopathic primary disease. This is observed most of all in the newborn, 
or at least in young children. 

Little is known with certainty about the causes of chronic hydrocephalus. The 
assumption is very frequently made that the condition is the result of an inflam- 
mation of the ependyma of the ventricle, which itself occurs either before birth or 
very soon after, but the autopsy often fails to support this idea. Our knowledge 
is equally uncertain as to the existence of a stasis due to mechanical obstruction 
(obliteration of the foramen of Magendie, etc.). Syphilis, drunkenness in the 
progenitors, etc., have been regarded as predisposing causes; whether justly or 
not, is uncertain. It has been repeatedly observed that the disease has attacked 
several children of a single family. 

The most important physical sign of hydrocephalus in children is enlargement 
of the head. The circumference of the skull may even in the first year of life be 
sixty to eighty centimetres. Usually the frontal bones and the parietal eminences 
are especially prominent. The cranium becomes gradually almost as thin and 
translucent as paper. The fontanelles and sutures gape widely. The brain is 
flattened out, so as to seem almost like a bag, filled with the hydrocephalic fluid. 
In well-marked cases the entire thickness of the hemispheres is frequently not 
more than an inch. The space within, containing the serous effusion, represents 
the enormously distended ventricles, particularly the lateral ventricles, although 
the third and fourth ventricles are quite often distended also. The walls of the 
ventricles are often strewn with minute granulations, or they present a reticular 
hypertrophy. The hydrocephalic fluid usually has the appearance of colorless 
serum, and contains a very slight amount of albumen, if any. The specific grav- 
ity is about 1004 to 1006. The amount of fluid may be a quart or more ; but, of 
course, there is a great variation in this respect in different cases. 

Congenital hydrocephalus is often associated with other peculiarities or de- 
fects in the structure of the brain, which we can not mention here. 

Clinical History. — Sometimes a child is born with hydrocephalus so far devel- 
oped as to occasion dystocia. Usually, however, the parents notice nothing pecul- 
iar about the child for some weeks. Then they are alarmed by the gradual swell- 
ing of the head. As a basis for determining abnormal size, we may mention that 
under normal conditions the circumference of the head at birth is about thirty-five 
to forty centimetres, at the end of a year about forty-five centimetres, and from 
that age to puberty there is a gradual approach to a circumference of about fifty 
centimetres. The possible dimensions in chronic hydrocephalus have been already 
stated. The increase in circumference is often quite rapid, amounting in a 
fortnight or three weeks to one or two centimetres. Usually the swelling is tol- 
erably symmetrical ; but sometimes the greater increase is in the antero-posterior 
diameter, making the skull dolichocephalic. At times the rate of expansion may 
be particularly rapid, and then at other times it may seem to be suspended. That 
the fontanelles and sutures remain widely open has already been mentioned; 
sometimes it is even possible to get fluctuation through them. An intravascular 
murmur can now and then be heard in the head, but it has no great importance 
with regard to diagnosis. The veins are often so greatly distended as to form 
72 



1138 



DISEASES OF THE NERVOUS SYSTEM 



a bluish network underneath the scalp. The face remains small, in striking con- 
trast with the great, heavy cranial portion of the head. The head almost always 
hangs over forward, from its own weight. The eyes generally look down, partly be- 
cause the roof of the orbit is depressed, and partly because of impairment of the 
nervous supply to the motores oculi. 

A very important symptom is the defective intellectual development of hydro- 
cephalic children. They can not learn to talk well, if at all. If they play, it 
is in a silly manner. They can not concentrate their attention upon anything, 
and they are heedless and dirty. It must, however, be mentioned that sometimes, 
in spite of considerable hydrocephalus, the patient now and then evinces an unex- 
pected activity of mind — thus, he gradually becomes able to distinguish the differ- 
ent objects and individuals about him. 

There is almost invariably motor disturbance also. The legs, more rarely the 
arms, are decidedly paretic, or there may be even complete paraplegia. There are 
usually spastic symptoms and increased tendon reflexes. Few patients learn to 
walk or stand alone. The arms seldom present any great paresis, but their move- 
ments often betray an awkwardness and uncertainty suggestive of ataxia. It is 
noteworthy that sensation almost always remains intact; at least the patient 
reacts vigorously to the prick of a pin, etc. Of the special senses, sight is most 
frequently affected ; choked disk and atrophy of the optic nerve have been observed 
repeatedly. Symptoms of motor irritation are of very frequent occurrence, such 
as general convulsions and spasm of the glottis. General nutrition is pretty well 
maintained in many cases, but, as a rule, hydrocephalic children are atrophic and 
ill developed. 

The chronic hydrocephalus of children almost always terminates unfavorably. 
Only a few patients survive the fifth year, although now and then striking excep- 
tions occur. Death is generally the result of marasmus; or a convulsive seizure 
may prove fatal. The possibility of recovery has not yet been demonstrated. The 
progress of the disease may, however, be arrested, and the child continue for years 
in statu quo. 

Hydrocephalus in adults is a very rare, chronic, and apparently idiopathic dis- 
ease. Its cause again is assumed to be chronic inflammation of the ventricular 
ependyma (so-called meningitis serosa ventriculorum) . The symptoms are some- 
times very like those of a tumor of the brain (with predominant general symp- 
toms), and sometimes there is a remarkable absence of characteristic cerebral 
disturbance, except that spastic paralysis of the extremities (compare page 1012) 
is gradually developed. 

Diagnosis. — A pronounced case of congenital hydrocephalus can be recognized 
without difficulty, inasmuch as the excessive size of the head betrays the disease 
upon the first glance. Less extreme cases may indeed be somewhat obscure, and 
we have especially to avoid confounding the condition in question with rachitic 
enlargement of the skull. We should always, therefore, take into consideration 
the intellectual powers, the presence or absence of motor disturbances, and other 
similar symptoms, as well as the cranial peculiarities. In the hydrocephalus of 
adults there is often no enlargement whatever, so that a diagnosis can hardly ever 
be made positively. 

Treatment. — Thus far, no remedy has been applied with success in chronic 
hydrocephalus. The following may be tried: Applications of mercurial oint- 
ment and of tincture of iodine to the scalp, methodical compression of the skull, 
and iodide of potassium internally. The hydrocephalic fluid has often been drawn 
off, to a certain extent, by tapping, but only rarely with permanent success, and 
usually with merely temporary benefit, if any. Quincke was the first to suggest 
drawing off the hydrocephalic fluid by so-called lumbar puncture ; that is, puncture 
of the vertebral canal. This can be done most easily in the region of the second, 



MENIERE'S DISEASE 



1139 



third, or fourth lumbar vertebra. Some favorable results from this method have 
been reported. 

In most cases we confine ourselves to purely symptomatic treatment, and to 
recommending intelligent care for the child. 



CHAPTER XI 

MENIERE'S DISEASE 

( Vertigo ab aure Icesa. Labyrinthine Vertigo) 

In 1861, Meniere, a French physician, first called attention to a peculiar affec- 
tion which may be apparently primary or may result from chronic aural disease 
and which is characterized mainly by excessive vertigo and loud tinnitus aurium. 
At first the symptoms appear in distinct paroxysms. These are ushered in by a 
shrill ringing in the ears, which is often compared "to the whistling of a locomotive, 
and which is perceived in but one ear. At the same time, or shortly after, comes on 
a very pronounced dizziness, of a unique sort. The patient has a feeling as if his 
whole body were moving, as if he were falling forward or were whirling around. 
Consciousness is unimpaired, but the patient feels wretched, the skin is pale and 
cool, and the face is bathed in cold perspiration. Frequently there is vomiting 
toward the close of the attack. The first paroxysms are of brief duration. As 
the disease progresses the attacks become more and more frequent, and at last 
the vertigo may be constant, being extremely annoying to the patient and perhaps 
confining him to bed. Even now there are occasional paroxysmal exacerbations 
of the disorder, usually ushered in by the shrill tinnitus. The tokens of chronic 
aural disease on one side, or less frequently on both sides, also persist. Some- 
times there is purulent otorrhoea; often the aural speculum reveals lesions of 
the drum or of the middle ear ; and almost invariably there is more or less deaf- 
ness on the affected side. This condition may persist for years, until finally it 
ceases of its own accord, after the deafness on that side becomes complete. 

The apoplectiform occurrence of Meniere's symptom-complex in persons whose 
ears were previously healthy is especially characteristic and interesting, but very 
rare. The disease begins suddenly, or at least very acutely, with an attack of ver- 
tigo or with loss of consciousness. In a very short time total deafness sets in, 
with extreme tinnitus, vertigo, and, as we have seen in one case, a very unsteady 
gait (as in cerebellar ataxia). In such cases we may suspect an effusion of blood 
into the labyrinth ; but there may also be, perhaps, an acute inflammatory process. 
Later the symptoms may gradually become less severe, but there is hardly ever 
complete recovery. 

We possess scanty information as to the origin of these subjective phenomena. 
That they are due to a disease of the internal ear (labyrinth) can scarcely be 
doubted ; and it is further probable that in every case the vestibular nerve and the 
semicircular canals are involved. Numerous experimental investigations have 
demonstrated that these last-named structures bear a part in maintaining the 
equilibrium of the body. Acquaintance with this variety of vertigo is valuable 
to a nervous specialist, inasmuch as Meniere's disease has been more than once 
confounded with epilepsy or disease of the cerebellum and other parts of the 
brain. On the other hand, of course, we must also add that purely neurasthenic 
and hysterical conditions may sometimes simulate the type of Meniere's disease 
very perfectly, so that a correct diagnosis often can not be made until the 
patient has been carefully observed for a long time. 



1140 



DISEASES OF THE NEEVOUS SYSTEM 



Treatment is not wholly unavailing. Charcot has discovered that the persist- 
ent use of quinine gives great relief — at least in many cases — and it may even com- 
pletely cure the disease. Eight to fifteen grains (gramme 0.5-1) of quinine 
should be given daily, in two or three doses, and continued for at least several 
weeks. Persevering galvanic treatment (anode to the ear, cathode to the back of 
the neck) also seems to us to be at times of decided service. The particulars of 
such special treatment of the ear as may be necessary must be sought elsewhere. 



EPILEPSY 



1141 



VI.— NEUROSES WITHOUT KNOWN ANATOMICAL 

BASIS 



CHAPTEE I 

EPILEPSY 

{Falling Sickness. Morbus sacer) 

iEtiology. — Epilepsy is a peculiar disease of rather frequent occurrence, the 
main symptom of which is paroxysmal loss of consciousness. In typical cases 
the unconsciousness is associated with violent general convulsions ; but there are 
many anomalous and rudimentary forms of epilepsy without any symptoms of 
motor irritation. " Genuine epilepsy " is a functional neurosis — that is, with our 
present means of investigation we can discover no constant objective lesion of the 
nervous system as its basis. It is, indeed, true that attacks similar to those of 
true epilepsy not infrequently occur in the course of tumor, syphilis, and other 
diseases which do present an anatomical lesion ; but such attacks are merely symp- 
tomatic, and are therefore termed " epileptiform," in distinction from the genuine 
epileptic paroxysms. 

Of the actual causes of epilepsy we know nothing. We are acquainted only 
with certain factors which are favorable to the development of the disease, and are 
to be regarded, therefore, as predisposing or exciting causes. Heredity is decid- 
edly the most important of these. About one third of all cases of epilepsy occur 
in persons who have inherited a nervous diathesis, and one or more of whose blood- 
relations have suffered from diseases of the nervous system. It should not be 
understood that we must find other cases of genuine epilepsy in the family, in 
order to establish the fact of congenital predisposition. The question is merely 
whether the ancestors have exhibited a general tendency to nervous disease. The 
more accurate and careful our investigations, the oftener do we find among the 
relatives of the patient instances of nervous trouble — sometimes genuine epilepsy, 
sometimes insanity, hysteria, or general " nervousness." Of course these 
" nervous families " present, besides those that are actually ill, others who are 
more or less peculiar and odd, and yet others gifted with extraordinary talents, 
although frequently somewhat ill-balanced. It is said that the children of parents 
who are related to each other are somewhat predisposed to epilepsy, as well as to 
other nervous diseases; but certainly this factor is very rarely of importance. 
Perhaps drunkenness in the parents is somewhat more prejudicial in this regard. 
It is said to have been repeatedly observed that children begotten while the father 
was intoxicated became epileptic. 

There are other influences which are assumed to have setiological importance, 
but whether justly or not is difficult to decide. Alcoholic excesses can seldom act 
in this way (although epilepsy is said to attack absinthe-drinkers in France quite 
frequently). Venereal excesses probably have still less importance. It should 
also be borne in mind that not infrequently excesses in these directions are the 
result of neurotic tendencies already existing. Syphilis has no direct connection 
with genuine epilepsy. Epileptiform convulsions may, as we have seen, be symp- 
tomatic of syphilis, being due to the cerebral lesion caused by this latter disease. 
Certain factors may determine the onset of epilepsy, although they can not be 



1142 



DISEASES OF THE NERVOUS SYSTEM 



said to cause the disease (except the symptomatic epilepsy which develops after 
a previous encephalitis). Such are over-exertion of mind or body, repeated emo- 
tional disturbance, certain general conditions of the system, such as anaemia or 
malnutrition, on the one hand, and plethora on the other; and, in particular, 
acute febrile diseases, such as scarlet fever, measles, and gastric diseases. [The 
individual attack is often brought on by some disturbance of digestion or indis- 
cretion in diet. — K.] Another important point is that the first attack is some- 
times brought on by great mental excitement, especially fright. But here, too, 
it is probable that the terror is merely the exciting cause, a tendency to the disease 
already pre-existing. We must also be on our guard against confounding genuine 
epilepsy with the convulsive form of hysteria (q. v.), which very frequently de- 
velops after fright. 

In some instances there is an evident connection between epilepsy and a pre- 
vious injury to the skull at birth or from a fall, or blow, etc. At a certain 
interval after the trauma, attacks begin which seem precisely like those of genu- 
ine epilepsy. This is known as " traumatic epilepsy." These are not cases of genu- 
ine epilepsy, however, inasmuch as there is really some anatomical lesion of the 
cortex cerebri which, in some way as yet unknown, causes irritation of the motor 
centers of the cortex (vide infra). It is often the case that this variety of 
epileptiform attacks is peculiar in that the convulsions are at first unilateral, or 
confined to a single limb, corresponding to the seat of the injury in the opposite 
cerebral hemisphere. 

" Reflex epilepsy " remains to be mentioned. This name is applied to cases 
where each convulsive attack seems to be excited by reflex influences originating 
in some remote part of the body. Most cases have followed injury of peripheral 
nerve trunks (retained splinters, or scars), and have ceased upon removal of 
the exciting cause. Other causes are new growths in the nerves, foreign bodies 
in the ear, otitis, intestinal parasites, and, apparently, diseases of the female 
sexual organs. It seems probable that sufferers from these attacks have had 
a tendency to disease of the nervous system. We must hesitate to rank re- 
flex epilepsy in the same class with the genuine form. The whole subject of 
" reflex epilepsy " needs a new and thorough investigation. It has been in the 
past so often confounded with hysterical (" traumatic-hysterical ") attacks, that 
we are personally disposed to doubt the occurrence of any real reflex epilepsy. 

Both the traumatic and the reflex varieties of epilepsy have repeatedly been 
the object of experimental investigation. Brown-Sequard has shown, by a great 
number of experiments, that epilepsy can be excited in rabbits by injuries to the 
medulla, the spinal cord, and the sciatic, as well as other peripheral nerves. A 
certain time after the operation the animals undergo spontaneous convulsive 
paroxysms. These occur at frequent intervals and for a long time, and they may 
be voluntarily excited at any time by irritation of a certain portion of the skin 
called the "epileptogenous zone." An interesting observation in this connection 
has been made by Brown-Sequard, which is that sometimes the progeny of these 
animals, who have been made epileptic, suffer from spontaneous epilepsy. West- 
phal induced epilepsy in guinea-pigs by blows upon the skull. Immediately after 
the blow general convulsions occurred, but soon entirely ceased. Afterward, how- 
ever, there were repeated epileptiform attacks. Westphal thought that the causa- 
tive lesion in these instances was the minute haemorrhages which were found in 
the upper part of the cervical division of the cord and in the medulla. 

These and other experiments, which will be spoken of later, interesting as they 
may be in themselves, have contributed absolutely nothing to our knowledge of 
genuine epilepsy. In regard to the latter we have nothing left but to assume that 
there is a congenital, abnormal predisposition of the brain, and especially of its 
motor centers, but the nature of this predisposition is still wholly unknown. 



EPILEPSY 



1143 



[Various writers have maintained that the epileptic attack was due to an accu- 
mulation of toxic products in the blood — in many cases an auto-intoxication from 
intestinal disturbances. An increase in the toxicity of the urine has been noticed 
before the attack, and the attack may sometimes be provoked by the ingestion of 
certain toxic substances. The toxic origin of the trouble, however, is not yet estab- 
lished. — K.] 

Clinical History. — In describing the symptoms of epilepsy, we shall first con- 
sider the various forms of the epileptic paroxysm, and then describe the general 
course of the disease. 

1. The fully developed epileptic paroxysm is usually described, for the sake 
of greater clearness, as made up of several stages. First is the prodromal stage, 
or, according to Galen's expression, still in vogue, the stage of the epileptic aura 
(aura = breath). !N~ot infrequently, however, there is no aura whatever, the con- 
vulsions coming on without warning; but in many cases the prodromata are 
well marked, and are repeated with noticeable regularity and- similarity before 
^ach individual attack, although the different cases of epilepsy differ greatly as 
to the special phenomena of the aura occurring in each. 

The best manner in which to distinguish the various forms of aura is accord- 
ing to the nature of the nervous phenomena, whether sensory, motor, vaso-motor, 
or psychical. Of these the most frequent is, beyond a doubt, the sensory. Here 
we have peculiar paresthesia, beginning in the arm or leg, or perhaps in the 
region of the heart or stomach, and thence usually " mounting to the head." It 
is seldom that the peculiar sensation is actually like a " breath " or puff of air. 
The aura which proceeds from the epigastrium is sometimes associated with a 
very disagreeable feeling of oppression and anxiety, and often also with nausea 
.and vomiting. The aura may be referred to the nerves of special sense. In cer- 
tain instances the patient perceives an unpleasant odor, which he likens to some 
familiar one. An aura of taste also occurs, but it is very rare. An optical aura 
is much more frequent, consisting of a subjective sensation of color or light (usu- 
ally a sensation of red appears first), of an apparent increase or diminution of the 
size of surrounding objects, or finally of actual hallucinations of vision, such as 
heholding all sorts of human or brute shapes. An auditory aura is not very 
Tare: it produces a sudden feeling of deafness in one ear, or various subjective 
sounds, like whistling, humming, roaring, etc. 

The motor aura takes the form of mild premonitory contractions, affecting the 
head, face, arm, or leg. There may be aphasic disturbance at the same time ; or 
we may observe symptoms of irritation of the unstriped muscles (strangling, or 
a desire to go to stool). Sometimes there are prodromal vaso-motor phenomena, 
where the aura consists of a sensation of cold or warmth, often associated with 
excessive pallor or redness of the face or hands. An attack may be ushered in by 
■chilliness, perspiration, or palpitation. 

Finally, the name of psychical aura is applied to those initial symptoms which 
•consist of vertigo, confusion of thought, or other pronounced disorders of con- 
sciousness. A particularly frequent form for this to assume is excessive mental 
uneasiness and excitement. We may also add that various forms of aura are not 
infrequently seen in combination. 

The aura lasts sometimes only a few seconds. It may persist long enough for 
the patient, who knows from experience what is coming, to He down or take 
other precautionary measures (vide infra). In some few cases the aura may last 
liours, and even days. This is especially true of the psychical variety. Some- 
times the aura passes away without being succeeded by any true epileptic fit ; but 
it is usually followed by the second stage of the attack — the convulsive stage. 

The convulsive stage of the epileptic attack almost invariably begins abruptly. 
Perhaps there is no aura, or only a very brief one, before the patient falls suddenly 



11U 



DISEASES OF THE KEEVOUS SYSTE1E 



tothe ground, usually on his face, although sometimes on the side or back. Con- 
sciousness is entirely suspended. Insensibility is complete, and often the patient 
sustains severe injury from his fall. Some patients utter a loud " epileptic cry " 
at the commencement of the attack, but they are already entirely unconscious. 

The convulsive attack begins with a brief period of general tonic spasm of the 
muscles. The head is usually strongly extended, the teeth are pressed firmly 
together, the trunk is curved backward in opisthotonos, the extremities are ex- 
tended, and the fingers are clenched over the flexed thumb. Inasmuch as the 
respiratory muscles participate in the seizure, breathing stops, and the original 
pallor of the face soon gives place to deep cyanosis. This general tonic convul- 
sion ordinarily is but brief, perhaps fifteen to thirty seconds. It is followed by 
the second period of the convulsive stage — that of the clonic convulsions. The 
facial muscles now exhibit the most violent contortions ; the eyeballs roll, or oc- 
casionally present a conjugate deviation toward one side; the tongue is thrust 
out and retracted convulsively; the head beats violently against the floor; and 
the muscles of the arms, legs, and trunk undergo the severest clonic spasms. The 
pupils are probably contracted for a short time at first, but during the convulsive 
stage they are widely dilated and do not react at all. The pulse is somewhat accel- 
erated, but not greatly. The temperature is normal, or elevated a small fraction 
of a degree. The cutaneous reflexes are still suspended directly after an attack; 
but the tendon reflexes are generally somewhat exaggerated, although sometimes 
they also are diminished or absent. "Not infrequently an involuntary dejection 
takes place during the fit, or the bladder is emptied ; and in men there may be a 
seminal emission. During these violent convulsions the body is often severely 
injured. The tongue is frequently bitten. The face, which is usually pale at the 
beginning of the attack, becomes extremely cyanotic. The veins in the neck are 
distended, and the venous stasis is so extreme that sometimes minute haemor- 
rhages occur into the conjunctiva, the skin of the face, and other parts. 

The convulsive stage usually lasts several minutes. Then the contractions 
cease, often after a deep, long-drawn sigh ; and the patient passes into the third 
stage of post-epileptic coma. He lies unconscious, but his respiration grows 
quiet, and the cyanosis vanishes. Gradually the coma yields to slumber, which 
may persist for some hours ; but some patients remain only a very brief time in 
this stage, and recover from their attack with surprising rapidity. It is, however, 
not infrequently the case that for some days after-pains are felt ; there are head- 
ache, languor, and exhaustion, and mental despondency and irritability. For 
some time there may be severe pain in the muscles, particularly those of the 
trunk. There may be slight paresis of one limb or one side of the body after an 
attack, but this speedily vanishes again in cases of pure epilepsy. In the first 
urine passed after the seizure is often f ound a trace of albumen, and perhaps a few 
hyaline casts. JSfot infrequently there is also decided polyuria for some time sub- 
sequent to the fit. Almost always after recovery of consciousness there is no 
recollection of what has happened, or it is very imperfect. On careful investiga- 
tion we often find that the memory of events immediately preceding the attack 
(for fifteen minutes to two hours before) has also entirely disappeared. A 
student, for example, who had an epileptic attack at the author's clinique, later 
had absolutely no knowledge of how he came to the clinique or of what he had 
seen or heard there before his attack. In a few cases (especially after traumatic- 
epilepsy) this retrograde amnesia may extend over a much longer period. 

2. The Milder, Rudimentary Forms of Epileptic Seizure. Petit Mai. — Be- 
sides these violent paroxysms just delineated (" grand mal "), there are very often 
witnessed in epilepsy milder attacks of so-called "petit mal." Sometimes there 
is only a transitory dizziness, or slight faintness, or perhaps a brief loss of con- 
sciousness, but without accompanying symptoms of motor irritation. These- 



EPILEPSY 



1145 



milder attacks may or may not be preceded by an aura. Cases have been repeat- 
edly seen where the patient suddenly pauses in the midst of conversation, card- 
playing, piano-playing, or other occupation, stares absently for a moment, and 
then, with equal abruptness, goes on with what he was doing, as if nothing had 
happened. In other instances the patient pursues his occupation during this 
brief suspension of consciousness. For example, if seized while upon the street, 
he walks on mechanically, but takes the wrong turning, or goes into a strange 
house, when suddenly he comes to himself and wonders to find himself where he 
is. Cases of " sudden somnolence " are also almost all of them ascribable to epi- 
lepsy. There are all sorts of transitional forms between the slight attack of 
vertigo and the typical epileptic fit. Not infrequently the patient falls down 
unconscious, but he has only a slight twitching of the face or arm, and in a few 
minutes is entirely himself again. Very often, especially in children, the attack 
consists of a short, piercing cry, loss of consciousness, a few convulsive movements 
of the arms — and in a few seconds all is over. Such attacks come on in the day- 
time and often in the night as well. In other patients the attacks consist of sud- 
den pallor, springing to the feet, rushing to the door, the ejaculation of some short 
words, etc. In short, it is hardly possible to describe all the different manifesta- 
tions of the rudimentary and atypical epileptic attacks; but persons who suffer 
from such slight attacks not infrequently have perfectly typical and fully devel- 
oped epileptic attacks besides, and this is of especial importance in diagnosis. 

[The medico-legal bearings of epilepsy, in its mild as well as in its severe form, 
are very important, but they can be only alluded to here.] 

3. Epileptoid Conditions (Epileptic Equivalents). — Cases of petit mal are gen- 
erally rudimentary forms of the typical epileptic paroxysm, and consist merely 
of a simple impairment of consciousness, possibly associated with slight motor 
symptoms; but in the epileptoid state the characteristic features of the typical 
epileptic attack are quite subordinate. The disturbance is paroxysmal, and it can 
often be shown to be connected with genuine epileptic seizures, else its undoubted 
relation to epilepsy would never have been recognized. The greatest practical im- 
portance attaches to the "psychical equivalents of epilepsy" (Samt). These are 
attacks of mental disturbance, which either immediately succeed a typical epileptic 
fit (" post-epileptic insanity ") or occur independently. These attacks are mani- 
fested by states of complete mental confusion, in which the patient may do the 
strangest things — may strip himself, steal, jump into the water, or commit incen- 
diarism. Besides these " states of epileptic confusion " there are also attacks of 
violent psychical excitement, associated with terror, frightful hallucinations, and 
resultant maniacal excitement. Not infrequently the patient is led to acts of vio- 
lence against those about him. In the young the attack may take a peculiar f orm : 
the child runs about in a peevish way, collects all sorts of things together, makes 
strange motions, etc. We have also frequently seen in children brief states of dis- 
turbed consciousness of sudden onset, with dominant ideas of apparent anxiety, 
often associated with some twitching. Many cases of so-called pavor nocturnus 
are certainly epilepsy, although it is sometimes not easy to exclude hysteria. Nu- 
merous and valuable particulars upon this subject, and a consideration of its great 
medico-legal importance, must be sought in text-books on insanity, as we can not 
discuss them further here. 

Among the rarer forms of epileptoid attack are the epileptoid sweatings 
(Emminghaus), a spontaneous outbreak of excessive perspiration in epileptics, 
which may or may not be associated with impairment of consciousness, and also at- 
tacks of epileptic tremor (Fere), procursive epilepsy (attacks when the patient 
runs impulsively forward), etc. 

General Course of the Disease. — In a large majority of cases epilepsy begins 
before the thirtieth year. Often the disease appears in early youth, and some- 



1U6 



DISEASES OF THE NERVOUS SYSTEM 



times even in the earliest years. Many a child has " convulsions from teething," 
which later on are seen to have been epileptic. It is only in rare instances that 
the first appearance of trouble occurs in advanced life. 

It is impossible to give any general rule as to the frequency of the paroxysms. 
Different cases differ very much. There are persons who during their whole life 
have no more than three or four seizures, at intervals of ten or fifteen years, while 
in most cases there is an attack every two to eight weeks. In severe types the fits 
may even recur daily. One very often sees certain variations in the course of the 
disease; at some periods the intervals between the attacks will be longer, and 
at others shorter. In severe cases the patient may have for several days very fre- 
quent seizures, so that he does not regain consciousness at all between them. This 
is termed the epileptic state (Stat de mal, status epilepticus). The condition is 
quite rare. It is often fatal, death being ushered in by a great rise of tempera- 
ture. 

External influences sometimes affect the frequency of epileptic attacks. Alco- 
holic or sexual excess, [indiscretions of diet,] mental excitement, and physical 
over-exertion almost always exert a malign influence. An opposite effect is often 
experienced where a quiet life is led, with every attention paid to hygiene and pure 
air. In women, the appearance of the catamenia is not infrequently the signal for 
the occurrence of an attack. In many instances the disease begins with the first 
establishment of menstruation. Sometimes, however, epileptic girls grow better 
when they arrive at puberty. Pregnancy sometimes increases and sometimes 
diminishes the frequency of the paroxysms. Intercurrent diseases seem frequently 
to exert a beneficial influence upon the frequency of the attacks. 

There is a practical distinction between diurnal and nocturnal epilepsy. Many 
patients have attacks only during the day, while others again have them only 
at night. A case of pure nocturnal epilepsy may go on for a long time un- 
suspected, particularly if the patient sleeps alone. He seldom has, on the next 
morning, the slightest recollection of his attack during the night. He usu- 
ally perceives, however, from a confused feeling in his head, or from certain in- 
juries, such as a bitten tongue, or from the disordered state of the bed, that 
something must have happened to him during the night. In some cases of noc- 
turnal epilepsy the patient wakes up out of sleep before he enters into the epi- 
leptic state of unconsciousness. Probably he is aroused by the aura. Besides 
cases where the fits occur during the day or the night only, mixed forms are fre- 
quently seen. 

With regard to the occurrence of the different varieties of epileptic seizure, all 
sorts of combinations are possible. Many cases never have any but the typical 
convulsions ; but in many others there are also a greater or less number of attacks 
of petit mal. The latter may even be for a long period the sole indication of the 
disease. Often there are no epileptoid conditions whatever, while in other in- 
stances the " psychical equivalents " are the most prominent feature of the 
disorder. 

During the interval between the individual attacks many epileptics seem per- 
fectly well, both physically and mentally. They are not infrequently, to be sure, 
somewhat peculiar and nervously excitable, or again dull and lethargic ; but this 
does not by any means apply to them all. Many epileptics, and particularly such 
as have comparatively infrequent paroxysms, are very capable; and history 
furnishes numerous examples of eminent men who suffered from this disease — 
for instance, Ca?sar, Mahomet, Rousseau, and Napoleon I. 

Much effort has been devoted to the discovery of " signs of physical degener- 
acy " in epileptics. Relying upon numerous measurements, Benedikt believes 
that a majority of epileptics exhibit craniometric anomalies, such as asymmetry 
of the cranium, macrocephalia, or steepness of the vertex. It is also not unusual 



EPILEPSY 



1U7 



to meet with anomalies of the ears, teeth, or hands * in such cases. Indeed, all 
peculiarities of this sort are, in general, more frequently observed in neuropathic 
families than in healthy ones. 

When the disease has lasted some time, and particularly if the attacks come at 
very short intervals, the general condition of the patient often undergoes a 
gradual but marked change. This rule is by no means invariable. The mind 
becomes more and more affected; the intellect grows feeble; memory grows 
weaker, and occasionally there is at last dementia. In such cases the body also 
suffers. There are emaciation, paresis, tremor, and other persistent disturbances 
of cerebral origin. 

In regard to the duration of epilepsy, it must be termed a life-long disease. To 
be sure, it is no rare thing for the paroxysms to cease and not return for years. 
But one can never rest satisfied that all trouble is at an end; some cause or other 
may excite another attack after a long interval. In general, an epileptic has a 
shorter life-expectancy than healthy persons, especially as he may be carried off 
by chronic pulmonary or other intercurrent disease. 

The prognosis is obvious from what has been already said. The individual 
seizure is only exceptionally dangerous of itself. The so-called " status epilepti- 
cus " often ends fatally, as above stated. In general, those cases may be called 
the most favorable where the separate paroxysms are infrequent and mild ; but 
even here the disease may suddenly assume an aggravated form. With regard 
to the distinction between nocturnal and diurnal epilepsy, the nocturnal is. in 
our opinion, the milder of the two. 

Pathology. — The very fact that in the intervals between attacks the patient 
often betrays no sign of disease, shows that epilepsy can not be due to any per- 
sistent macroscopic lesion of the tissues. Indeed, in many cases nothing is found 
at the autopsy, or, at most, changes which can not be regarded as essential, such 
as osteosclerosis of the cranium or thickening of the cerebral meninges. Epi- 
leptic subjects who were during life decidedly demented usually present atrophy 
of the hemispheres. Meynert states that changes in the pes hippocampi major are 
noticeably frequent in epilepsy; but these changes are not at all constant, and 
their significance remains to be established. 

"We must therefore, for the present, be content to assume that the cause of the 
epileptic seizure is an intermittent functional condition of irritation. A natural 
question is, Where shall we locate this irritation, and what may be its nature? 
The opinion was long current that the medulla oblongata must be regarded as the 
true seat of the disease. Schroder van der Ivolk was the first to express this 
opinion. It afterward received support from the experimental investigations of 
Nothnagel, who demonstrated that irritation of a particular spot (" convulsive 
center ") in the pons, in rabbits, invariably excites general convulsions. Xever- 
theless, most pathologists have now abandoned this view, because experiment and 
clinical observation indicate with increasing distinctness that the origin of epi- 
leptic convulsions is to be sought, at least in the great majority of cases, in the 
cerebral cortex. The clinical evidence is the invariable combination of con- 
vulsions and impairment of consciousness ; the circumstance that the milder and 
the masked forms of epilepsy, now known to be intimately related to the true 
epileptic convulsions, also, almost without exception, indicate psychical disturb- 
ance; that attacks, the symptoms of which are perfectly analogous with those of 
epilepsy, are often found to be the result of anatomical lesions of the cerebral 
cortex; and, finally, that these convulsions in man and the convulsions of " cortical 
epilepsy" (vide infra'), experimentally produced in animals, extend over the 
different groups of muscles in a way which corresponds precisely with the ana- 



* We have seen an epileptic who had six fingers on each hand. 



ms 



DISEASES OF THE NERVOUS SYSTEM 



tomical position of the different motor centers in the cortex (Hughlings Jackson). 
For example, if the convulsion begins in the distribution of the facial nerve, it 
extends from this point to the arm before it affects the leg. 

^ There is also experimental evidence that epileptic paroxysms are of cortical 
origin. A great number of observers (Hitzig, Ferrier, Albertoni, Luciani, Franck, 
and Pitres) have proved that electrical irritation of the motor regions of the 
cortex in animals will produce epileptiform convulsions. Unverricht has made 
some of the latest and most thorough investigations in regard to this point upon 
dogs. He found that when a motor center is stimulated the convulsions spread 
from the corresponding group of muscles to others in a way which corresponds 
precisely to the anatomical position of the separate centers. If one of the centers 
in the cortex be destroyed, the convulsions of the corresponding muscles cease at 
once. This proves that the motor centers must be intact in order to render the 
occurrence of epileptic seizures possible. Just how the stimulation extends from 
one center to another we have as yet no certain information. Probably it travels 
horizontally through the cortex. 

We see, therefore, that in all probability the seizures in man also originate in 
the cortex of the brain. The phenomena of the aura are likewise referable to 
some stimulation of the cortex, probably of the sensory region in most cases, as in 
the optical aura. The starting-point of the irritation is probably usually in the 
motor cortex, but it does not seem impossible that an irritation developing in the 
posterior cortical regions may extend secondarily to the anterior motor portion of 
the cortex (Unverricht). The manner in which the irritation is created is as yet 
entirely conjectural. Kussmaul and Tenner proved that epileptiform convulsions 
can be excited by a general cerebral anaemia ; and this fact was the main founda- 
tion for the assumption that the genuine epileptic convulsions are also due to a 
temporary cerebral anaemia, caused, it may be, by local vaso-motor constriction. 
Definite proof has not yet been furnished on this point. In the artificial epilepsy 
which Unverricht produced, and that also which Magnan excited by absinthe, the 
cortex of the brain was not strikingly anaemic. In regard to the occurrence of 
the attacks in true genuine epilepsy we can therefore provisionally make the im- 
perfect assumption that, as the result of a diseased condition, the motor cortex 
of the brain has lost the power to store up its motor energy and to give it out 
again in normal fashion, and that therefore there arise, from time to time, morbid 
" discharges of energy " and an outbreak of the convulsive movements already 
described. We will omit a further discussion of this theory, since we would soon 
be lost in the realm of mere hypothesis. 

Diagnosis. — Most cases of epilepsy are easily recognizable. It needs only to be 
borne in mind that epileptiform convulsions may also occur as a symptom of 
cerebral diseases which do have an anatomical basis, such as tumor, abscess, mul- 
tiple sclerosis, and hydatids. As a rule, however, such diseases are readily distin- 
guished by the state of the patient between the seizures, or by the further course 
of the illness. It should also be understood that unilateral convulsions, or such 
as are confined to a single member (Jacksonian epilepsy, vide supra, page 1073), 
are usually not true epilepsy, but symptoms of some circumscribed affection of the 
cortex. We will return once more to the differentiation from hysterical convul- 
sions in the chapter on hysteria. Weight should be laid on the general character 
of the attack, the complete loss of consciousness in epilepsy, the dilatation of the 
pupils, which do not react to light, the initial pallor not infrequently observed, 
and the subsequent cyanosis of the face. We may also consider the character of the 
onset and the duration of the attack (in true, genuine epileptic attacks the con- 
vulsive stage seldom lasts longer than a few minutes), the biting of the tongue, 
the condition of the patient immediately after the attack (deep, continued sleep 
is in favor of epilepsy), the possibility of exciting the hysterical attacks volun- 



EPILEPSY 



1149 



tarily (by suggestion, by pressure on a " hysterogenous " zone, etc.), which we 
can not do with epileptic attacks. The same factors (especially the condition of 
the pupils and the biting of the tongue) are the chief means of discovering 
simulated epileptic attacks. 

Treatment. — Although no remedy is capable of working a certain and perma- 
nent cure of epilepsy, yet a favorable influence can be exerted upon the disease in 
many ways, so as to lessen the frequency and severity of the paroxysms, and to 
avert many of their evil results. 

In the first place, regimen is of great importance. Any excessive exertion of 
mind or body must be forbidden. Temperance must be exercised in eating and 
drinking. Alcohol, strong coffee, and tea, can be used only moderately; nor is 
too much smoking permissible. The diet should be simple and unirritating, and 
vegetable rather than animal. It is said that in some cases decided improvement 
has been brought about by confining the patient to milk and vegetables. In 
summer the patient should live quietly in the country or the mountains. We 
have also the individual constitution to consider: a weak and anaemic person 
must have iron and abundant nourishment; and a full-blooded, corpulent indi- 
vidual should drink the natural aperient waters, and live abstemiously. 

Proceeding to the treatment of the disease itself, we shall only rarely, when 
dealing with "reflex" epilepsy (vide supra), have to consider aatiological condi- 
tions. The excision of old scars, the extraction of foreign bodies, or trephining the 
skull, where the disease has followed an injury, are said to have brought about 
permanent recovery in a few cases. VTe should also deal with any nasal or aural 
disease, in order, by rational treatment of any such trouble, to exert, if possible, a 
favorable influence upon the convulsive attacks. If we discover any intestinal 
worms they should be expelled. In genuine typical epilepsy we have no such indi- 
cations to fulfill, and we must have recourse to such treatment as experience shows 
can influence favorably the outward manifestations of the disease. 

Among these remedies, potassic bromide has an undisputed right to the first 
place. It should be the first remedy tried in any severe case. Apparently it acts 
by directly lowering the sensitiveness of the motor centers of the cortex to irrita- 
tion. Eather large doses are requisite. Beginning with about one drachm 
(grammes 4-5) a day, we may find it advisable to increase up to two or two and one 
half drachms (grammes S-10). It may be prescribed in water (1 to 10 or 15), or in 
powders which the patient himself is to dissolve in water, sweetened if desired. 
The remedy in almost all cases needs to be used for months and years, and it is 
therefore often advisable for the patient to buy a half pound or a pound at a time 
and weigh it out himself into the proper doses. It should always be taken in a 
good deal of water, half a tumbler or more, to avoid irritating the stomach. The 
total amount for the day is usually divided into two or three portions; but the 
whole may be dissolved in a large amount of water (seltzer water) and drunk 
gradually through the day. The other bromide salts, the bromides of sodium and 
ammonium are also frequently employed. They have the advantage of disturb- 
ing the stomach less than does the potassium salt. It is well to combine the various 
bromides. Erlenmeyer strongly recommends a mixture of two parts each of 
potassic and sodic bromides with one of ammonic bromide in so-called " bromine " 
water. 

In using the bromides, persistence is necessary for at least months, and otten, 
with occasional interruptions, for years, if benefit is to be obtained. In case there 
are unpleasant symptoms due to the remedy, such as excessive acne, a bad breath, 
muscular lassitude and tremor, cardiac weakness, dyspepsia, impotence, or mental 
depression and weakness of memory, we must diminish the dose, or even omit the 
medicine for a time. Many patients are greatly annoyed by pustules due to the 
bromide ; this can sometimes be avoided by giving Fowler's solution at the same 



1150 



DISEASES OF THE NERVOUS SYSTEM 



time. If the attacks are decidedly abated, the dose may be gradually diminished, 
to be increased again, however, if there be any tendency to a relapse. 

There is no doubt that the frequency of the attacks can be lessened by the 
continued use of bromides. This action is of course manifest only in those cases 
where the individual attacks occur rather frequently (every three or four weeks 
or oftener). If we are treating epileptics who have intervals of six months to 
a year or more between the individual attacks, it is hardly possible to decide 
with certainty whether the bromide treatment has any efficacy, and the long- 
continued use of bromide which is necessary is often attended by unpleasant 
accompaniments. We are therefore usually disposed in such cases to abstain 
wholly from the bromide treatment. Elechsig recommends combining the bromide 
treatment with the use of opium. We should give at first simply the extract of opi- 
um, beginning with two and a half grains (gramme 0.15) a day, and gradually in- 
creasing to six or eight grains (gramme 0.25-0.35) or more, always divided into 
two or three doses in the day. After using opium for six weeks we stop it abruptly 
and begin with a bromide treatment, continuing about two months. Whether 
this method has any special advantages can be told only after longer experience. 

Recourse to other remedies is seldom had, unless potassic bromide fails, or for 
some cause must be discontinued. We may then try valerian in powder, eight to 
thirty grains (grammes 0.5-2) several times a day, or as an infusion. It is a very 
good plan to give patients who are taking bromide a cup or two of valerian tea at 
bedtime. Belladonna may also be exhibited, or a pill of atropine, grain 
(gramme 0.0005), three to five times a day; or zinc oxide in the dose of one to 
three grains (gramme 0.05-0.20), perhaps combined with one fourth of a grain of 
extract of belladonna [IT. S. P.], and fifteen grains of valerian, as a powder, three 
times a day, and finally chloral in small doses (five to ten grains a day, gra m mes 
0.3-0.5, divided into several doses). Combinations of the bromide salts with some 
one of the remedies mentioned have seemed to us very advantageous in many cases. 
We have sometimes seen a decidedly favorable action from a mixture of the bro- 
mides with small doses of chloral or with atropine, especially where there are fre- 
quent rudimentary attacks. Bechterew recommends the combination of bromides 
with adonis vernalis (an infusion of two or three parts of adonis vemalis in 180 
parts of water, to which eight to twelve parts of bromide are added). Many rem- 
edies formerly recommended are not worth mentioning, as they are wholly in- 
efficacious. 

Electricity is apparently beneficial in occasional instances, and it may be tried 
in connection with other remedies. The galvanic current should be cautiously 
applied to the head and the sympathetic nerves. Still greater benefit is some- 
times obtained from a carefully conducted cold-water cure. Cold sponging with 
friction at night helps most cases, and it is sometimes very advisable to send the 
patient in summer to some appropriate establishment for cold-water treatment. 
We can not hope for any benefit from the surgical treatment of epilepsy except 
in those cases where the epilepsy is symptomatic, and we can expect, by the opera- 
tion, to remove or render harmless some actual local lesion in the brain (a de- 
pression of the skull, a cicatrix, a cyst, a meningeal adhesion, etc.). [In some cases 
of Jacksonian epilepsy an attempt has been made to relieve the attacks by removing 
the cortical center in which they apparently originate. After the brain is exposed 
this center is determined by faradization of the cortex. In a number of cases the 
center has been excised even when there was no macroscopic evidence of disease. 
The convulsions have often ceased for a time, but they have usually returned 
later, and the removal of the cortex is apt to cause permanent paralysis. — K.] 

Treatment during the Paroxysm. — In most cases we can do little during the 
seizure except to take such precautionary measures as common sense suggests. 
We possess no means of suppressing an attack when once under way: nor. 



INFANTILE CONVULSIONS (ECLAMPSIA INFANTUM) 1151 



indeed, is it often dangerous. In individual instances the patient finds out from 
experience some method to cut short the paroxysm during the aura. For 
instance, there are cases where tightly bandaging or vigorously rubbing the part 
in which the aura originates will avert the convulsions. A number of cases have 
also been known where the ingestion of a generous quantity of common salt dur- 
ing the aura has had the same effect. In these cases the aura usually starts from 
the epigastrium. A patient of our own, whose attacks began with a feeling of rec- 
tal tenesmus, maintained that she could almost invariably suppress the convul- 
sions by promptly going to stool, if she had time and opportunity. It was for- 
merly a frequent manoeuvre to seek to ward off the attack by compressing the 
carotids ; but this usually fails. Berger recommends the inhalation of nitrate of 
amyl at the commencement of the fit, having repeatedly seen benefit follow its use. 

In the " status epilepticus," narcotics are the most deserving of trial, and in 
particular chloroform or ether given by inhalation, and the internal use of chloral 
(forty-five to seventy-five grains a day, grammes 3-5). Amyl nitrite may also 
be of service. 

[It is sometimes desirable to withhold the knowledge that he is an epileptic 
from the patient, whose ordinary life should be interfered with as little as is 
possible. 

Especially in cases characterized by headache and heat in the head, Brown- 
Sequard finds the application of ice directly to the back of the neck and between 
the shoulders useful.] 

APPENDIX 

INFANTILE CONVULSIONS (ECLAMPSIA INFANTUM) 

Convulsions in childhood are of such frequency and importance as to justify 
brief special mention here. 

Every practitioner learns from daily experience that the young are especially 
predisposed to convulsions. Probably this is due in part to excessive reflex excita- 
bility of the brain in childhood. Thus children not infrequently undergo con- 
vulsions under circumstances in which adults would very rarely have them. 
They sometimes are seen in children in the beginning of acute febrile diseases, 
such as pneumonia, scarlet fever, measles, febrile sore throat, etc. They also occur 
from indigestion, particularly when the stomach has been overloaded; sometimes 
on account of teething ; or because of intestinal worms. In these cases they are 
usually regarded as of reflex origin, although they may possibly be due to the 
action of toxines (especially with intestinal worms). 

Convulsions may occur in very early life without ascertainable cause. In 
many cases they are really the commencement of epilepsy, as is seen afterward. 
Again, they may be due to some actual lesion in the brain. For example, if one 
recalls the initial stage of the acute poliomyelitis and acute encephalitis of chil- 
dren (vide pages 1015 and 1111), it will not seem unlikely that many rapidly fatal 
cases of " convulsions " are really instances of the diseases mentioned. This 
point has not yet been at all satisfactorily investigated by pathologists. At any 
rate, it does not seem satisfactory to us to regard the " oedema of the meninges " 
found in such cases as an independent disease and the sufficient cause of death. 
Often convulsions occur suddenly in children and then cease, never to recur, with- 
out our being able to find any explanation of the attack. Experience shows that 
rachitic children are especially liable to suffer from eclampsia — possibly because 
of cranial rachitic changes (?). 

The symptoms of the eclamptic attacks are on the whole analogous with those 



1152 



DISEASES OE THE NERVOUS SYSTEM 



of epileptic paroxysms. The child's eyes become staring and fixed, and there 
are tonic and clonic spasms of the face, trunk, and extremities. Such seizures 
may continue for days with brief intermissions. In such cases the prognosis is 
dubious, particularly if the child be weakly, but it is by no means absolutely bad. 
The cause and the significance of the convulsions can seldom be determined 
immediately. 

Symptomatic treatment consists of applying cold to the head, wet packs, sina- 
pisms on the chest and the calves of the legs, and perhaps an enema (to which 
vinegar may be added. These measures generally answer for mild cases. If the 
fits are very frequent and violent, we may allow even small children to inhale 
chloroform, often with great advantage. A dessertspoonful is to be poured upon 
a handkerchief and administered cautiously. 

Of course, we must also try to discover and remove the cause (acute diseases, 
intestinal worms). The attacks due to overloading the stomach usually occur in 
not very young children, and are apt to be greatly benefited by a prompt emetic or 
purge. 

[A bath at a temperature of 90°-95°, while cool water is applied to the head, 
seems often to be of service ; if the child be exhausted by diarrhoea, the cold to the 
head should be omitted. In a teething child it can do no harm, and it sometimes 
has a very marked beneficial effect to lance the gums thoroughly. Enemas con- 
taining chloral with or without bromide of potassium are more used in this coun- 
try than is chloroform by inhalation. 

A drop of nitrite of amyl by inhalation is said by Eustace Smith to exert a 
controlling effect on the muscular movements.] 



CHAPTER II 
CHOREA 

( Chorea Minor. Sydenham's Chorea. St. Vitus' 's Dance) 

^Etiology.— Centuries ago the name chorea (dance) was applied mainly to 
those strange states of " dancing mania " which were endemic in certain places, 
being due to excessive mental excitement and to the innate propensity to imita- 
tion. The specific for this condition was held to be a pilgrimage to some shrine 
of St. Vitus. At the present time, however, chorea is used to designate a perfectly 
definite disease, of which the characteristic symptom is the appearance of certain 
peculiar motor phenomena due to irritation of the nervous centers. It is some- 
times called chorea minor, in contradistinction from what was formerly termed 
chorea major or magna. This latter is, however, not a genuine, independent dis- 
ease, but a manifestation of hysteria (q. v.), or apparently in many instances of 
epilepsy. 

Chorea proper is mainly a disease of childhood. It occurs 'most often between 
the fifth and fifteenth years, although it may be seen both earlier and later. 
There is a slightly greater liability to it in girls than in boys. Hereditary neuro- 
pathic tendencies are also a factor in its aetiology, but not a very important one. 
(See the appendix to this chapter for chronic hereditary chorea.) 

As to causation, in many cases nothing definite can be made out. Mental ex- 
citement, as from fright, seems in some few instances to favor the onset of the 
trouble. It is also certain that the imitative impulse will often lead to choreic 
movements in healthy children who come in contact with choreic patients, but it 
is doubtful whether this " imitative chorea " can be regarded as true chorea. It 



CHOKEA 



1153 



seems to us far more correct in such cases, which are very amenable to psychical 
treatment, to speak of a hysterical chorea. There is a very interesting connection 
between chorea and acute articular rheumatism. Although the statement of cer- 
tain authors, that almost every case of acute articular rheumatism in children 
is followed by chorea, is far too strong, yet this sequence is comparatively fre- 
quent. Chorea i's sometimes seen also in children who have a mild form of 
chronic rheumatism, or especially in such as have valvular cardiac disease, 
whether preceded by articular rheumatism or not. This undoubted and close con- 
nection existing between chorea, articular rheumatism, and valvular heart disease, 
indicates the possibility that in true chorea there is an intoxication arising from 
some infection. 

Pregnancy exerts a special influence upon the development of chorea in women. 
Chorea gravidarum is most frequent in comparatively youthful primiparse. The 
nature of the connection between chorea and pregnancy is still utterly obscure. 

Clinical History. — Chorea usually begins gradually, and without any special 
prodromata. Sometimes, however, there are prodromal symptoms, chiefly a cer- 
tain mental depression and irritability, with indisposition to intellectual effort. 
There may be slight rheumatic pains or anorexia, and other evidences of constitu- 
tional disturbance. 

Ordinarily the peculiar motor disturbances are the first thing to attract the 
attention of the patient or its parents. There are involuntary and irrepressible 
movements in the most diverse groups of muscles. Both single contractions and 
also complicated movements occur, independently of the will, and in all parts of 
the body, now in one place, now in another, sometimes in a single member, and 
sometimes in several at once. The movements may be made in rapid succession, 
or may be separated by long intervals of quiet. The facial muscles may be 
involved, causing an occasional wrinkling of the brow or distortion of the mouth. 
When there is marked chorea of the facial muscles, as usually happens in severe 
•cases, the patients often make the strangest grimaces, sometimes with some par- 
ticular expression of emotion (laughter, anger, etc.). The eyes also may take 
part in the involuntary movements, being moved from side to side, or opened 
and closed. The pupils are frequently dilated. If the patient be asked to pro- 
trude his tongue and keep it quiet, it will often be involuntarily withdrawn into 
the mouth or thrust to one side. The tongue may even be sufficiently affected 
-to impair speech, which is explosive and indistinct. The laryngeal muscles have 
also been observed to make choreic movements. The arms are frequently the 
most affected of any part ; they are twisted, flexed, elevated, put behind the back — 
in short, moved in every conceivable way. The trunk is generally but little dis- 
turbed in the milder cases, but in severe ones the whole body participates. The 
patient stands up, lies down again, turns upon his side, etc. The legs are 
seldom as much disturbed as the arms and face, but slight movements of the 
lower limbs are very frequent — the foot is thrust forward or extended, the 
knee is flexed, and so on. In general, it may be said to be characteristic of chorea 
that the abnormal motor irritation usually affects a considerable number of 
muscles simultaneously, thus exciting all sorts of combined movements; and, 
secondly, that choreic movements, for the most part, are not short twitches, but 
-take place in a manner decidedly similar to that of voluntary movements. 

The vigor of the movements varies greatly in different cases. At first they 
may be too slight for the unpracticed eye to catch. Many children in an incipient 
stage of chorea are unjustly punished at school because they write ill or do not 
sit quietly. Many cases are mild throughout, never having very severe disturb- 
ance. Others, though considerably annoyed, can nevertheless walk or stand 
alone. In the severest cases, however, the whole body is continually in active 
motion. The patient throws himself about in bed, and all the extremities exhibit 
73 



1154 



DISEASES OF THE NERVOUS SYSTEM 



constant violent and irregular movements. The ingestion of food is extremely 
difficult, sleep is disturbed, and the patient's flesh and strength are rapidly and 
greatly diminished. 

Further, each individual case presents variations in severity at different times. 
If the patient be left quietly to himself, the contractions are comparatively very 
slight. As soon as he is conscious of being watched or as soon as any one speaks 
to him, his condition usually becomes much worse. On the other hand, of course, 
the movements may also be somewhat influenced by the will. The patient some- 
times becomes quieter if the body is completely supported and gently restrained, 
etc. During sleep the choreic movements usually cease altogether. 

In many cases all the. voluntary muscles are involved ; but sometimes the dis- 
ease is limited to certain groups of muscles. Very frequently the disturbance is 
mainly unilateral (hemichorea) ; the opposite side of the body then exhibits few 
involuntary movements, or, it may be, none. As already stated, the face and 
upper extremities are often more affected than the trunk and lower limbs. 

These motor disturbances often constitute the sole or the predominant symp- 
tom of chorea. There is hardly ever muscular weakness or paralysis. It is 
remarkable how little feeling of fatigue there usually is, despite the incessant 
activity. In a few cases only, of genuine chorea, have we seen actual paresis, 
affecting, for instance, one arm, or in hemichorea the choreic half of the body. 
Sensation is unimpaired. The reflexes do not exhibit striking peculiarities. The 
tendon reflexes we have usually found normal, more rarely very weak or even a lit- 
tle increased. There may be isolated spots in the spinal column tender on pressure, 
but this is not at all constant. That chorea may be complicated by arthritis and 
valvular cardiac disease has already been stated. Some caution should be exer- 
cised in making a diagnosis of cardiac lesion here, for experience shows that 
choreic patients are apt to have functional murmurs and slight irregular cardiac 
action. [Osier has found that the endocarditis of chorea is very apt to lead to 
organic valvular disease. Of 110 choreic patients that he examined more than 
two years after the attack, 54 presented signs of organic heart disease. — K.] The 
temperature is not elevated, in spite of the constant muscular contractions, nor is 
the amount of urea excreted by the kidneys increased. 

Slight mental disturbance is frequently observed. The patient is often rude, 
peevish, capricious, incapable of mental exertion, irritable, and inclined to tears. 
More marked mental disturbances (confusion, hallucinations) are sometimes met 
with in the severer cases, especially in chorea gravidarum. [These mental dis- 
turbances sometimes become very severe (chorea insaniens) . The patient becomes 
excited and delirious, and is very apt to die in a few weeks of general exhaustion, 
with considerable fever, 104-105° F. — K.] 

The entire process generally occupies several months. In mild cases, however, 
recovery may ensue at the end of a few weeks, while, on the other hand, cases 
may last a year or even longer. Variations in the intensity of the chorea are 
often witnessed. These are sometimes spontaneous, and sometimes are due to 
outward influences. Even when the disease is apparently extinguished, we must 
be prepared for a possible relapse. The disease may appear repeatedly in the 
course of a few years, in such a way that it is not easy to determine whether the 
different attacks are relapses or new illnesses. The protracted cases are, as a rule, 
comparatively mild; and many cases that begin with great violence end compara- 
tively early. In adults, and still more frequently in the aged (chorea senilis), 
however, the chorea sometimes assumes a chronic form and becomes stationary. 

The termination of chorea, in the great majority of cases, is favorable. Now 
and then severe cases do occur which end in death. In these the choreic move- 
ments are extremely violent. The patient is tossed about in his bed, and can eat 
little and sleep none. We have ourselves observed three such cases, in girls four- 



CHOKEA 



1155 



teen to seventeen years of age, which proved fatal within the first two or three 
weeks. Two died from general exhaustion and collapse, and the third from 
gangrene affecting numerous cutaneous traumatic lesions, which had occurred 
despite every possible precaution. 

Nature of the Disease.— All cases of genuine chorea thus far examined by 
pathologists have failed to furnish any lesions which can be regarded as essential. 
In the three cases above mentioned the autopsy revealed absolutely nothing 
abnormal in the central nervous system. We are at present, therefore, obliged to 
classify chorea as a " neurosis " — that is, as a disease that produces functional dis- 
turbances, for which latter there is no anatomical basis known to us. The symp- 
toms themselves show that the disorder must affect principally some motor region 
of the nervous system; but just which motor region is involved can at present 
only be conjectured. It seems very probable, however, that the true seat of chorea 
is to be sought in the brain. In the first place, the frequent occurrence of hemi- 
chorea would indicate this; as would also the fact that slight mental anomalies 
are frequently combined with chorea ; and, finally, " choreiform " movements may 
occur as the sole symptom of undoubted cerebral disease, as in post-hemiplegic 
hemichorea. We have, however, no hint as to whether the motor regions in- 
volved are those located in the cortex, or others. The surmise has quite often 
been expressed that chorea is due to embolism of a mild type; but, in our opinion, 
this view entirely lacks proof, and is even extremely improbable. As has been 
said above, we believe that the most probable theory is that genuine chorea is of 
toxic and usually post-infectious origin. 

Diagnosis. — The diagnosis is almost always easy, and it can often be made at a 
glance. The motor symptoms of athetosis, paralysis agitans, and of alcoholic, 
senile, saturnine, and mercurial tremor are so characteristic as to be readily dis- 
tinguished from the movements of chorea. It is not difficult to perceive the 
difference between genuine idiopathic chorea and the symptomatic choreiform 
movements occasioned by some other cerebral lesion. 

Prognosis. — As has been stated, the prognosis of ordinary chorea is almost in- 
variably favorable, although the disease may prove very tedious. The possibility 
of relapses should be borne in mind. The prognosis is doubtful, only in the worst 
cases of acute chorea, where there is great and rapid failure of the general 
health. Chorea gravidarum must also be regarded as of far more serious progno- 
sis than the ordinary chorea of childhood. 

Treatment. — Even in mild cases the patient must be kept from school and at 
home, in order to avoid all unnecessary excitement from ridicule and the like. 
If the chorea be only moderately severe, it is not necessary that the child should 
be in bed; we may even allow moderate exercise in the open air. Where the 
motions are violent, we should seek to guard the patient from self-injury by means 
of pillows and cushions. 

Among the remedies recommended for chorea, the chief place is occupied by 
arsenic and potassic bromide. Arsenic in particular seems often to be of value. 
We give Fowler's solution alone, or with equal parts of peppermint water or com- 
pound tincture of cinchona ; we may begin with five drops, in water, two or three 
times a day, gradually increasing to eight or ten drops. [In severe cases larger 
doses may be given. It should be pushed up to twenty drops or more, stopping 
for twenty-four hours if symptoms of poisoning appear, and beginning again at 
the same dose. It should be freely diluted. — K.] In children under six, the dose 
should be made somewhat smaller. If the child be anssmic, iron may be given 
in addition ; or, if there be great restlessness and loss of sleep, narcotics may also 
be administered. Antipyrine, in doses of seven to fifteen grains (grammes 
0.5-1) several times a day, is sometimes of decided service in severe cases. We 
give it especially in cases associated with rheumatism. Many observers have seen 



1156 



DISEASES OE THE NERVOUS SYSTEM 



good results from sodic salicylate, fifteen to thirty grains three times a day 
(grammes 1-2). If these remedies have no effect we may also try bromide 
of potassium in large doses, a drachm or more (grammes 3-5) a day. In severe 
chorea we have seen frequently undoubted benefit from the bromides. Numerous 
other drugs have been recommended : oxide of zinc, valerianate of zinc, nitrate of 
silver, and sulphate of copper. The efficacy of all these remedies is doubtful and 
at present they are very rarely used. Reiss has lately recommended physostigmine, 
one sixth to one third of a grain a day (gramme 0.001-0.002), best subcutaneously. 
[Sulfonal, three to five grains (gramme 0.2-0.4) three times a day, acts well, as 
an adjuvant to arsenic, in cases where there is much excitement. Exalgine, two 
or three grains (gramme 0.1-0.2) three times a day, has also been recommended. — 
K.] Narcotics should be employed very cautiously in chorea. Although chloral 
has been recently recommended for grave cases, there are instances known where 
this remedy has been followed by unfortunate results ; but we may try the contin- 
ued and cautious use of small doses of chloral, giving to children two to five grains 
(gramme 0.1-0.3), and to adults ten to fifteen grains (gramme 0.5-1) daily, or a 
few larger doses at night. 

Hydrotherapeutics of a mild kind do good, and can easily be carried out in 
most instances. Thus, we may use lukewarm baths, a wet pack, or gentle spong- 
ing with water at 72°-82° (18°-22° R.) to great advantage. In some obstinate 
cases sweating seems of service. We have also repeatedly seen decided benefit 
from the use of methodical gymnastic exercises, consisting of regular flexion and 
extension of the arms, marching in time, etc. 

Electricity may also be tried. A feeble current of galvanic electricity is ap- 
plied to the head (in the region of the motor centers), or the spinal cord is gal- 
vanized. If there be points along the spinal column where pressure causes pain, 
it is said to be an excellent plan to apply the anode to them; but the results of 
electrical treatment are seldom very brilliant. 

In the chorea of pregnancy, which sometimes is a very violent disease, the 
same remedies may be employed. If they do no good, artificial delivery may 
be required ; after which, as we can attest, there may be a rapid abatement of all 
symptoms. 

APPENDIX 

CHRONIC HEREDITARY CHOREA. ELECTRICAL CHOREA. PARAMYOCLONUS (MYOCLONIA) 

1. Chronic Hereditary Chorea (Huntington's Chorea). — Chronic chorea also 
manifests itself by severe choreic movements of the body, but in its nature it is 
a wholly different disease from ordinary chorea. It is notably of family (generic) 
or hereditary occurrence. The symptoms of the disease begin as a rule between 
thirty and forty. The choreic movements gradually become more severe and 
increase to the most curious and strange movements of the face and the whole 
body. The ability to walk and to use the arms in eating, dressing, etc., is retained 
for a long time ; but every action is accompanied by distressing associated move- 
ments and twitchings of the whole body. The sensibility and the other nervous 
functions are unaffected, but mentally we notice a decided but gradual failure as 
time goes on, which may increase to complete dementia. The anatomical basis 
of this remarkable disease is still unknown. The disease is incurable. The 
remedies used in ordinary chorea never mitigate the symptoms. 

2. Electrical Chorea. — Henoch gave this name to a form of chorea in children 
which differed from the ordinary chorea by the much quicker, lightning-like con- 
tractions coming on in single muscles (especially of the neck and shoulders). 



PAEALYSIS AGITAXS 



1157 



The contractions give the impression that the muscles have been put in contraction 
by single galvanic shocks. They come on at rather long intervals of three to 
five minntes. The same name, " electrical chorea," has also been given to a pe- 
culiar disease, said to be endemic in Lombardy, which was first described by 
Dubini, and which is therefore known by the name of " Dubini's disease." In this 
affection also muscular twitchings occur, usually beginning in one arm and grad- 
ually involving all the extremities. After several weeks or months paralysis and 
muscular atrophy set in, and not infrequently, it is said, epileptiform convulsions 
and fever. Xothing definite is known as to the anatomical changes. 

3. Paramyoclonus Multiplex (Myoclonia). — This name was first used by 
Friedreich for a case observed by him, in which there were clonic spasms in sym- 
metrical groups of muscles of the arms and legs, which came on in paroxysms 
without any disturbance of consciousness. There was also a considerable increase 
of the tendon reflexes. Such cases have since been described in considerable num- 
bers, but undoubtedly very different morbid conditions have been confounded with 
one another. We can regard as genuine paramyoclonus — that is, as a specific dis- 
ease sui generis — only those cases where lightning-like contractions come on in 
single muscles, often without any visible effect of movement. The muscles of the 
trunk and extremities are most frequently involved. This peculiar morbid condi- 
tion is on the one hand most closely allied to electrical chorea mentioned above, 
while, on the other hand, according to our own experience, it has a decidedly close 
relation to the different forms of tic convulsif (clonic facial spasm, clonic ac- 
cessory spasm, q. v.). A large number of the cases described as myoclonia or 
paramyoclonus, however, are undoubtedly to be classed as hysteria (vide infra). 

Unverricht and others have described a special form of myoclonia. It is char- 
acterized by its occurrence in various member? of one family, by the extension 
of the twitchings to the lingual and pharyngeal muscles, and by its complication 
with epileptic attacks. 



CHAP TEE III 

PARALYSIS AGITANS 

(Shaking Palsy. Parkinson's Disease) 

etiology. — In 1817 Parkinson described for the first time a disease which he 
named " shaking palsy." It is not of very frequent occurrence, and as yet 
little has been ascertained with regard to its aetiology. In most cases it develops 
very gradually, without any demonstrable cause. It almost always attacks elderly 
persons, being very rare before the thirty-fifth year. Sex does not seem to exert 
any great predisposing influence. Hereditary neuropathic tendencies can indeed be 
traced in some instances, but they are certainly of less potency in paralysis agitans 
than, for instance, in epilepsy. Special exciting causes have sometimes been ob- 
served, such as catching cold, violent emotional excitement, and traumatic influ- 
ences (blows, falls, injuries, etc.). Berger reports two cases where the first symp- 
toms appeared after an acute febrile disease (typhoid fever). 

Clinical History. — Paralysis agitans has two characteristic symptoms, viz., (1) 
peculiar evidences of motor irritation, evinced by tremor, and (2) a condition of 
stiffness and persistent shortening of certain muscles, consequent upon which is a 
series of peculiar motor phenomena. 

The trembling is generally the earliest symptom to attract the patient's atten- 
tion. It usually begins in the hands, especially in the right hand, and then 
gradually involves the arm and leg on the same side, next the other arm and 



1158 



DISEASES OF THE NEKVOUS SYSTEM 



leg, and finally, in well-marked cases, the entire body. The form of tremor is 
very characteristic. There are rapid, uniform, oscillatory movements of varying 
extent. The tremor is usually greatest in the hands and arms. At the same time 
the thumbs and half -flexed fingers exhibit a movement which suggests spinning 
or pill-rolling. The forearm is generally flexed and extended in rapid alterna- 
tion, but it is always very difficult to determine just what muscles contract. With 

regard to the trunk, it is often a question whether its 
tremor is of independent origin, or due merely to the 
motion of the extremities. Charcot states that the 
head and the facial muscles are never implicated, but 
there is doubt about this point. We ourselves, as well 
as other observers, have repeatedly seen independent 
tremor of the head. As to the face, the muscles about 
the chin seem to suffer chiefly. 

The trembling of paralysis agitans is almost con- 
tinuous. It may, indeed, cease for a moment in a 
limb, but only to recur immediately. The quieter the 
patient is in mind and body, the less violent are the 
movements. If he is excited, or begins to speak, or is 
watched, the tremor at once becomes exaggerated, and 
may be violent enough to jar the whole body vehe- 
mently. Active motion does not intensify the tremor. 
On the contrary, it may often be observed that the 
trembling abates when the muscles undergo vigorous 
voluntary contraction, as when a weight is lifted, or 
the hand of another is firmly grasped. 

The second symptom is almost more characteristic 
than the first. It consists of a peculiar rigidity of the 
muscles. We generally notice, even in the face, a 
peculiar tension of the muscles. This often produces 
a stolidity of expression, so that the emotions are less 
clearly depicted than upon the countenance of a 
healthy person. We have been especially impressed 
in several cases by the infrequency of winking. The 
head gradually becomes more and more flexed. When 
the disease has lasted some years, the chin may even 

^%f 78 th£ h body te ^ rest upon tlie sterimm - Tne muscles of the trunk and 

agitans. extremities also stiffen gradually, and lead to peculiar 

and almost pathognomonic appearances. The body is 
bent over forward; the arms cling to the trunk, and are flexed at the elbow joint; 
the fingers are flexed, especially at the metacarpo-phalangeal joint; the thumbs 
rest against the fingers, as if holding a pen, or else are flexed inward upon the 
palm; and the legs are somewhat bent at the knee. The accompanying picture 
(Fig. 178) is from the photograph of a patient who was for, a long time under 
observation at the clinique in Leipsic, and gives a good representation of the 
characteristic posture. 

The stiffness of the muscles also operates to impair motion in various ways. 
In particular all movements of the trunk are greatly impeded. In advanced cases 
the patient can not get upon his feet, if he is lying in bed, without help. Inas- 
much, however, as the muscular strength usually remains good (vide infra), he 
requires to exert but a slight traction upon some helping hand in order to attain 
an erect posture. On the other hand, the patient is often utterly unable to turn 
in bed from one side to the other. In severe cases, therefore, it is often neces- 
sary to alter the patient's position several times in a night, especially as lying long 




PAEALYSIS AGITANS 



1159 



in one attitude makes him feel very uneasy. If the patient is in a chair, he can 
not get up of himself, because it is impossible for him to bend his body forward 
in the necessary manner; but with just a little help he can stand up, and he is then 
able to walk alone or even to run. Then, since the flexion of the trunk forward 
brings the center of gravity forward also, and the trunk can not be sufficiently 
bent backward, he is apt to "get going," so that he can not stop until he brings 
up against a post or a wall. If such a patient, with a considerable degree of 
anteflexion and rigidity of the trunk, is slightly pushed from behind, he will 
have to start into a run to avoid falling. This phenomenon is termed " propul- 
sion." A push backward, which brings the center of gravity behind the point 
of support, is very likely to make such a patient fall, as he will seldom succeed 
in moving backward fast enough to recover his balance (retropulsion). Both pro- 
pulsion and retropulsion are conceived by Charcot to be " forced movements " 
(see page 836) in the strict sense of the term. We are, however, convinced, as 
the result of numerous observations, that these phenomena can in every case be 
explained simply by the mechanical conditions arising from displacement of the 
center of gravity and the muscular rigidity. Again, the reason why many pa- 
tients are prone to keep their arms behind them as they walk is that such a posi- 
tion contributes slightly toward bringing the center of gravity farther back- 
ward. 

The movements of the extremities are less impaired than those of the trunk, 
but they often betray a certain slowness and stiffness. The strength of the 
muscles may be preserved for a long while, but often there is at last evident 
paresis. Even in the early stages of the disease the muscles may become easily 
fatigued. The impairment of facial expression has already been referred to. In 
many cases the muscles of the eye also seem to participate in the rigidity, making 
it difficult for the eye in reading to follow rapidly along each line, or to pass from 
the end of one line to the beginning of the next. [The voice is often affected; 
the patient talks in a high-pitched monotone. — K.J 

The muscular rigidity is almost more characteristic of paralysis agitans than 
is the tremor. Indeed, there would seem to be cases, as we have ourselves ob- 
served, where, at least for a time, the posture of the patient is typical, and yet 
there is no trembling. Such cases might be called paralysis agitans sine agita- 
tione. In uncomplicated cases all other nervous functions remain perfectly 
normal. Sensation is never impaired. Sometimes some pain is felt at the com- 
mencement of the disease, particularly in the shoulders. There is no striking 
disturbance of reflex action or of the bladder. In a few cases of paralysis agi- 
tans, cerebral and mental symptoms have been observed; but they are so rare that 
it is impossible to say whether they belong to the disease or are merely accidental 
complications. It is also noteworthy that many patients complain of a subjective 
feeling of excessive warmth. The internal temperature is normal ; but it is said 
that the temperature of the surface of the body is frequently somewhat elevated. 
Sometimes there is a tendency to excessive perspiration. [Mosse and Banal have 
found that the excretion of urea and the total excretion of phosphoric acid is in- 
creased in paralysis agitans, but that the excretion of imperfectly oxidized phos- 
phoric acid is diminished, thus showing that there is increased combustion. — K.] 

The disease runs a very chronic course, perhaps for twenty years or more. 
From the first, it keeps on slowly but gradually developing. The symptoms 
rarely exhibit marked alterations of mildness and severity, but for long periods 
the progress of the disease may be apparently arrested. Recovery has never yet 
been observed. The final and fatal termination is not brought about by the dis- 
ease itself, but is due to some intercurrent affection or to general marasmus. The 
original of the picture on the opposite page came to a pitiable end by tumbling face 
downward into a puddle of water. He could not get up, and was drowned. 



1160 



DISEASES OF THE NERVOUS SYSTEM 



Nature of the Disease— The true nature of the disease is unknown. Inas- 
much as the disorder is purely a motor one, the corresponding lesions must be 
sought somewhere in the motor system. As yet, however, post-mortem examina- 
tions of the nervous system, even with the microscope, have revealed no charac- 
teristic changes ; at least we can ascribe no significance to the statements in this 
respect made by some observers. We must, therefore, confess that we have even 
had a doubt whether it is justifiable to claim that paralysis agitans is an affection 
of the nervous system at all, or whether it may not possibly be of purely muscular 
origin. Certainly it would not be impossible for abnormal processes in the mus- 
cles to excite the tremor and tonic contraction. But, as has been said, there is 
at present no ground for deciding this question; we would merely suggest it. 

[Gordinier has found some perivascular sclerosis in the posterior portion of 
the spinal cord, with pigmentation and degeneration of the ganglion-cells and 
some dilatation of the vessels. He thinks the symptoms are due to irritation from 
an increase of the neuroglia in the posterior columns, causing excitability of the 
reflex collaterals of the posterior nerve-roots which arborize about the motor cells 
in the anterior horns. This causes an increased discharge of energy, which gives 
rise to tremor and rigidity. Other observers have found somewhat similar 
changes in the white matter of the cord, and also in the gray matter. — K.] 

Diagnosis. — Any typical case of paralysis agitans can be easily and certainly 
recognized, often at the first glance. The important factors are the peculiar 
tremor, the characteristic carriage, and the rigidity of the muscles of the trunk 
and extremities. It was formerly a difficult matter to distinguish between paraly- 
sis agitans and multiple sclerosis ; but to-day the peculiarities of the two diseases 
are better known, and confusion is seldom possible. The character of the tremor 
varies in the two. In paralysis agitans it persists even when the patient is quiet, 
and it is decidedly oscillatory. The motion in multiple sclerosis (q. v.) is almost 
always an intention tremor only ; and, what is of still greater importance in dis- 
tinguishing between them, the general appearances of the two diseases are essen- 
tially unlike. 

Treatment. — As has already been implied above, we possess no means of con- 
trolling the disease. In most cases, therefore, the treatment is confined to general 
hygienic measures. Good may be done by lukewarm baths of considerable dura- 
tion, and by gentle massage of the muscles. Among internal remedies Erb has 
lately recommended hyoscine, as having the most palliative and soothing influ- 
ence. It is best given subcutaneously, and we must always begin with very 
small doses, as otherwise unpleasant symptoms, such as vertigo, headache, etc., may 
arise. We inject one two-hundredth to one one-hundredth of a grain (milligramme 
in aqueous solution (solution of hyoscine muriate, 1 to 1,000, seven to 
fifteen minims). If well borne we can cautiously increase the dose. [Atropine 
and hyoscyamine have also shown good results, especially when given subcu- 
taneously. — K.] Arsenic, ergotine, potassic bromide, physostigmine, and curare 
may also be tried. Erancotte praises the action of sulphate of duboisine (subcu- 
taneously or in pills of Tib" grain, gramme 0.0005, three to six times a day) ; this 
also must be used with care. If electricity is to do any good at all, the case must 
be a recent one. It is said that in some instances stretching of the nerves has 
diminished the tremor considerably; but our own observations would not lead us 
to recommend the procedure in this disease. 



ATHETOSIS 



1161 



CHAPTER IV 
ATHETOSIS 



In 1871 the American neurologist Hammond described under the name of 
athetosis {aSeros, without fixed position) a peculiar symptom of irritation of the 
motor centers, differing in 
a characteristic manner 
from all other forms of 
involuntary movements, in- 
cluding the epileptiform 
and choreic. The move- 
ments of athetosis (see 
page 836) are often very 
complicated and peculiar. 
The part affected by them 
is in continuous unrest. If 
the facial muscles (usually 
those of the lower division 
of the facial nerve) and the 
muscles of mastication be 
attacked, the face and 
mouth are constantly being 
twisted and distorted. If 
the tongue suffer, as in one 
case which we saw, speech 
is difficult and indistinct. 
If the muscles of the back 
of the neck be implicated, 
the head is usually drawn 
backward or to one side, 
and is turned and twisted 
in all sorts of ways. Most 
characteristic of all, how- 
ever, are the movements ex- 
hibited by the hand and 
fingers when affected. The 
fingers are incessantly be- 
ing separated, extended, 
flexed, and intertwined, as- 
suming the oddest posi- 
tions. The accompanying 
pictures may serve to il- 
lustrate this (Fig. 179). 
The character of the move- 
ments reveals that the in- 
terossei must be chiefly 
involved. It is a very fre- 
quent result of the unceas- 
ing stretching of the articu- 
lar ligaments of the fingers 
that at last the articuia- 

v i j Fig. 179.— Example of the position of the fingers in the movement 

tions become relaxed to of athetosis (personal observation). 





W 



1162 



DISEASES OF THE NERVOUS SYSTEM 



such a degree as to permit of such a hyperextension of the fingers, as it is impos- 
sible for a healthy person to imitate. The arms are generally less severely affected 
than the hands ; and in the lower limbs the trouble is not often so severe as in the 
upper. The toes may, however, exhibit motions analogous to those of the fingers. 

Although in general the movements are continuous, their vigor frequently 
varies. Thus they almost always are aggravated if the patient becomes excited. 
During sleep they generally cease, although in certain instances they have per- 
sisted even then, only being diminished. When voluntary motions are made 
they ordinarily grow feebler; but they may, on the contrary, become exaggerated, 
taking the form of sympathetic movements. 

We must distinguish between genuine idiopathic athetosis and a symptomatic 
form, which also occurs. 

Symptomatic athetosis is seen in various nervous diseases. The first observa- 
tions reported by Hammond were, most of them, made in cases of epilepsy, or in 
severe psychoses, and the like. [In Hammond's original case the athetosis was 
symptomatic and due to a lesion involving the optic thalamus, the lenticular 
nucleus, and the most posterior portion of the internal capsule. — K.] By far the 
most frequent source of the phenomenon, however, is hemiplegia, producing what 
is known as post-hemiplegic chorea, or better, post-hemiplegic hemiathetosis. 
This is, to be sure, a very rare sequel to the ordinary hemiplegia of elderly per- 
sons, but follows rather infantile paralysis of cerebral origin (vide page 1112). 
Some traces of athetosis are seen in a majority of the cases of infantile 
hemiplegia. 

Idiopathic athetosis is rare. Here the peculiar movements are the chief, if 
not the sole, symptom of disease. A few cases of this sort have been reported 
where the athetosis began without known cause, and usually was limited to some 
one region. It attacked elderly individuals who were previously healthy. Of espe- 
cial importance is an apparently congenital form of athetosis, dating from the 
earliest infancy. Of this we have ourselves seen several instances, which closely 
resembled one another. The condition is a permanent one, not progressive, nor, on 
the other hand, capable of any great amelioration. The movements are almost al- 
ways most pronounced in the face, head, and fingers. Other nervous disturbances, 
paralysis or impairment of sensation, are entirely absent or are associated with 
the athetosis in various ways. The intelligence of the patient is sometimes, but 
not always, diminished. 

Of the nature of athetosis, or the locality or nature of the irritation, we possess 
no information as yet. It is extremely probable that the lesion is in every case a 
cerebral one. Perhaps it is in the cortex. In symptomatic athetosis we find 
post mortem the changes caused by the original trouble. In idiopathic athetosis 
no changes have thus far been reported. In a case of our own which came to 
autopsy, absolutely nothing abnormal was found in the brain. The patient was 
an elderly female, who displayed typical movements of the arm and hand. 

It is not yet known whether recovery is possible. A certain amount of im- 
provement sometimes follows the administration of Fowler's solution, bromide 
of potassium, or galvanism. 



CHAPTER V 

TETANY 

{Intermittent Tetanus. Tetanilla) 

iEtiology. — Tetany, a name originating with Corvisart, is applied to a pe- 
culiar neurosis, characterized mainly by paroxysmal tonic convulsions, usually 



TETANY 



1163 



painful, in certain symmetrical and bilateral groups of muscles. The disease 
attacks by preference children and young adults between fifteen and thirty years 
of age. The physiological processes peculiar to the female sex seem to have an 
especial tendency to excite the disorder. It is comparatively so frequent in 
nursing women that Trousseau has called it " contracture des nourrices." It is 
also remarkable that tetany is especially common in certain occupations, particu- 
larly in cobblers and tailors. 

Among exciting causes, catching cold deserves particular mention. Hence the 
earlier observers describe the disease as " intermittent contracture of rheumatic 
origin." In other cases the disorder has appeared as a sequel to other acute dis- 
eases, such as typhus or typhoid fever, small-pox, and intestinal troubles. A very 
remarkable fact was pointed out by N. Weiss — namely, that tetany is apt to follow 
operative extirpation of goitre. We have once observed attacks of tetany in a pa- 
tient with exophthalmic goitre. Its occurrence in gastric diseases is also interest- 
ing, it being seen especially in dilatation of the stomach due to cicatricial stenosis 
resulting from ulcer of the pylorus with hypersecretion of gastric juice. The tet- 
any of childhood is seen chiefly in patients with dyspeptic and intestinal symp- 
toms. All these observations suggest the action of some toxic substance, and it is 
therefore worthy of note that attacks precisely like tetany have been observed in 
different intoxications (ergotine, alcohol, chloroform). In chronic alcoholic sub- 
jects tonic spasms like tetany are not very rare. Reports from various quarters 
indicate that tetany may sometimes be epidemic. Most cases ordinarily occur in 
the winter and spring (February and March) . On the other hand, endemic influ- 
ences also seem to us to have some importance. At any rate, the published ac- 
counts would seem to indicate that tetany is much more frequent in Heidelberg 
(Erb, F. Schultze), Breslau (Berger), and Vienna (N. Weiss), than in Leipsic, 
for instance, where it is one of the very rarest nervous diseases. [It is also very 
rare in America. Crozer Griffith a few years ago was able to collect only seventy- 
three reported cases, while forty or fifty eases have been treated at the hospital 
in Vienna in a single year. — K.] 

From what has been said it is evident that we should probably not regard 
tetany as one single disease serologically. Just as we distinguish in epileptic 
attacks between genuine epilepsy and symptomatic epileptic (epileptiform) con- 
vulsions, so we may distinguish between " idiopathic " and symptomatic tetany. 

Clinical History. — The paroxysm of tetany usually has certain prodromata, 
consisting of slight general discomfort and pain, and of a feeling of weakness and 
stiffness, most marked in the arms. These symptoms last some hours (at least) 
before the true convulsive stage begins. The extremities, and more particularly 
the fingers, almost always suffer first; and then, after the arms, the lower ex- 
tremities become involved. The spasm usually affects the toes before it seizes 
upon the other parts of the leg. The symptoms are almost invariably bilateral 
and symmetrical. Exceptionally, the disturbance commences in the leg, or is 
confined to one side of the body. In most cases the flexor muscles are pre- 
dominantly affected, giving rise to very characteristic postures. The fingers 
are in apposition with one another, and placed as if holding a pen, or, as Trous- 
seau says, as if the hand were about to be thrust into the vagina, during labor ; 
but in the attack the fingers may also be closed in a fist. The hands are flexed, 
the elbows are also slightly flexed, and the upper arm in severe cases is pressed 
against the chest. In the lower extremities, the toes are flexed, and the feet are 
in the posture of talipes equinus. The muscles of the thigh are less frequently 
affected, as are also the muscles of the trunk, the muscles of mastication, the 
facial and ocular muscles, and the diaphragm. 

The intensity of the tonic spasm is very great. The affected muscles feel as 
hard as a board, and are usually rather sensitive to pressure. The attack some- 



1164 DISEASES OF THE NERVOUS SYSTEM 



times continues only a few minutes, but not infrequently it may occupy several 
hours or days. Other nervous symptoms are less prominent ; the most noticeable 
are paraesthesise, tearing pains, etc. Anaesthesia is very rare. The reflexes 
are generally normal. There is no impairment of consciousness. In only a few- 
cases has a combination of tetany and hallucinatory confusion been seen. In a 
few instances slight cedematous swelling and other trophic disturbances have been 
observed, and sometimes profuse perspiration. The temperature is normal, or 
sometimes subnormal or slightly elevated (100.5° to 101° [C. 38°-38.4°]), and the 
pulse is often quite rapid. Polyuria has sometimes been observed. 

When the attack ceases, which it always does gradually, and never suddenly, 
the patient feels perfectly well, save for a slight pain and stiffness in the mus- 
cles, but all the muscles often feel weak and uncertain during the whole period 
of the disease. Even in the interval between the paroxysms there are also some 
few objective symptoms, which have a most important bearing on the pa- 
thology of tetany. In the first place, the peripheral nerves are generally abnor- 
mally sensitive to electricity (especially to galvanism, less regularly to faradism). 
The complete demonstration of this fact we owe to Erb. The weakest current will 
frequently produce violent contractions. The different sensory nerves and nerves 
of special sense also seem often to exhibit a similar abnormal irritability (Hoff- 
mann), and finally we very often find a considerable increase in the mechanical 
irritability of nerves, which is seen with especial frequency in the facial (Chvostek, 
"N. Weiss). Thus, if the face be vigorously stroked from above downward, with 
the finger or the handle of a percussion hammer, almost all the muscles contract 
energetically, one after the other. Similar contractions are, of caurse, obtained by 
light percussion of the different branches of the facial. The direct mechanical 
excitability of the muscles, on the other hand, is not increased (F. Schultze). 

Another very characteristic symptom was discovered by Trousseau — " Trous- 
seau's sign." It is found in most cases, although not in all, and is this : a fresh 
paroxysm can at any time be artificially excited by pressure upon the larger 
arteries and nerves of the arm (particularly the median nerve and the brachial 
artery) . It is not definitely known how compression accomplishes this ; but com- 
pression of a nerve seems to be the main point, as the corresponding experiments 
on animals show, in which an artificial tetany is produced by extirpation of the 
thyroid. Berger found that mechanical or electrical irritation of certain painful 
points situated along the spinal column produces the same result. 

The frequency of the attacks varies greatly in individual cases. As a rule, 
there are several paroxysms daily; but the intervals may last for days, or again 
may be almost inappreciable. The entire duration of the disease is generally sev- 
eral weeks, but many cases last for months or even years. It is noteworthy that 
when the paroxysms grow less frequent and violent there is also a gradual diminu- 
tion in the hypersensitiveness of the nerves and in the reaction to Trousseau's 
test. As long as these symptoms persist, spontaneous attacks are also possible. 
Many persons seem especially disposed to tetany, so that the affection repeatedly 
recurs in them. 

The termination of tetany is, as a rule, favorable, but in some cases death 
results, which of course is usually due to complications. In children the dis- 
ease may have an unfavorable termination if the spasms involve the diaphragm or 
the laryngeal muscles. Nothing definite is known as to the special nature of 
tetany. No essential or positive anatomical lesions have yet been detected. The 
symptoms leave us in doubt whether the disease affects the peripheral nerves or 
the nervous centers. 

Diagnosis. — The diagnosis is not difficult if we only consider carefully the 
symptoms presented, the nature of the paroxysms, and the other phenomena above 
enumerated. It is of fundamental importance, however, after determining that 



TETANUS 



1165 



the attacks are tetany, to discover, if possible, their special cause, and especially 
to determine whether we have to do with " idiopathic " or symptomatic tetany. 
It should also be said that tonic spasms, like tetany, may also occur in the hands 
in hysteria. The peculiar tonic spasms of young children are not, in our opinion, 
to be regarded indisputably as tetany; a special form has already been described 
(vide page 881) under the name of arthrogryposis. This is characterized by per- 
sistent tonic contracture, not paroxysmal, and most pronounced in the distribu- 
tion of the ulnar nerve on both sides. In such cases there is no incerased me- 
chanical irritability of the nerves. 

Treatment. — The main treatment, besides general hygienic measures (es- 
pecially rest and nursing) and the consideration of all discoverable causes 
(gastric and intestinal diseases, chronic intoxications, excessive work with the 
hands, etc.), is electricity. The stabile current is passed upward through the 
nerves affected; the galvanic current is also applied to the spinal cord, and the 
anode is applied to the various nerve-trunks, with, the cathode on the sternum. 
This last procedure sometimes dissipates a spasm actually present. Internal 
remedies, such as bromide of potassium, arsenic, and belladonna, rarely produce 
brilliant results. Tepid baths and the cautious use of cold sponging, with friction 
and massage, may be tried. The internal exhibition of thyroid preparations may 
sometimes be attended with good results. 



CHAPTEE VI 

TETANUS 

(Lock-jaw) 

Tetanus is an acute infectious disease whose chief symptom consists of the 
occurrence of severe, extensive, tonic (" tetanic ") muscular spasms. The specific 
cause of tetanus, the tetanus bacillus, was first discovered by Nicolaier in garden 
earth. Rosenbach first cultivated the same bacilli from the secretion of the 
wound of a man who died of traumatic tetanus. Since then the specific signifi- 
cance of the tetanus bacillus has been positively confirmed beyond any doubt by 
numerous investigations. These bacilli are distinguished by a little head (spur) 
at one end. If a small amount of these bacilli be injected under the skin of 
mice, the most violent tetanic spasms ensue in the animals thus treated. Since 
the development of the bacteria remains limited to the seat of the wound or the 
injection, it is a priori probable that the spasms are not excited immediately by 
the bacilli, but by a chemical poison produced by them during life. In fact, 
Brieger has lately succeeded in producing several alkaloid-like substances from 
tetanus-cultures, so-called toxines, which he terms tetanine, tetanotoxine, and 
spasmotoxine. All these substances are violent poisons, and, like strychnine, pro- 
voke the most violent tetanic spasms in the animals experimented on. 

In regard to the method of infection in man, it occurs by far most frequently 
through open wounds (operation wounds, or small accidental injuries). Since 
the tetanus bacilli are found chiefly in the soil, we can readily understand that 
injuries of the feet in persons who go barefoot, or injuries of the hands in 
gardeners, farmers, etc., most frequently give rise to tetanus. Such cases were 
formerly called traumatic tetanus, in distinction from rheumatic tetanus, follow- 
ing exposure to severe cold, or idiopathic tetanus, which was thought to occur with- 
out any discoverable cause. In the cases last mentioned there was probably some 
wound infection which was overlooked (just as in erysipelas) on account of the 



1166[ 



DISEASES OF THE NEKVOUS SYSTEM 



smallness of the wound. It of course would not be impossible for the infection 
sometimes to take place in some other manner. Tetanus neonatorum is undoubt- 
edly an ordinary wound tetanus, almost always arising from an infection of 
the umbilicus. 

In Germany [and temperate latitudes generally] tetanus is a comparatively 
rare disease. Men are much of tener attacked than women. Tetanus is much more 
common in the tropics than in our climate. The frequency of the disease in 
negroes is well known. Tetanus is also not equally frequent at all times. En- 
demics and epidemics of tetanus have often been observed, especially in time of 
war. These have arisen in part from the unfavorable influence of certain external 
conditions, such as poor care, bad weather, sleeping on the wet ground, etc. 

Clinical History. — In so-called " rheumatic " tetanus the symptoms usually 
begin soon after exposure to the exciting cause. There may be, however, an in- 
terval during which the patient feels perfectly well, or at most has only certain 
mild and indefinite premonitory symptoms, such as languor and headache. Simi- 
lar prodromata may occur in the apparently idiopathic cases. 

Traumatic tetanus seldom begins immediately after the injury has been 
received. Several days or even weeks may intervene previous to the outbreak of 
the disease. Here, too, there may be mild prodromata for a brief period preceding 
the graver phenomena. The patient's wound presents no specific appearances. 
Tetanus may be associated with either slight or severe injuries, whether treated 
carelessly or kept apparently aseptic. 

The symptoms of the disease proper are the same in both rheumatic and 
traumatic tetanus. They usually begin gradually. Ordinarily, the first thing 
noticed is a feeling of rigidity and tension in the muscles of the face, lower jaw, 
and back of the neck. The stiffness spreads by degrees to the muscles of the back 
and abdomen. The disease is sometimes completely developed in a few hours, but 
sometimes not till after several days. 

The persistent tension of the facial muscles gives the countenance a strange 
immobility. The brow is usually wrinkled, and the corners of the mouth are 
often drawn back in a " sardonic grin," or the face has a tearful expression from 
the deepening of the naso-labial folds and the drawing down of the corners of 
the mouth. Most prominent of all is the tonic spasm of the masseters, or trismus. 
The teeth are so firmly pressed together that it finally becomes impossible to 
open the mouth more than one or two millimetres. The eyes are staring, the 
pupils usually contracted. The muscles at the back of the neck draw the head 
somewhat backward, but in many cases it can still be moved quite well, although in 
other cases it is fixed by the spasm. The spinal column is bent forward, so that 
the trunk is convex anteriorly, permitting the hand to be passed between it and 
the bed — opisthotonos. The muscles of the back are hard and contracted. The 
epigastrium and the anterior part of the abdomen are flat. The abdominal mus- 
cles are as hard as a board. The lower limbs may be rigidly extended at the 
knee, and the adductors are also contracted, but as a rule the feet and toes are 
free from spasm. The arms generally can be quite freely moved, but the move- 
ments at the shoulder are usually decidedly impaired. Convulsive dysphagia, as 
seen in hydrophobia (q. v.), may occur, but it is rare (vide infra). 

In many cases the continuous tonic spasm is occasionally interrupted by sud- 
den and irregular paroxysms, during which all the affected muscles become still 
more tense. In severe cases this gives the whole body a violent shock, and makes 
the opisthotonos even more pronounced. In a very bad case the paroxysms are 
very frequent ; in a mild case they are rare or almost indistinguishable. Some- 
times they are apparently spontaneous, and sometimes they are evidently of reflex 
origin, being superinduced by external irritation. In severe cases the cause may 
be comparatively insignificant, such as a slight jar or noise. 



TETANUS 



1167 



If there are other nervous derangements, little is known about them — partly, 
no doubt, because it is seldom possible to make an extended examination of the 
patient. Sensation is said to have been impaired in some instances, but in others 
it is perfectly normal. The muscles affected by the spasms are usually the seat 
of severe pain. The cutaneous reflexes are almost always greatly exaggerated. 
In two cases which we saw very recently, the patellar reflex was much increased, 
and in one there was distinct ankle-clonus. Paralysis is extremely exceptional. 
There is often profuse perspiration. The forehead is usually studded with many 
beads of sweat. The intellect remains perfectly unclouded. 

There is a special form of tetanus which must be briefly mentioned. It was 
first described by E. Eose, and is called " hydrophobic tetanus," or " cephalic 
tetanus." It occurs only in connection with injuries situated in the distribution 
of the cranial nerves — that is, in the face and head — and is characterized in most 
cases by violent spasm of the pharynx and oesophagus. This is in addition to the 
other ordinary phenomena of tetanus. The disease in many ways reminds one of 
hydrophobia. Another characteristic point is that in most cases there is facial 
paralysis on the injured side. 

Tetanus, as a rule, gives rise to no disturbances referable to the internal vis- 
cera. In one case, however, in the Leipsic hospital, croupous pneumonia and acute 
nephritis came on a few days before the end. Often there are dyspnoea and a 
most harassing sense of thoracic oppression — symptoms due mainly to the convul- 
sive rigidity of the muscles, by which the thorax is constantly maintained in the 
position it normally assumes during inspiration. Expectoration is impeded; and, 
finally, there may be such an accumulation of secretions in the mouth and air- 
passages as to cause a secondary diffuse bronchitis, or an inhalation pneumonia. 
Another occasional source of extreme dyspnoea is spasm of the glottis. 

The pulse often remains normal for a long while, but it is usually accelerated, 
not infrequently reaching 120 or 160 beats a minute in severe cases. Such a 
pulse is small, and may be somewhat irregular. The temperature is at first usu- 
ally normal, or slightly elevated (100°-102° [38°-39° C.]). Later it is almost sure 
to rise ; and, as Wunderlich pointed out, it is often very high shortly before death 
— for instance, 107° to 111° (42 -44° C). It is not rare for the temperature 
to keep on rising for a short time after death. ]STo explanation of this terminal 
elevation of temperature has yet been furnished. It can not be the result of the 
increased production of heat occasioned by the muscular spasm, for in earlier 
stages the most violent convulsions are unattended by any such change. Au- 
thorities are, therefore, inclined to assume that at the last there is a paralysis 
of the centers which regulate the warmth of the body,, just as is seen in other 
severe nervous disorders, such as meningitis, injury to the cervical portion of 
the cord, and uraemia. 

Interesting observations have been made with regard to tissue-metamorphosis 
during tetanus. The excretion of urea is not increased. This fact agrees well 
with Voit's view, that muscular activity has no relation to the breaking down 
of albuminoids. Senator failed to find any increase of kreatine and kreatinine in 
the urine. Probably the production of carbonic dioxide is abnormally large in 
tetanus. At least, physiological considerations would strongly indicate this, al- 
though it has not yet been actually demonstrated. Occasionally traces of albumen 
and sugar have been detected in the urine. There is usually obstinate constipa- 
tion, probably due to the persistent rigidity of the abdominal muscles; and, 
indeed, micturition is not a little impeded from the same cause. 

It may be said, in regard to the general course of the disease, that there are 
severe and mild forms of the disease. What has been said above applies mainly to 
the severe form. In this, all the symptoms reach their extreme violence in a few 
days, the paroxysms occur in quick succession, and death usually takes place 



1168 



DISEASES OF THE NERVOUS SYSTEM 



within a week or two. The fatal result is brought about by the suspension of 
respiration and by cardiac failure. Of course, the extreme difficulty of taking an 
adequate amount of food has an unfavorable influence. The bad cases seldom 
outlast the first week. If they do, there is some slight hope of recovery; the 
paroxysms may gradually become less frequent and less severe, until they finally 
cease altogether. The severer form, however, so rarely ends favorably that the 
prognosis is always very grave. The mild form, on the contrary, usually runs a 
much more favorable course. In it, all the symptoms are from the -first much 
less severe. Often there is only more or less trismus, accompanied by no marked 
spasm in the muscles of the trunk, if any at all. There is little constitutional 
disturbance. The temperature is normal, and the prognosis is rather favorable. 
The disease may sometimes drag on for some weeks, but it often ends in complete 
recovery. It must not be forgotten, however, that what at first seems a mild case 
may develop into the severe form. 

The anatomical changes in the nervous system in fatal cases are almost wholly 
negative. Further investigations are necessary to determine how far the finer 
changes in the motor cells of the spinal cord, which have repeatedly been found 
of late, are of pathological significance. Any small haemorrhages, etc., have, if 
they be present, only a secondary significance. 

Diagnosis. — In most cases, tetanus can be easily recognized from the peculiar 
convulsions and the general aspect of the disease. It might be confounded with 
acute meningitis, for this may cause rigidity of the neck and back; but here 
there are usually certain cerebral symptoms also present, such as headache and 
impairment of consciousness; and, on the other hand, in tetanus, trismus is an 
almost constant phenomenon, although exceptional in meningitis. Strychnine 
poisoning produces convulsions similar to those of tetanus, but they generally 
affect the extremities in a more marked degree. Hydrophobia is distinguished 
from tetanus by the aetiology, the absence of trismus, the predominance of the 
pharyngeal convulsions, and the greater distinctness of the individual paroxysms. 
The hysterical conditions similar to tetanus can usually be easily distinguished 
from genuine tetanus by the discovery of specific hysterical symptoms (anaes- 
thesia, etc.). 

Where trismus is the only symptom, we must guard against mistaking for 
tetanus the symptomatic rigidity of the jaws which occurs with severe sore throat, 
diseases of the teeth, or inflammation of the maxillary articulation. 

Treatment. — Through the recent bacteriological investigations the treatment 
of tetanus seems to be directed into entirely new channels. Animals may be 
rendered immune to tetanus by inoculation with attenuated cultures of the 
specific germs just as they can be to many acute infectious diseases. The blood 
serum of such animals then contains substances (" antitoxine " or " alexine ") 
which annul the action of the tetanus toxine (Tizzoni, Behring). A considerable 
number of experiments upon the therapeutic usefulness of the tetanus serum have 
also been tried on man, but the reports upon the therapeutic benefits are still very 
contradictory. It is, however, not only justifiable, but urgently desirable to inject 
the tetanus serum as early as possible in every severe case of' tetanus infection. 

If the physician can not obtain an antitoxic serum, he must look to the 
methods of treatment heretofore employed. We have ourselves treated all the cases 
we have seen in the last few years with salicylic acid (eight grains, gramme 0.5, 
every hour), and we believe that we have repeatedly seen a favorable influence 
from this remedy. Otherwise narcotics are to be used. Those chiefly recom- 
mended are subcutaneous injections of morphine, opium in large doses, and 
chloral, of which thirty grains (grammes 2) should be given two or three times a 
day, and the amount gradually increased. If deglutition be very difficult, the 
chloral may be given by enema. Bromide of potassium should also be mentioned 



CONGENITAL MYOTONIA 



1169 



(at least two and a half to four drachms, grammes 10-15, daily), and calabar-bean 
(a sixth of a grain of extract of physostigmine, gramme 0.01, three to five times 
a day). The above remedies diminish the irritability of the nervous centers. In 
curare we possess a means of lowering the excitability of the terminations of the 
motor nerves in the muscles. It has therefore been employed by many, but by 
few with success. It is difficult to say what the dose of curare is, inasmuch as 
the strength of different samples varies. The best way is to determine the 
strength of the solution to be employed by experimenting on some animaL Usu- 
ally a one-per-cent. solution of curare in water is employed, and an amount equal 
to one quarter of the contents of a Pravaz's syringe is injected, the dose being 
gradually and cautiously increased. [Such a syringe contains about thirteen 
minims (0.8 gramme).] 

It is very desirable to put the patient by himself in a darkened and quiet 
chamber. Nourishment should be liquid, and lukewarm stimulants, such as 
alcohol and camphor, should be given from the first. Protracted warm baths 
may be given cautiously. We know from personal observation that such baths 
are very grateful to some patients. 

It need hardly be saiol that in traumatic tetanus the primary wound should 
Teceive careful attention. Since, according to recent investigations, the tetanus 
bacilli remain limited in their growth to the seat of the wound, it may be indi- 
cated in the beginning of tetanus, if possible, to amputate the wounded part or 
to excise the wound. Of course, from present experience, we can not promise a 
successful result. 



CHAPTEK YII 

CONGENITAL MYOTONIA 

( Thomsen>s Disease) 

In 1876, Thomsen, a Schleswig physician, described a peculiar disease which up 
to that time had escaped observation. He had had experience of it in himself and 
numerous members of his own family. Thomsen called it " tonic convulsions of 
the voluntary muscles," an appropriate but somewhat clumsy name, for which 
we suggested instead " congenital myotonia." Apparently the disease is very 
infrequent; but a considerable number of cases have already been reported in 
Germany, Prance, and Italy. 

The disease is probably always congenital; at least, the symptoms invariably 
date from the earliest infancy. It is very often generic and hereditary; and 
males of the same family seem to suffer oftener, and also more severely, than do 
females. The essential symptom of myotonia is this: whenever any voluntary 
muscle has been inactive for a time and is then made to contract, it falls into 
a state of more or less persistent contraction, a mild sort of tetanus, so that it 
can not be immediately relaxed. It is obvious that this would interfere with any 
series of motions, and make voluntary movement difficult. The patient is not 
paralyzed at all, but he has a feeling of great resistance to be overcome in per- 
forming any act. Quick and accurate motions are often out of the question, 
so that, for instance, the patient can not perform military duty. It is noteworthy 
that the stiffness temporarily disappears after the patient has been moving his 
muscles for some time. On going up-stairs, the first steps are often very stiff and 
laborious, while succeeding ones grow easier and easier. Mental excitement 
invariably exerts a very unfavorable influence, exaggerating the stiffness of the 
muscles. 

74 



1170 



DISEASES OE THE NERVOUS SYSTEM 



Upon physical examination, the observer is usually struck by the extraordinary 
development of the muscles. The size of the extremities, in particular, almost 
deserves the term " genuine muscular hypertrophy," although the strength is not 
always proportionately great. Certain extremely interesting variations in the 
electrical excitability of the nerves and muscles are, however, very remarkable. 
These were first studied in detail by Erb and given the name of " myotonic reac- 
tion." The motor nerves show quantitatively a normal faradic and galvanic 
excitability. All single shocks give short contractions, but on continued excita- 
tion (faradic current, labile galvanic current), a very characteristic persistence 
of the contraction occurs after the cessation of the irritation. The muscles are 
very easily excited by faradism, and, with rather strong currents, always show 
the above-mentioned persistence of the contraction. When the current is applied 
continuously peculiar wave-like, oscillating muscular contractions occur. On gal- 
vanic excitation of the muscles a slight increase of excitability is manifest. 
With rather strong currents the contractions are decidedly slow, tonic, and 
also persistent. They occur only on closing the current, not on opening. Finally 
we almost always see in the muscles a very remarkable phenomenon, discovered 
by Erb : rhythmical wave-like contractions occur in the muscles, under the action 
of a stabile current, which start from the cathode and go to the anode. The direct 
mechanical excitability of the muscles, on percussion, is usually increased, but 
this does not apply to the idio-muscular contractions. The reflexes, sensation, 
and, indeed, all other nervous phenomena, are normal. 

These facts render it very probable that the cause of the disease is to be sought 
in the muscle itself, and that myotonia is due to a congenital peculiarity of the 
muscular system. This hypothesis is supported especially by the interesting his- 
tological discoveries of Erb on excised bits of muscle. He found a considerable 
increase in the volume of the individual fibers, whose transverse striation was 
often very fine and indistinct, at times the formation of vacuoles in the fibers, a 
great increase of nuclei, and a moderate increase of interstitial connective tissue. 
Nothing is known at present in regard to anatomical changes in the nervous 
system. Erb reports that, upon microscopic examination of minute particles of 
muscular tissue which were excised, he found marked hypertrophy of individual 
muscular fibers, and an increase in the number of nuclei in the sarcolemma. 

The disease persists through life. The patient gradually becomes accustomed 
to it, and learns to conceal his misfortune as much as possible. There may be no 
constitutional disturbance. Sometimes there is melancholia. Therapeutic efforts 
have not yet been attended with much success. We might try cold sponging, 
with friction, gentle massage, and methodical exercise of the muscles. 

[Eulenburg describes a congenital family affection, which he calls congenital 
paramyotone, allied to myotonia, where tonic spasm was produced by cold. Gow- 
ers has found the association of tonic spasm with ataxia — ataxic paramyo- 
tone. — IL] 



CHAPTEE VIII 
CATALEPSY 

Formerly catalepsy was regarded as a special form of disease, but at present 
the opinion is almost universally held that it is merely a symptom of several differ- 
ent diseases. As was mentioned on page 837, " cataleptic rigidity " is a term de- 
scriptive of that peculiar condition of the muscles in which the limbs maintain 
involuntarily any position into which the observer puts them. If we change the 



CATALEPSY 



1171 



position of the members which are cataleptic, the patient does not make the 
slightest effort to alter the posture in which we leave them, however strange, 
awkward, and apparently insupportable, it may be. The limbs may be moved in 
this way almost like wax, and they are therefore said to exhibit a "waxy flexi- 
bility." 

~No real explanation of the cataleptic state has been given. We have not yet 
advanced beyond the study of the circumstances under which it appears, and of 
the associated phenomena. As has been said, the tonic muscular spasm of cata- 
lepsy is never very great, being little more than sufficient to overcome gravity and 
maintain the limb in the posture given to it. This shows that there must, in every 
case, be a due proportion in the vigor of the contractions of antagonistic muscles ; 
and this relative force must vary with every change of position. How this con- 
tinuous and remarkable regulation of motor nervous energy takes place is an 
unanswered question. Perhaps reflex action has something to do with it. A 
further interesting point is, that changes of position induced by electrical stimula- 
tion of the nerves or muscles are not permanent ; when the stimulus ceases to act, 
the limb falls back into its old place. 

Catalepsy occurs oftenest as a symptom of hysteria (see the following chapter). 
In this case it is usually associated with other disturbances, chief among which 
are impairment of consciousness and anaesthesia. The anaesthesia is especially 
marked in the muscles. For example, the patient will stand for an hour with 
arms extended, and yet experience not the slightest sensation of weariness. At 
last, however, the arms sink slowly down. Closely allied to hysterical catalepsy 
is hypnotic catalepsy, a condition which can be artificially produced by certain 
procedures in many hysterical subjects at will (see the next chapter). Charcot 
has reported cases where the lethargy of hypnotism could invariably be trans- 
formed into catalepsy by opening the previously closed eyes. These cases also 
presented, in addition to the catalepsy, the strange phenomenon called " sugges- 
tion." If the patient were put into any posture associated with some definite 
mental conception (such, for example, as the attitude of prayer, or that assumed 
in terror, or to express detestation), then the corresponding thoughts would come 
into the mind, as a hallucination, but with all the vividness of reality. Ample 
proof of this was visible in the expression of the face and in the whole bearing 
of the subject. An analogous fact has been observed by Duchenne, Lasegue, and 
ourselves — namely, that sometimes a hysterical person can be brought into the 
cataleptic state by artificial closure of the eyes (compare what is said in the next 
chapter about hysterical anaesthesia). 

Catalepsy is also seen in many psychoses, particularly in certain grave forms 
of melancholia (melancholia attonita, katatonia), and sometimes in progressive 
general paralysis. (For particulars see works on insanity.) The cataleptic state 
may also develop in connection with grave organic cerebral disease, as in menin- 
gitis and apoplectic coma. It may finally be mentioned in passing that quite well- 
marked catalepsy is sometimes observed in young children of one or two years 
when they are ill. Probably they fall into a sort of stupor; or often it seems 
that they are rendered hypnotic, as it were, by the presence of strangers. 

Catalepsy has been regarded as a special disease in those very rare cases where 
otherwise healthy persons are liable to " cataleptic fits." The condition comes on 
suddenly, unprovoked, and passes off spontaneously after, a variable length of 
time. It is, however, very probable that such of these cases as are not hysterical 
are epileptoid, and deserve to be classed with genuine epilepsy. 

Prognosis and Treatment. — Since catalepsy is a symptom of so many different 
diseases, it is impossible to make any general statements with regard to prognosis 
or therapeutics. The reader may gain some light from the remarks on the treat- 
ment of hysteria in the next chapter. 



1172 



DISEASES OE THE NERVOUS SYSTEM 



CHAPTER IX 
HYSTERIA 

iEtiology and Definition.— It is impossible to give a definition of hysteria that 
shall be at once brief and accurate, for the aspects of the disease are so manifold 
that there is no one symptom which can be called pathognomonic or even 
universally characteristic. Hysteria is therefore symptomatically not a well- 
rounded morbid unit, although the nature of all those pathological conditions 
which we term hysterical may very well be regarded from a single point of view. 
Hysteria thus has its peculiarities and its rules like any other disease. Only 
because its laws have been sought elsewhere than where they really are, has the 
claim often been made in the past that the morbid symptoms of hysteria were 
subject to no law. 

The fundamental condition for a right understanding of hysteria seems to be 
that we should free ourselves from the old untenable idea that hysteria is a " gen- 
eral functional disease of the whole nervous system, where now this and now that 
portion of it may be disturbed in its functions." We regard hysteria as a disease 
which relates to the cerebral activity immediately associated with the psychical 
processes — that is, one may say, with a psychosis, but in the broader sense of the 
word; the disturbance affects not only the normal course of the psychical pro- 
cesses, but also their association with the purely corporeal processes of innerva- 
tion. We therefore call any symptom hysterical which is due to a disturbance of 
the normal relations between the processes of our consciousness and our cor- 
poreity. Between our ideas of volition and our muscles, as between the excitations 
of our sensory nerves and our consciousness, there exist under normal conditions 
very definite and very well ordered connections. If there comes a loosening, a 
displacement, a false estimate in these connections, it gives rise to a " nervous " 
disturbance of motion or sensation, a " hysterical n symptom ; but the starting- 
point of the disturbance always lies ultimately in the psychical domain. If, 
for example, the idea of volition suffers a morbid change in the sense that it 
can no longer arouse a corporeal motor excitation in any muscular territory, 
a " hysterical " paralysis follows. If the consciousness turns permanently from 
definite sensory impressions that come to it, we have to do with a hysterical 
anaesthesia. Later deductions will prove more plainly this characteristic psycho- 
genetic origin of all hysterical symptoms. 

In the meantime we may add to what has been said the following characteristic 
features of hysterical affections : 

1. All hysterical disturbances, no matter how severe the functional nervous 
derangement attributable to them, are without visible anatomical basis. The best 
proof of this is the fact that any hysterical affection, however severe, may some- 
times develop and then may recover completely in a very short time. 

2. The hysterical affection is very often most intimately associated with 
discoverable causes of a psychical nature. "Not only is its appearance and incipi- 
ency most closely linked with emotional excitement, but later on the mind is the 
main if not the only channel through which causes can operate to change the con- 
dition of the patient, whether favorably or unfavorably. 

3. It is therefore evident that the origin of all hysterical disturbances must be 
sought in the most central portions of the nervous system — those regions which 
are most directly concerned in the mental processes. Hysterical phenomena are, 
however, exhibited in all parts of the nervous system, so far as these depend upon 
psychical processes or may be altered by them. The symptoms of hysteria are 
therefore more manifold than those of almost any other disease. Although so 



HYSTERIA 



1173 



manifold, certain symptoms predominate with such frequency as to be character- 
istic of hysteria, and therefore to be regarded as especially valuable in diagnosis. 
Following Charcot, we term such symptoms " hysterical stigmata." These symp- 
toms are most constantly present, and therefore they can easily be found at any 
time. 

4. Besides the permanent symptoms — the " stigmata " — we see in many cases 
of hysteria peculiar nervous attacks. These are also highly characteristic of 
hysteria, since they come on in forms which are seen in no other disease ; but there 
are also patients who suffer from hysteria who nevertheless are never visited 
by attacks. The possibility of the occurrence of an attack is, however, always 
present. Very often the attacks are provoked by easily discoverable psychical 
causes. 

After this brief introduction, turning to the special aetiology, psychical causes, 
as has been said, are of first importance. In numerous instances hysteria comes 
on as an immediate sequel to violent emotional excitement or to a "psychical 
trauma," if we may use such an expression. Hysterical convulsions or paralysis 
may be excited by great terror or violent anger or any unusual agitation. Here 
the efficient psychical cause is often hidden by some attendant circumstance. 
If, for example, a patient falls into the water, or gets burned, or tumbles down- 
stairs, and thereupon develops hysteria, the mistake is often made of ascribing 
the subsequent nervous disease to catching cold, or to the injury received, 
although really it was the mental excitement which produced it. The various 
physical injuries (falls, blows, burns, etc.) play a far greater, and perhaps the 
greatest, part in the genesis of hysterical conditions. In such cases it is not 
the physical injury itself, but the terror it causes, or rather the whole disturbance 
of consciousness due to the trauma (terror, anxiety about the consequences, 
fright, etc.), which produces the hysterical symptoms. These nervous affections 
produced by physical injury (traumatic hysteria, traumatic neuroses) are of 
such great practical importance that we will devote special consideration to them 
later. 

What is very remarkable in such cases is that the special attendant circum- 
stances of the psychical disturbance often influence the localization of the hys- 
terical phenomena : that part, to which attention was particularly directed at the 
time, not infrequently becomes, later on, the seat of the nervous disturbance. In 
hysterical joint-affections (page 821) the cause not infrequently proves to have 
been an injury to the particular joint now suffering from hysteria. A young 
girl, who was awakened at night by the smoke of her burning mattress, and who 
had a severe laryngitis from inhaling the vapors, exhibited later an indubitably 
hysterical paralysis of the vocal cords. In the case of another girl, who in jump- 
ing from a carriage fell upon her side, we afterward saw hemianesthesia of the 
same side. Many such instances could be cited. 

Certain hysterical cases, therefore, have for their obvious cause a single occa- 
sion of mental agitation; but in many others the disease is not thus abruptly 
excited. As, in poisoning, we can distinguish between the sudden action of a 
large dose and chronic cases where minute amounts of poison are absorbed daily 
for a long period, so hysteria may come on not only after a single violent shock, 
but also as the final consequence of psychical influences insignificant in them- 
selves, but potent because of their frequent repetition or persistency. It is in 
cases of this sort that the causes do not become evident to the physician until he 
has gained the entire confidence of his patient ; for the root of the trouble is often 
entwined about the most private affairs. Anxiety, sorrow, disappointed expecta- 
tions, abandoned hopes, and, in brief, everything which can depress and over- 
whelm the mind — these are factors which may at last excite the functional nerv- 
ous derangements of hysteria. 



1174 



DISEASES OF THE NERVOUS SYSTEM 



Finally, we must state that hysteria may often develop without any specially 
noticeable cause. We see this particularly in young- people with a marked 
hereditary nervous taint. Here the ordinary daily demands upon a central 
nervous system, which had originally an abnormally weak constitution, sometimes 
suffice to disturb in a measure its normal equilibrium. 

This leads us to a second extremely important point in the aetiology of hysteria. 
The blow which brings a feeble body to the ground rebounds without effect from a 
massive frame. Exactly the same may be said of the " blows " to which the 
nervous system is subjected. Few entirely escape these influences, but there 
are some " strong natures " who resist the psychical assault without wavering, 
while others have a feebly resistant (" inferior ") nervous organization and are 
overpowered. We see, therefore, that the predisposition of different individuals 
to diseases of the nervous system varies. This fact is a very important one in 
the pathogenesis of all functional nervous disorders. In what this predisposition 
consists we do not know, being acquainted only with its results and with some 
of its causes. 

In many cases this predisposition is hereditary. Hysteria is most prominent 
among those neuroses which attack different members of a family — one suffering 
from one disease and another from another (vide page 1141). It is also possible 
to acquire such a predisposition. At least it may be developed and fostered, on the 
one hand, or, on the other, checked and repressed. In these directions physical as 
well as psychical factors are of importance. Anything which weakens the con- 
stitution diminishes the resistant power of the nervous system. Among psychical 
influences, nothing favors the development of hysterical tendencies more effi- 
ciently than does a bad education. Hysteria is often ascribable to an irritability 
and feebleness of the nervous system thus engendered. The whims of the child 
are not controlled, its will is not strengthened, or its energy developed; its 
imagination is unsuitably and excessively stimulated, or its intellectual powers 
are overtaxed and prematurely ripened. 

It is well known that hysteria occurs more frequently in the " feebler " female 
sex than among men; but it is by no means a rare thing for men to exhibit 
hysterical convulsions, paralysis, contracture, or other well-marked disturbances. 
Most cases occur between puberty and the end of middle life. It is quite common 
to see pronounced hysteria in children, especially such as are over eight or ten 
years old. The disease very frequently begins to develop a year or two previous 
to puberty. Nationality and race also seem to exert some influence — for instance, 
the severer forms of hysteria are decidedly more frequent in France than in Ger- 
many, but severe hysteria is by no means rare in Germany. The Jewish race are 
particularly subject to hysteria, and to nervousness in general. 

One matter remains to be considered with regard to aetiology, to which a 
greatly exaggerated importance was formerly ascribed. It is the influence of dis- 
ease of the sexual organs. The very name " hysteria " (vo-repa = uterus) reveals 
what the old view was, namely, that hysteria invariably originated in disease of 
the female genitals. Not to speak of the fact that the disease occurs in men and 
children, an unprejudiced consideration of the matter will show that the above 
assumption is entirely groundless even in regard to women. A large number of 
hysterical women present no anomaly of their sexual organs ; and even if the lat- 
ter be diseased, we are not justified in assuming at once that the hysteria is 
secondary to the sexual disorder. In these cases, also, we usually find, on careful 
inquiry, that psychical causes have been at work; and these are incomparably 
more potent in exciting hysteria than is malposition of the uterus or constriction 
of the cervical canal. It is true, however, that disease of the genital organs 
may depress the spirits more than some other diseases would, and so indirectly 
promote hysterical disturbances. In the same indirect way, menstruation, preg- 



HYSTEKIA 



1175 



nancy, and parturition exert an important influence upon the development and 
course of hysteria. Sexual excesses or total abstinence from sexual indulgence 
also produce their effects indirectly through the mind. 

The Symptoms and ^Manifestations of Hysteria 
Considering the great differences in the external morbid symptoms under 
which hysteria may manifest itself, it is not easy to give in a brief summary a 
comprehensive, intelligible, and yet accurate description of its clinical manifesta- 
tions. "VTe believe that we can best attain this end by speaking first of the most im- 
portant and most frequent of the single symptoms of hysteria, by describing next 
the hysterical attacks, and finally by trying to evolve a general picture of the 
disease. 

l. The Hysterical Stigmata, especially Sensory Anaesthesia and Hyper- 
esthesia. — In every case vrhere the diagnosis of hysteria has already been estab- 
lished or where it is to be confirmed, we must examine the patient for certain 
symptoms, which, as we have said, are very common in hysteria, and in part so 
peculiar to it. that by themselves they are often of decisive diagnostic significance. 
These symptoms are termed " hysterical stigmata.'"' A knowledge of them is the 
more important for the physician in that we often detect them only by a special 
examination directed to that end. Patients only exceptionally inform us as to 
these symptoms. It is not at all unusual for patients to have no inkling of their 
existence until after an examination. 

The most important, because the commonest, of these hysterical signs relate to 
sensibility. The more carefully we examine, the more rarely will we meet with a 
case of severe hysteria in which in some sensory region we do not find manifest 
disturbances, especially a diminution of sensibility. We must therefore test 
accurately not only the sensibility of the whole surface of the body, but also the 
functions of all the special senses (sight, hearing, smell, and taste). 

The sensory disturbances of the skin must first be mentioned. Xot infre- 
quently we find a diminution of sensibility over the whole surface of the body, 
especially a more or less complete analgesia. In such cases we can stick a pin in 
deeply anywhere, or pierce a fold of skin with a pin, without the patient's com- 
plaining of pain. As is well known, it often happens that hysterical patients, in 
order to appear interesting or from some other reason, produce upon themselves 
deep injuries and wounds ; this is almost always connected with the patient's anal- 
gesia. Very often, however, the anaesthesia is not general, but it is limited to a 
definite region. We find complete anaesthesia of one arm or leg. or we find on the 
trunk or the extremities single areas of anaesthesia, in which the anaesthetic parts 
are bounded by the normally sensitive skin; these areas may take all possible 
forms, and may often be very peculiar. The sensibility to pain is almost always 
the most disturbed, even when the other forms of cutaneous sensibility may be 
quite unaffected, but changes in the sensibility to temperature, pressure, etc., may 
also occur. It may be added that in the severer forms of anaesthesia the deeper parts 
may also be insensitive, so that the so-called muscular sense is absent, and pa- 
tients with their eyes shut have not the slightest idea of the position of the 
anaesthetic limbs. [The skin reflexes are usually diminished or absent over the 
anaesthetic regions. In hemianaesthesia the gagging reflex from irritating 
the back of the pharynx, palate, or tongue, may be absent on the anaesthetic 
side. — K.] 

Besides cutaneous anaesthesia, disturbances in the sensibility of the other sen- 
sory organs (other " sensory anaesthesias ") are among the commonest signs of 
hvsteria. Sometimes the patients say, when asked, that they see indistinctly and 
dimly. If we examine the eyes we often find a loss of visual acuteness and a 
rapidly induced fatigue on using them. A limitation of the visual field is the 



1176 



DISEASES OF THE NERVOUS SYSTEM 



most characteristic sign — that is, an anaesthesia of the peripheral portions of the 
retina. The degree of this limitation sometimes shows manifest differences for 
the different colors. Hysterical achromatopsia is a common symptom — that is, a 
partial or complete loss of the color sense. According to Charcot, in the hysteri- 
cal the perception of violet usually first disappears, then green, and lastly blue and 
yellow; but we must not hold too strictly to all these rules; for, although the 
French investigators are otherwise deserving of great praise in adding to our 
knowledge of hysteria, in this respect they seem decidedly too schematic, and to 
have generalized too rashly. Diminution of the auditory acuteness in one or both 
ears is also not uncommon. Anaesthesia of smell and taste is still more common. 
Salt, quinine, vinegar, sugar, etc., either excite no sensation of taste at all, or the 
tongue is anaesthetic for one or another of these substances. The same holds for 
the sense of smell. All these symptoms are especially important in diagnosis, be- 
cause in organic diseases they seldom reach such a degree as in hysteria. 

The sensory anaesthesias above described may of course be combined in various 
ways in different cases, but none of these combinations is so characteristic and 
individual as hysterical hemianaesthesia, a symptom-complex which occurs almost 
solely in hysteria, and is therefore of distinct diagnostic value. 

Hysterical hemianaesthesia is one of the most common symptoms of profound 
hysteria. It must often be sought for, inasmuch as the patient herself frequently 
has no suspicion of its existence until her attention is called to it. It seems just 
as if one half of the body had been entirely lost to consciousness ; the patient does 
not know whether it is or is not capable of feeling. 

In a typical and fully developed case the hemianaesthesia does actually affect 
just one half of the body. There are rudimentary forms ; but in these complete 
ones, the boundary between the anaesthetic parts and the parts retaining normal 
sensitiveness accurately corresponds to the median line of the body. The skin on 
the affected side is entirely insensible to the prick of a needle or to heat. Often 
it seems somewhat blanched, and its blood-vessels seem to be constricted ; at least 
the skin very often bleeds surprisingly little if wounded. The mucous membranes 
upon the abnormal side are all equally anaesthetic, including the conjunctiva, and 
the corresponding half of the buccal cavity and of the tongue. The deeper parts, 
such as the muscles and joints, are also almost invariably anaesthetic. The patient 
can no longer feel in what position the limbs of the affected side are ; and if they 
are moved passively, no sensation is communicated to her. The organs of speciaL 
sense are usually involved. Hearing is impaired upon the affected side ; the corre- 
sponding half of the tongue can not taste ; the corresponding nostril can not smell ; 
and sight upon that side is affected in a peculiar manner. There is no hemianopsia, 
but a total amblyopia, or possibly amaurosis. If the amaurosis be not complete, we 
find at least a limitation of the visual field and the signs of the above-mentioned 
achromatopsia. 

Apart from other hysterical symptoms with which hemianaesthesia as well as 
all the other sensory anaesthesias may be associated, we must mention here one 
symptom which is in close relation to anaesthesia, and which was first described by 
Duchenne under the name of " loss of muscular sense " (perte de la conscience 
musculaire) . The patient, whose arm, for example, is anaesthetic, can not move 
it if she closes her eyes, although with the eyes open she can move it as well as ever. 
When the eyes are shut the arm remains motionless in the position it has pre- 
viously occupied. If its position be altered by passive motion, the new position is 
maintained with equal persistency. There is, with the eyes shut, pronounced 
catalepsy. Duchenne referred this peculiar symptom to the loss of a special 
sense which he termed "muscular sense" (conscience musculaire). According to 
our present conception of hysteria it would be more correct to regard the symptom 
as purely psychical. 



HYSTERIA 



1177 



[The various anaesthesias and many other symptoms of hysteria might often be 
termed more properly " delusions of not-feeling.'* Patients with hysterical blind- 
ness, for example, when prisms are placed before their eyes, so that they imagine 
they are looking with the sound eye when they are really looking with the " blind " 
eye. can sometimes see very well. When hypnotized such patients can recall that 
they have been touched or pricked in the anaesthetic area, etc. This is often mis- 
taken for deliberate simulation, but it is really another instance of the psychical 
nature of the disease. — K.] 

The much-discussed and peculiar symptoms of transfer, as well as metal- 
loscopy and allied symptoms, will be mentioned below. 

Thus far we have spoken only of anaesthesia, but we very often find in the hys- 
terical certain hyperaesthetic regions. These hypersesthesias are so characteristic 
that we must reckon them among the hysterical stigmata, and must therefore look 
for them in every case. Sometimes the physician's attention is called to these 
places because they are the seat of constant slight or severe pain. In other cases 
the tenderness appears only upon pressure. The hyperaesthesia may be so great 
that the patient can scarcely bear the slightest touch. Of course, the hyper- 
aesthesia is very closely connected with the condition of the patient's attention. 
If the thoughts be diverted, even firm pressure is often not at all noticed. We see 
clearly, then, that we usually have to do here with a "psychical hyperaesthesia." 

The hyperaesthetic spots are either quite extensive or quite circumscribed, or 
even limited to one definite spot. They may lie near to or in the midst of anaes- 
thetic areas. They are relatively rarest in the extremities and more common on 
the head and trunk, especially on the sternum, on the sides of the chest, under the 
mammae, etc. Most common, and therefore especially characteristic, is the hyper- 
aesthesia of the vertebral column, and, in women, of the lower abdominal region 
(" ovarian pain,"' " ovarie '"). The latter term is convenient but by no means cor- 
rect, since really we have only a tenderness of the soft parts in general, which is at 
once noticeable on deep pressure, and we do not have solely or chiefly a tender- 
ness of the ovary. We usually find ovarie only on one side, oftener on the left 
than on the right. Analogous symptoms in men — tenderness in the groins or the 
testicles — are less common. Hyperaesthesia of the vertebral column, hysterical 
" spinal irritation/'* is even more important for diagnosis than ovarie. The hyper- 
aesthesia affects either the whole spine or merely single portions of it, often only 
single vertebrae. It may attain so high a degree that the slightest touch of the 
skin over the vertebrae, or somewhat deep pressure, may cause the liveliest out- 
cries and shrinking. This symptom is almost pathognomonic of hysteria. 

The relations which these hyperaesthetic regions have to the hysterical attacks 
are very important, and they have therefore procured for them the name of " hys- 
terogenous zones.'"' We will speak further on this point in describing the hysteri- 
cal attacks. 

Hyperaesthesia in other sensory regions — abnormal sensitiveness of the eye, 
ear. etc. — also occurs. Thus certain cases of hysterical blepharospasm seem to be 
due to an immoderate sensitiveness to light. Unusually sharp hearing is noted, 
especially during the hysterical attacks. Here, too, belongs the aversion of many 
patients to certain odors and flavors, and the like. 

We may also mention in this place hysterical pains. They can scarcely be 
separated strictly from hysterical hyperaesthesia; at least, almost all hysterical 
patients, who complain of pain (in the back, in the face, in the arms and legs, 
and very often " all over " !), state that these pains are increased by motion and 
pressure. The more the patient's general disposition is disturbed, the more he 
thinks of his pain, and the worse it becomes. If the patient is busied with other 
things, he forgets his pain entirely. Suggestive influences (vide infra) are of 
great effect. There can therefore be no doubt that these feelings of pain are of 



1178 



DISEASES OF THE NERVOUS SYSTEM 



a purely psychical nature ; they are, so to speak, " imaginary pains," hallucina- 
tions of pain. Hysterical pains sometimes become very important because they 
render the patient inactive. There are hysterical patients who lie the whole day 
on the sofa, because they can not stir a limb " on account of pain." Mobius and 
others have described such especially pronounced cases under the name of 
" akinesia algera." In our opinion, there is no reason for wishing" to make a 
separate disease of such cases, because such conditions often enough occur alone 
or associated in various ways with other symptoms in severe neurasthenia and 
hysteria. 

2. Hysterical Paralysis. — Hysterical paralysis is frequently an immediate 
sequel to some violent mental excitement (for example, " paralysis from fright ") ; 
but it may come on gradually. Hysterical paralysis is indubitably of central 
origin. It is a paralysis of the will. The patient has lost the power to will a 
contraction of the affected muscles. One always has the feeling that the patient 
could move the paralyzed limb perfectly well if she only desired to; but she can 
not bring the will to bear on it, and this inability is the real trouble. It also 
seems a remarkable circumstance that hysterical paralysis often, but of course 
not always, affects only certain combined movements. Many patients, for in- 
stance, can move their legs very well in bed, but they can not walk a step 
("abasia" vide infra). We have seen a hysterical writing paralysis; the right 
arm was not paralyzed, but it utterly refused to make any attempt to write. 

The extremities are most frequently paralyzed, particularly the lower limbs; 
but hemiplegia is not especially rare. A very common manifestation is loss of the 
power to stand or walk. The patient lies in bed or on a sofa, and sometimes while 
thus reclining she can flex and extend the legs very well; but as soon as she is 
urged to stand up or walk, the knees double up, the patient begins to tremble, the 
respiration grows rapid and convulsive, and there is not the slightest effort made 
to move the legs. In France the names " astasia " and " abasia " are used for 
these common hysterical symptoms. If only one leg be paralyzed, the gait is 
often very peculiar and characteristic. The sound limb makes long strides, while 
the paralyzed one is held perfectly rigid, and often is dragged along with a loud 
shuffling sound. The arms are much less often affected. The facial muscles are 
hardly ever paralyzed, although they may be involved in hemiplegia. We once 
saw hysterical diplopia. 

In regard to the more precise form of the paralysis, both flaccid and spastic 
paralyses occur in hysteria. In many cases of hysterical paralysis the tendon 
reflexes may be so exaggerated — nay, there may even be, as we have repeatedly 
seen, such a lively ankle clonus — that one is at first disposed to think of actual 
spinal paralysis. In other cases, as in paralysis of an arm, the paralyzed limb 
hangs down completely flaccid. The paralyzed parts are often at the same time 
completely anaesthetic (a circumstance which may often be distinctive in 
diagnosis), but in other cases they are normally sensitive or even hyperses- 
thetic. 

Hysterical paralysis of the vocal cords is very often seen. The voice is gener- 
ally lost suddenly, and the patient can talk only in a whispers-hysterical aphonia. 
On laryngoscopic examination, we are often struck, at the outset, by the anaes- 
thesia of the pharynx and its lack of reflex excitability. We find no trace of any 
anatomical lesion of the cords, but merely that they are paretic. The glottis can 
not be completely closed, and sometimes the vocal cords actually become wider 
apart upon every effort at phonation. The patient then speaks exclusively in a 
whisper. — Hysterical mutism quite rarely follows hysterical aphonia. The pa- 
tients entirely lose voluntary control of their speech apparatus, and finally be- 
come completely dumb. We will also mention here hysterical stammering, al- 
though it should more properly be classed with the spasmodic hysterical symp- 



HYSTEEIA 



1179 



toms. The voluntary quiet innervation of the muscles of articulation is affected, 
so that the speech is altered in the most peculiar way, by needless spasmodic at- 
tendant movements, grimaces, etc. We have very often observed such hysterical 
disturbances of speech (stammering or mutism), especially in children (as a result 
of fright). A loss of the power of writing may sometimes be associated with the 
dumbness in an interesting way. 

Hysterical paralysis of deglutition is much less frequent than paralysis of 
the vocal cords. If there be dysphagia, it is often not an easy matter to determine 
whether it is due to paralysis or to spasm, which comes on at any attempt to 
swallow. 

3. Hysterical Contractures. — Contractures may occur as isolated phenomena, 
or in combination with other symptoms, such as anaesthesia or paralysis. They 
are caused by unusually strong tonic muscular contractions. The starting-point 
of the irritation is certainly in the central nervous system. Sometimes the con- 
tractures are temporary, but often they are characterized by their intensity and 
their great persistency. The extremities suf- 
fer most frequently, although the trunk or 
the back of the neck may be affected. In the 
hands and feet, especially in the toes, flexor 
contractures predominate, but in the larger 
joints extensor contractures are the rule. 
Although many varieties occur, single forms 
of contracture are especially characteristic. 
As an example, we will refer to the accom- 
panying illustrations (Figs. 180, 181). 

The relations of hysterical contractures 
to the articular neuralgias have already been 
mentioned (page 821). They may occur in 
hemiplegic, paraplegic, or monoplegic form. 
They often follow a hysterical convulsive at- 
tack (vide infra). All hysterical contrac- 
tures disappear completely in chloroform nar- 
cosis, after the use of an Esmarch bandage, 
and in deep sleep. 

4. Vaso-motor Disturbances. Secretory 
Disturbances. Symptoms in the Internal 
Organs. — Besides the sensory and motor 
symptoms just described, other symptoms oc- 
cur in hysteria which fall under the domain 
of the vaso-motor and secretory nerves; but 

in our opinion we should cite here with positiveness only those symptoms which 
we find to be dependent directly or indirectly upon psychical processes. In this 
domain, however, the credulity of many physicians has brought to light a mass 
of apparently wonderful and inexplicable observations, which are not proof 
against rigid criticism. 

In the first place abnormal anaemia or abnormal fullness of the vessels (a cool, 
pale skin in the one, a hot, red skin in the other) is not infrequent, and points 
to vaso-motor influences. Since we know that the vascular nerves are influenced 
in a high degree by the emotions, we can probably assume a central origin for 
these symptoms. Haemorrhages from internal organs are harder to explain ; they 
are apparently not uncommon in hysteria, and they have often been referred 
to " nervous vaso-motor influences," but in our opinion we must be extremely 
guarded in such an assumption. We most frequently see hysterical haematemesis 
or hysterical haemoptysis — that is, the evacuation of blood from the mouth, either 




Fig. 180.— Hysterical contracture. (From 
Bourneville and Regnard's Iconographie 
de la Salpetriere). 



1180 



DISEASES OF THE NERVOUS SYSTEM 



with cough or in a way suggestive of choking. Inexperienced physicians have 
thus often been led to a false belief in dangerous pulmonary disease or gastric 
ulcer; but if we look more closely we shall find that the blood evacuated is of a 
clear raspberry-red color, is mixed with a good deal of mucus and saliva, and is 
of a thin fluid consistency. The whole amount is seldom more than two or three 
ounces (grammes 50-80). If we inquire more carefully as to its origin, we can 

usually find a source for the blood in the gums 
or in the oral or pharyngeal mucous membrane. 
There are often spasmodic chokings or hic- 
coughs, by which a hemorrhage of the mucous 
membrane is mechanically produced. It is also 
certain that in many cases intentional decep- 
tion on the part of the patients may lie at the 
bottom of the haemorrhage. We must be ex- 
tremely cautious in haemorrhages from the 
genitals, from the skin, from the palms in the 
" stigmatized," etc. We once exposed a hysteri- 
cal woman who had for years produced the most 
extensive gangrenous spots upon her skin by 
caustic soda! 

Finally, among the vaso-motor disturbances 
we must mention one symptom whose signifi- 
cance, in our opinion, has not yet been satisfac- 
torily explained — we mean hysterical fever. In 
severe hysteria, especially at the time of severe 
attacks and psychical disturbances, other ob- 
servers, and we ourselves, have repeatedly seen 
high febrile temperatures, 106° (41° C.) and 
more ; and these temperatures come on in a very 
irregular manner. In none of the cases under 
our own observation, however, could we wholly 
exclude the possibility of simulation — that is, 
of producing a rise of the mercury by rubbing 
and pressing on the thermometer. In all the 
measurements we made ourselves in the rectum 
the temperature was normal, while the high 
fever was always said to occur in our absence. 
We therefore recommend the greatest caution 
with reference to this point. 

Anomalies of the secretory and excretory 
organs have also been met with in hysteria. 
Many patients have a remarkably dry skin, 
while others sometimes perspire very freely. 
The secretion of saliva is subject to similar 
modifications. Very remarkable observations 
have been made in a few cases with regard to 
hysterical ischuria; for days only a very small 
amount of urine has been passed, although there has been no retention. In one 
case of this sort, observed by Charcot, there was violent vomiting at the same 
time, and the vomitus was said to contain a comparatively large amount of urea 
(vicarious excretion). Such observations, which are very few in number, are at 
present not susceptible of an exact explanation, but the suspicion of simulation 
does not seem to us wholly excluded. Hysterical polyuria occurs more frequently 
than ischuria. A large amount of very light-colored urine of low specific gravity 




Fig. 181.— Contracted position of the left 
foot in traumatic hysteria. (Personal 
observation.) 



HYSTEEIA 



1181 



is excreted. This polyuria is in many instances merely the result of excessive 
ingestion of liquids. Polydipsia (excessive thirst, or probably, to speak more cor- 
rectly, a morbid tendency constantly to drink water) is a very frequent symptom 
in hysteria, particularly at the close of a fit. 

The digestive disturbances which many patients have are mainly such as have 
already been discussed on page 463, under the head of " nervous dyspepsia." 
Colicky pains, obstinate constipation, occasional diarrhoea, and similar symp- 
toms, are by no means rare. Hysterical vomiting, especially, often plays 
a very great part, since it may very much impair the patient's nutrition. In 
other cases, of course, the patient's well-nourished appearance is in striking con- 
trast with her statement that she " has to vomit everything up again." Hys- 
terical tympanites also deserves mention. It is due to the accumulation of a 
large amount of air and gas in the primse vise. This may be in part the result 
of a sort of paralysis (" atony ") of the muscular coat of the stomach and intes- 
tines, but another frequent cause is the swallowing of large amounts of air. 
Perhaps the patient does this on purpose. The prominence and tension of the 
abdominal walls may be so considerable as to simulate grave diseases, such as 
peritonitis, a tumor, or pregnancy. Doubts of this sort can always be dispelled 
by inducing anaesthesia with chloroform. It is possible to remove the gas com- 
pletely in a short time by pressing upon the abdomen, or by introducing a long 
tube through the rectum. 

Sometimes there are symptoms referable to the genital organs. It has been 
already pointed out that too much prominence was formerly given to the influence 
of sexual diseases in exciting hysteria. It is also true that nervous derangements 
of the genital organs, as of all the other organs, may be among the symptoms of 
hysteria. Many pains and hypersesthetic conditions of the genital organs must 
in particular be so interpreted, while co-existing disturbances of menstruation 
are often to be regarded as co-ordinate symptoms. We can also readily under- 
stand that sexual relations often influence very excitable, hysterical individuals 
to no slight extent, as is indeed very frequently betrayed by the character of 
their hallucinations and their utterances when delirious. 

5. General Mental and Bodily Constitution of the Hysterical. — If we regard 
hysteria as a disease which is largely psychical, which is the only correct view, it 
will not seem strange if the whole mental constitution and nature of the patient 
show special peculiarities. In many cases, therefore, the psychical condition of 
the hysterical is so characteristic that the physician can, from the patient's nature 
and demeanor, form his conclusions as to the form of her disease. 

Hysterical persons are irritable and emotional, easily depressed, sensitive, 
whimsical, and subject to violent extremes of feeling. They are inclined to exag- 
gerate their sufferings, exact a great deal of attention, and are anxious to excite 
sympathy. They have little energy or force of will, but they are sly and obsti- 
nate in carrying out any pet desire. Again, they can be very amiable and attrac- 
tive if they take the fancy. They are often shrewd and active mentally, but hys- 
teria is also not infrequently seen in dull and stupid persons. 

This brief sketch represents many cases, as we have said, but not all. The 
patients to whom it refers as a rule present no very great disturbances, but com- 
plain merely of all sorts of general derangements, sometimes of one kind and some- 
times of another, and yet are able to perform their daily duties tolerably well. A 
case of paralysis, contracture, or other important localized hysterical trouble may 
not present any marked mental peculiarities. Often, of course, the patient conceals 
them from the physician, and the psychopathic nature of the whole mental con- 
stitution (" character ") is finally revealed .only by a closer acquaintance with the 
patient and her previous life. 

With regard to the general physical constitution of hysterical subjects, it has 



1182 



DISEASES OF THE NERVOUS SYSTEM 



already been mentioned that any bodily weakness favors the development of the 
disease; and yet hysteria is by no means confined to the ill-nourished, weakly, 
and anaemic. On the contrary, many patients seem to be in blooming health and 
well nourished. In a severe case of hysteria, however, the effects of the disease 
on general nutrition may be very distinct. Little food is ingested, sleep is dis- 
turbed, digestion is affected (vide infra), and the bodily health is gradually 
undermined. 

Hysterical Attacks, Conditions of Spasm, etc. 

While the symptoms thus far described are largely of a permanent character, 
paroxysmal nervous symptoms are also very common in hysteria. The diagnosis 
of the entire morbid condition is often made certain by the onset of such hysteri- 
cal attacks, which are often very characteristic, and their significance is readily 
perceived by the experienced physician. There are some cases of hysteria which 
run their course entirely free from these attacks, and present only certain per- 
manent nervous symptoms, such as paralysis, contractures, anaesthesia, etc.; but 
there are also other patients in whom the hysterical attacks dominate the whole 
scene, and are sometimes the only manifestations of the disease. A hysterical at- 
tack is not infrequently the beginning of the trouble, especially in those cases 
where the disease is excited by fright, etc., and where the attack follows immedi- 
ately upon the psychical excitement. 

In regard to the severity and the variety of the hysterical attacks, they are so 
manifold that an exhaustive account of all the possibilities can not here be given ; 
but certain features and details are so common in them, and recur so often, that a 
consideration of them is often in itself sufficient for a correct diagnosis. 

The mildest form of the hysterical attack consists of the development of a feel- 
ing of distress, anxiety, vertigo, and especially of a loss of voluntary control of 
the body. The patient sinks on a bed or chair, closes the eyes, and becomes inca- 
pable of action or speech. Mild symptoms of motor irritation usually ensue, 
most commonly an acceleration of respiration, general tremor, winking of the 
eyes, etc. Mild spastic symptoms in the pharyngeal muscles and the diaphragm 
are not uncommon. There is very often a lively palpitation during the attack. 
The face is sometimes quite red, but in other cases pale. 

In such mild attacks any impartial observer has decidedly the impression that 
the patient is humoring her inclinations. If, therefore, she be encouraged, or if 
cold water be thrown in the face or on the back without too great regard for her 
feelings, she usually soon regains her will-power and rapidly recovers. 

In an unbroken series these mildest forms of attack pass over into the severer 
types, where the clouding of consciousness is greater and the symptoms of motor 
irritation are more severe. Complete loss of consciousness, so common in epi- 
lepsy, is scarcely ever seen in hysterical seizures, but there is very often a marked 
clouding of consciousness, and in the severe forms morbid alterations of con- 
sciousness (vide infra). If hysterical attacks occur which resemble those of epi- 
lepsy (" hystero-epilepsy "), we must think of the possibility of a combination of 
the two diseases ; but usually the form of the hysterical convulsion is essentially 
different from that of the epileptic. In severe hysterical convulsions the con- 
vulsive movements are more varied, more extensive, and more complicated than in 
epilepsy. The arms make thrashing and thrusting movements, and often appar- 
ently quite well-co-ordinated movements. Patients strike the bed, and sometimes 
their own bodies, with clenched fists; they seize objects, such as the bedclothes 
or furniture, and cling fast to them. We also see clonic or tonic flexor and ex- 
tensor spasms in the legs. The eyes are almost always rolled up, more rarely 
they converge or are turned to one side, and they often roll about. The lids are 
tightly closed or occasionally open. There is almost always trismus, and there is 



HYSTEKIA 



1183 



often grinding of the teeth. The trunk usually twists and turns the most of any 
part of the body. The patient often hits her head violently against the wall or 
the bed. The whole body may assume positions which a healthy person can 
scarcely imitate without special practice. The best known, and in fact one of the 
commonest and most characteristic, is the arched position (arc de cercle), of 
which the accompanying illustration (Fig. 182) gives an idea. 

Many patients rest for a time on the floor supported only by the head and toes. 
At intervals they fling or roll their bodies to and fro, drum on the floor with their 




Fig. 182.— Hysterical arc de cercle (Bourneville and Regnard). 



legs, throw themselves into the air, etc. Any one who has once seen such a " grand 
hysterical convulsion " will never forget the picture. 

A different but yet a common form of hysterical convulsion is characterized by 
a pronounced implication of the respiratory muscles. The attack begins with a 
spasmodic acceleration of respiration, and the breathing becomes progressively 
shorter and more rapid. We have ourselves counted two hundred respirations a 
minute. Other peculiar spasms of the respiratory muscles, which occur in this 
way only in hysteria, are also common; hiccough, loud sobbing, grunting, etc. 
The muscles of the pharynx are usually implicated in producing these noises. Of 
course, all these spasmodic conditions may be joined in the most varied ways with 
spasms of the trunk and the extremities. We very often find during the hysterical 
attacks pronounced cataleptic states. If the patient lies in bed with the eyes 
closed and without marked convulsions, we can put the arms and legs into the 
strangest positions passively, and they are kept there for a long time (see 
Fig. 183). 

One of the most essential factors which often gives the most characteristic 
stamp to the grand hysterical attack, is the relation which the spasms often have 
to certain co-existing abnormal conditions of consciousness. During the attack 
the patient is usually not unconscious, but she is under the dominion of 
morbid delusions, and these often mirror themselves in the outward movements. 
The patient is wholly dominated by a definite circle of ideas ; she has hallucina- 
tions, and passes through some frightful or exciting event. All this is most 
strikingly manifested in her movements and her expression. Hence, in an attack 
the face often expresses terror, rage, threatening, concupiscence, serenity, etc. 
Very often the internal excitement breaks forth in words, and there is actual hys- 
terical delirium, the most marked emotional utterances, etc. We often observe, 
and it is a fact of especial interest, that in hysterical attacks which have come on 
immediately after a severe fright, or some exciting event, the same scene to some 
degree is rehearsed over in the patient's consciousness in each subsequent attack. 
If, for example, hysterical attacks come on in a nervous child who has been at- 
tacked by a dog, we can not infrequently recognize again the cries of terror at 



1184 



DISEASES OF THE NERVOUS SYSTEM 



the approach of the dog in each new attack, etc. The patients often talk continu- 
ally to themselves during the attack, usually very rapidly, with frequent repeti- 
tions of the same phrase or word. We can often succeed in giving the delirium a 
definite direction by questioning the patient, or converse regularly with the pa- 
tient during an attack, but usually the pure motor spasms again set in, or persist 
for some time in atonic form. 

We can not go further into the numerous details of the symptoms of the grand 
attack (" grande hysterie "), for an accurate knowledge of which we must thank 
the observations of Charcot and the school of La Salpetriere in Paris (Bourneville 
and Regnard, P. Richer). The descriptions of the French authors apply to the 
grand hysteria not infrequently seen in Germany. In regard to the whole picture 
of the attack the French neurologists distinguish several periods which corre- 
spond in general with the above-described conditions. The first period consists of 
severe epileptiform convulsions apparently associated with loss of consciousness. 




Fig. 183.— Hysterical attack with catalepsy. (Personal observation.) 



Then comes the period of "contortions and grand movements" (clownismus), 
and finally the period of plastic positions and passionate attitudes (attitudes pas- 
sionelles). The short and very significant expressions of this scheme are of prac- 
tical value, but according to our experience one can only rarely expect sharply de- 
fined " periods " in the individual case ; the grand hysterical attack is rather com- 
posed in the most varied ways of the different symptoms abdve mentioned. 

There remains one essential trait needed to complete the picture of the 
hysterical attack, and that is the " suggestibility " of the patient, which is so pe- 
culiarly characteristic of hysteria. By " suggestion " we mean the artificial pro- 
duction of a definite psychical state, or a physical state dependent on the mind, 
by arousing the appropriate ideas. In the general characteristics of the mental 
constitution of many hysterical persons we have already had to point out how 
much and how often such patients let themselves be dominated by their imagina- 
tions. Suggestion is merely the artificial fostering of this psychical peculiarity 
and its special application. The more we try to foster and preserve this pecul- 



HYSTEEIA 



1185 



iarity, the more we leave uncorrected the false ideas which the patients have, the 
better we succeed at last in making the patients merely a shuttlecock for their 
ideas. Hence the physician's daily experience teaches that, as suggestion experi- 
ments are repeated, the patients more easily become susceptible to them, so that 
finally we can actually " do everything with them." There can scarcely be any 
difference of opinion as to whether such an experiment is entirely justifiable, 
medically and morally; and even the fostering of suggestion for therapeutic pur- 
poses is a two-edged sword whose action is not always rigidly within the physi- 
cian's control. 

Suggestion is most easy during the hysterical attack itself, especially in those 
forms where the patients speak, hear, and answer. As soon as we give the 
patients' ideas a definite direction, and tell them in a convincing tone that 
they are in a garden or a wood, picking flowers or fruit, that they are 
attacked, bound, lying on the edge of a precipice or the water, etc., we see in their 
bearing and speech that they think they are actually experiencing all these con- 
ditions in their delirium and hallucinations. The emotional utterances of fear, 
terror, joy, or aversion are then often expressed with astonishing art. In the 
same way we can suggest paralyses, contractures, or anaesthesias. The most 
interesting feature of it all is, that when the attack is over every trace of recol- 
lection of what happened during it is lost. The same patients who just now were 
so much excited by some definite idea, a few seconds later, as soon as the attack 
has ceased of itself or has artificially been brought to an end (vide infra), know 
nothing more about it. They have not even a vanishing recollection like that of a 
dream about what they have just said and done, even if it be expressly described ; 
but it is still more remarkable that during the following attack they often re- 
member very well what they have experienced actually, or in their imaginations 
in the past attack. In such cases we can truly speak of " double conscious- 
ness." Processes of the conscious waking life, however, often remain in the con- 
sciousness during the attack. We have already said that the actual event (scene 
of terror, etc.) which has given rise to the first onset of the attacks, is often re- 
vealed anew in the delirium of subsequent attacks. 

Hypnotic symptoms are closely allied to the processes in suggestion. We can 
not give here a complete review of this field, which, as is well known, has been so 
much studied of late. The tendency of human nature to mysticism and the influ- 
ence of suggestions, which may be potent not only with the patients but even 
with the investigating physicians, are the reasons why the false and the true have 
often been mixed in the study of hypnosis. We can say only that one great ad- 
vance is now generally recognized, and that is, that most persons of scientific 
training have abandoned the hypothesis, once frequently accepted, of a special 
""magnetic power" (animal magnetism), by which the "magnetizers " could put 
their " mediums " into the " magnetic sleep " or other abnormal conditions. 

Hypnosis is nothing more than the intentional artificial production of a hys- 
terical attack, or a hysterical psychosis by suggestion — that is, by the action of 
definite ideas on the person to be hypnotized. Therefore, only those persons can 
be hypnotized in whom these ideas have a strong enough influence. JSTo man can 
be hypnotized to whom the nature of hypnosis is clear. The essential feature of 
all hypnotic procedures is merely to produce in the most lively way possible the 
idea, "It will happen as the hypnotizer says." All other things — the fixation of 
the eyes on bright objects, the vibrations of a tuning-fork, etc. — are side issues, 
and serve merely to support the suggestion. In all easily hypnotizable persons 
the mere closure of the eyes and the remark, " Now go to sleep," are enough to 
produce the hypnotic sleep. Patients (and here we may actually speak of " pa- 
tients ") reach this suggestibility, of course, only after they have often been hyp- 
notized; for the oftener the same action of an idea is produced the more easily 
75 



1186 



DISEASES OE THE NERVOUS SYSTEM 



it occurs — a law which follows also from many other experiments in the psychical 
domain. The different forms of hypnosis are not distinguishable from the various 
hysterical conditions. Hypnosis is an artificial hysterical symptom, designedly 
produced, and from this alone we note the danger of all hypnotic experiments 
if they are practiced by the ignorant. In this, too, it has often been shown 
that we can not become free again from the spirits which we call up. 

The Erench physicians (Richer) distinguish four chief forms of the hypnotic 
state, which show, however, many transitions : 1. The cataleptic state, in which 
the limbs retain all the positions artificially given them (see the previous chap- 
ter). 2. The state of "suggestion," of artificially produced hallucinations. If 
we put the body passively into certain positions corresponding to definite acts, 
we can produce in the patient all the appropriate ideas with the distinctness of 
a hallucination. To this category belong the well-known hypnotic exhibitions 
where hypnotized adult men dance dolls, eat raw potatoes with an expression of 
enjoyment, etc. 3. The lethargic state, that is, a state of apparent unconscious- 
ness, with the eyes closed, the muscles completely relaxed, and a marked increase 
of excitability in the muscles and nerves. A light pressure or a slight blow on a 
nerve, such as the facial, suffices to put all the muscles supplied by it into a tetanic 
contraction which outlasts the irritation. 4. By certain manipulations (for in- 
stance, rubbing over the vertex) we can change the lethargic state into one of 
hysterical somnambulism. The patients remain half unconscious, but answer 
automatically questions which are put to them, obey orders given to them, and 
sometimes show certain sensory hypersesthesias. We see that all these forms are 
precisely identical with the different forms of the hysterical attack. Only the 
increased mechanical excitability of muscles and nerves is not yet fully explained, 
but the reported observations upon this point have not yet been absolutely con- 
firmed. It is especially a question whether suggestion — that is, ideas which lead to 
unconscious muscular contractions — may not also play a part here ? 

We have thus far omitted to dwell upon an important point in the description 
of the hysterical attack — namely, the relation to it of " hysterogenous zones."' 
We have mentioned above how often in hysterical patients certain parts of the 
body (the ovarian region, the sides of the chest, etc.) are extremely sensitive to 
pressure. It is by no means uncommon that, in spite of the patient's resistance, 
somewhat longer pressure on such a spot may excite a hysterical attack. On the 
other hand, we sometimes succeed in causing an existing attack to cease by pres- 
sure on the same zone. We are of the opinion that in these manipulations also 
ideas become potent as connecting links; for we may, as we have often demon- 
strated in the clinique, by suggestive persuasion aloud or by all possible procedures 
excite and then inhibit attacks in hysterical patients. In such cases we never 
have to do with physiological reflex processes, but always with the action of ideas 
suggested to the patient. 

Einally, we must add that there are also milder forms of hysterical spasm 
which are limited to a definite muscular region, and are not associated with any 
marked clouding of consciousness. There are, for example, isolated spasms of the 
muscles of the neck, isolated respiratory spasms (spasmodic cough, etc.), not infre- 
quently associated with the strangest noises, and isolated spasms in the arms and 
legs; the laryngeal muscles may also be affected (hysterical spasm of the glottis). 
Spasms of the diaphragm and other muscles of inspiration are quite common 
under the form of hysterical hiccough, which may sometimes last in the severest 
way for days and weeks. To spasmodic conditions in the muscles of the pharynx 
and oesophagus we refer the well-known symptom of so-called globus hys- 
tericus : the patients feel as if a ball were moving up and down in the throat. 

We sometimes see spasmodic conditions which come on in a clonic fashion, or 
in single twitchings in this or that muscular territory; sometimes affect sym- 



HYSTEEIA 



1187 



metrical groups of muscles ; are not associated with disturbances of consciousness ; 
cease during sleep, and are often easily cured by appropriate mental treatment. 
Such conditions have often been falsely called paramyoclonus, or myoclonia (q. v). 
Among the forms of hysterical spasm we may also reckon the peculiar attacks, 
essentially of a psychical nature, when more complicated morbid excitations of 
volition occur with or without the ordinary convulsive movements. In such at- 
tacks the patients begin to ejaculate the filthiest words of abuse (coprolalia), 
or to repeat every word they hear (echolalia), or to practice peculiar " impulsive " 
movements (tearing everything to bits, etc.). We see no reason to regard such 
conditions as a special disease under the name of " maladie des tics." We have 
repeatedly observed such conditions (especially in children) which were undoubt- 
edly to be regarded as hysteria, and which could rapidly be made to- disappear by 
appropriate psychical treatment. The severer forms of these conditions of course 
belong to the pronounced hysterical psychoses. 

General Course of the Disease. — Our description of the symptomatology of 
hysteria has been confined to the most important and frequent phenomena; and 
yet even this meager outline shows what an infinite variety of shapes the disease 
assumes. 1. In one class of cases there are no severe symptoms whatever. The 
patient merely displays the general mental condition characteristic of hysteria : 
she is easily excited, prone to make much of her ills, has all sorts of symptoms, 
such as pain, cephalic symptoms, palpitation, dyspepsia, and dyspnoea, and these 
are aggravated by mental excitement, while at other times they may so nearly 
vanish that the patient does not appear to be ill. 2. A second class of cases has 
more severe disturbance, coming on after some unfavorable psychical or other 
influence (vide supra). The patient may have displayed a general hysterical 
tendency previously, or may have seemed perfectly well. Here we may observe 
all the symptoms above enumerated and described. There may be paralysis, 
spasm, contracture, anaesthesia, or paresthesia. The individual symptoms may 
persist obstinately for weeks and months; but again they may vanish suddenly 
or give place to other disturbances. Psychical influences are unmistakably 
potent, not merely in the incipient stage but also in the further course of the 
disease. Any aggravation of the symptoms is often referable to emotional ex- 
citement. This is particularly true of the hysterical convulsions. In other 
cases, of course, the hysterical attacks come on apparently quite spontaneously, 
just like epileptic states. 3. The third class comprises the most severe forms of 
hysteria, with those nervous disturbances briefly outlined above. They are as 
complicated as they are puzzling, and form manifold combinations with all the 
other hysterical phenomena, including anaesthesia, contracture, and paralysis. 

The entire duration of the disease varies greatly. The true root of all evil is 
the abnormal excitability of the nervous system, which always remains in un- 
stable equilibrium; and often it is not possible to cure this. If not, the trouble 
lasts almost indefinitely. ISTew manifestations of the disease succeed to periods of 
apparently perfect health. Usually the symptoms do not abate till quite late in 
life. There are, however, many instances of complete and permanent relief. 
This favorable termination is more especially to be hoped for where the patient 
comes into suitable and appropriate conditions of life, having some regular occu- 
pation which is not exposed to all sorts of unfavorable psychical influences. Many 
cases of hysterical disturbance, in previously healthy children or young adults, and 
due to some distinct cause, terminate comparatively soon, and never recur. It is 
never possible, however, to be sure that there will be no relapse, inasmuch as a single 
appearance of hysteria shows unmistakably that the nervous system is abnormally 
vulnerable to external impressions and the mental emotions excited by them. 

Diagnosis. — An experienced physician is seldom greatly puzzled by hysterical 
affections. Although the disease may at first simulate some grave organic disor- 



1188 DISEASES OF THE NERVOUS SYSTEM 

der, a careful physical examination and continued observation will almost invaria- 
bly disclose the true character of the case. In the first place, there are 
never any such symptoms as would absolutely prove the existence of some organic 
lesion. Eor example, we never find marked atrophy or loss of electrical reaction 
in connection with hysterical paralysis. We should also regard the whole psychi- 
cal behavior of the patient, the influence exerted upon her by emotional disturb- 
ances, the disappearance of the symptoms when the attention is diverted, and the 
aetiology of the illness — for instance, the development of the symptoms after some 
mental excitement or emotion. The discovery of specific hysterical symptoms, 
the so-called hysterical stigmata, sensory anaesthesia, hysterogenous zones, etc., 
are especially important. Many symptoms of hysteria, especially hysterical aba- 
sia, hysterical aphonia, hysterical hyperaesthesiae, certain forms of spasm, hemi- 
anaesthesia, etc., are in themselves so characteristic that from them alone a correct 
diagnosis can usually be made at the first glance. The very circumstance that 
hysterical affections do not keep to the laws of nervous anatomy and nervous phys- 
iology, and that they often can not be brought into harmony with them, is of im- 
portance in their recognition ; but, on the other hand, we must earnestly warn the 
physician against making the diagnosis of " hysteria " too readily. Pronounced 
hysterical symptoms are of course only rarely mistaken by an experienced physi- 
cian, but very often all sorts of symptoms may be due to concealed affections, which 
can not be positively determined (certain cases of gastric ulcer, gall-stones, renal 
calculi, beginning cerebral diseases [especially multiple sclerosis. — K.], arterio- 
sclerosis, etc.), and these symptoms may falsely be regarded as "hysterical," es- 
pecially when we are actually dealing with nervous patients. Repeated careful 
objective examination and observation is therefore imperatively necessary. In 
doubtful cases the diagnosis can sometimes be rendered certain only by the result 
of treatment. In doubtful cases, however, the physician should not proceed too 
roughly or too rapidly, since he may only too easily cause harm. 

Since an investigation of hysterical and epileptic attacks is of especial impor- 
tance, we will give here a synopsis of the most important distinguishing features. 

Epileptic Convulsions Hysterical Convulsions 

1. Sudden fall to the ground ; often con- 1. Slow sinking to the ground ; no exter- 
sequent external injuries. nal injuries. 

2. Sudden pallor of the face. Often marked 2. No striking pallor of the face. No 
cyanosis later. marked cyanosis. 

3. Pupils dilated ; do not react. 3. Pupils react. 

4. Convulsions according to the nature of 4. Convulsions consist of extensive move- 
cortical epilepsy in the form of convulsive ments, striking out with the arras or legs, 
twitching. Tongue often bitten. twisting of the body, etc. Respiratory spasms. 

No biting of the tongue. 

5. Often one initial cry, then total loss of 5. Hysterical disturbances of conscious- 
consciousness, ness, but no complete loss of consciousness ; 

spasmodic and continuous cries, laughter, 
weeping, etc. Talking during the attack, 
emotional disturbances, delirium, etc. 

6. Convulsions rarely last longer than a 6. Attack may last from half an hour to 
few minutes, followed by deep sleep. an hour or more. Patient often wakes sud- 
denly. 

7. Suggestive and hypnotic procedures, 7. The attacks may easily be excited arti- 
and also external irritation during the attack, ficially at any time by hypnotic or other sug- 
without any influence. gestive procedures, or they may be inhibited 

in like manner (pressure on definite parts of 
the body or the like). During the attack the 
convulsions may be influenced or even wholly 
suppressed by sprinkling with water, a cold 
douche, etc. 

8. Other hysterical symptoms are absent. 8. Other hysterical symptoms may co-exist 

and often remain after the attack (hysterical 
hemianaesthesia, paralysis, contractures, etc.). 



HYSTEEIA 



1189 



Treatment. — What has been said about the aetiology of hysteria at once sug- 
gests a possible method of prophylaxis. A watchful eye will often detect, even in 
childhood, the signs of abnormal nervous excitability, and in such, a case the 
parent will make it his duty to impose a suitable physical and mental regimen, 
that graver disturbances may be averted. 

If hysteria be already developed, the first and most important treatment is 
mental. There could be no greater mistake than to deride the patient or treat 
her as a malingerer; for hysteria 
is a disease, and its symptoms are 
just as independent of any con- 
scious volition on the part of the 
patient as those of any other dis- 
ease. It is, however, also abso- 
lutely essential to carry out the 
moral training, which the physi- 
cian must institute with all the 
proper strictness and energy, be- 
cause in this way alone can any 
good be accomplished. Therefore 
an absolutely positive diagnosis is 
the first essential in the success- 
ful treatment of hysteria. If the 
physician is in doubt as to the 
nature of the trouble (vide 
supra), he can not proceed with 
necessary inflexible consistency, 
and the therapeutic results are 
seldom satisfactory; but if the 
diagnosis is assured, then there is 
no need of making the slightest 
concession to the patient. Some- 
times this most important indica- 
tion can be fulfilled only after the 
patient has been withdrawn from 
the over-anxious and over-assidu- 
ous parents or relatives, and like 
unfavorable influences. In such 
cases, treatment in some institu- 
tion will often be vastly better 
than the best care at home; and 
our own experience leads us to 
recommend most urgently that 
the eventful necessity of removal 
to an asylum should be constantly 
borne in mind with regard to ag- 
gravated cases. Often the mere 
dread of removal to such a place 
has a favorable mental influence. 




Fig. 184, 



-Hysterical abasia. Exercise in walking. 
(Erlangen Medical Clinique.) 



Proper moral treatment achieves comparatively the best results where there is 
hysterical paralysis. When we are once certain that the paralysis is due to 
hysteria, the patient must be instructed how to regain by practice the lost power 
of the will over the paralyzed muscles. If the paralysis affect the lower extremi- 
ties, as it usually does, the patient must be set on her feet, regardless of all her 
opposition and complaints, and kindly but most firmly required to try to walk. 



1190 



DISEASES OF THE NERVOUS SYSTEM 



Of course, at first she must be well supported (see Eig. 184). This exercise must 
be methodically gone through with several times a day. Gradually the patient's 
gait becomes more and more secure. She regains confidence in her own ability, 
and, having once begun to improve, usually makes rapid progress toward complete 
recovery. Every experienced physician can recall numerous instances where hys- 
terical paralysis which had lasted weeks and months was cured in a few days by 
this mode of treatment. Faradization of the muscles, cold sponging, with fric- 
tion and bathing, are excellent adjuvants ; and the disagreeable element in these 
procedures of itself stimulates the patient to make every possible exertion to re- 
gain the use of her limbs. 

When there is hysterical paralysis of the vocal cords, a similar training (ener- 
getic efforts to make the vocal cords tense and to produce a loud tone) will be 
found both practicable and efficient. Electricity is also of great value. It may 
be applied externally or within the larynx. Often the patient, terrified by the 
sudden pain it causes, recovers her voice at once. The same holds true of all 
hysterical disturbances of speech and of hysterical dumbness or mutism. 

The treatment of hysterical contractures consists, first, of an effort to relax 
the contracture by massage and energetic passive motion. Earadism will be 
found of assistance here also. In order to remove the contracture permanently, 
the patient must be induced to exercise the muscles regularly by making voluntary 
movements. We sometimes have the greatest difficulty in getting the patient to 
make the first attempt to move. In such cases we can attain our end only by great 
patience and perseverance and by the suggestive aid of all sorts of manipula- 
tions (galvanism through the head, etc.). 

The treatment of hysterical spasmodic conditions often causes greater difficul- 
ties. The main thing is to bring the patient to control herself at the beginning 
of the attack, either by an energetic appeal, by diverting the attention, etc. In 
many cases a sharp sensory irritation, douching with cold water, or a bath with 
cold affusions, acts to restore the energy of the patient's will and the control 
over the muscles, and thus to check the spasms. The dread of the repetition of 
the bath does its part in restraining the patients from giving themselves up unre- 
sistingly to a repetition of the attack. The electric current (strong faradism dur- 
ing the attack) may also act favorably in the same way. The action of such 
measures, however, often gradually weakens, the patients become accustomed to 
the cold baths, and they remain without effect. 

The milder varieties of hysterical convulsion, such as hysterical hiccough or 
cough, are often controlled by a stern reproof. It is precisely in these cases that 
the moral effect of transfer to some institution frequently causes the abrupt disap- 
pearance of symptoms which have lasted for months. All the forms of hysterical 
spasm occurring in children especially are easily removed by proper treatment 
(especially isolation from the family!). The severe hysterical attacks, on the 
other hand, are often, of course, peculiarly obstinate, and they may resist for 
months, and even years, the most intelligent treatment. In all hysterical spasms 
limited to certain muscles methodical gymnastic exercises are often attended by 
the best results. We inhibit the abnormal motor innervations, and direct the 
will into other well-regulated paths: regular respiratory exercises in respira- 
tory spasms, gymnastic exercises with the arms for twitching of the arms, etc. 

Hysterical anaesthesia is best treated with the faradic wire-brush. The vigor- 
ous irritation restores the anaesthetic parts to the domain of consciousness. It 
should be said, however, that these cases may prove obstinate or relapse. 

The most difficult of all hysterical cases to treat are those where the symptoms 
are not strongly pronounced, but where there is a general hysterical condition, ex- 
pressing itself in a multitude of nervous derangements, such as palpitation, dys- 
pepsia, and general debility, or in purely subjective symptoms, or in emotional 



HYSTEKIA 



1191 



tendencies. Such patients are often advanced in years, so that little is to be hoped 
for from moral training; and their circumstances may be unfavorable without 
our being able to remedy the situation. Even here, however, the physician may 
greatly benefit the patient by means of psychical influences, if he once gains her 
complete confidence. We should also consider all such remedies as invigorate the 
nervous system; electricity should be given, either in the form of general faradi- 
sation, the faradic brush applied to the back and shoulders, or the galvanic cur- 
rent applied to the spinal column and the sympathetic nerve ; and of still greater 
importance is a methodical cold-water treatment, either by sponging, bathing, 
or douches. Such patients are often vastly improved by sea-bathing in summer, 
or by going to the mountains. 

The numerous internal remedies for hysteria are also of more use in these 
g'eneral conditions than where there are marked nervous disturbances in special 
parts of the body. In the latter, internal remedies do good only indirectly and in 
a psychical fashion by so-called suggestion, especially if the patient has great 
confidence in the virtues of the medicine or in the physician who prescribes it. 
This is the explanation of the frequent cases of rapid recovery after taking 
homoeopathic and " electro-homoeopathic " remedies, and those still more marvel- 
ous cures effected by means of holy water and relics. 

Among the " anti-hysterical " agents contained in our medical thesaurus, asa- 
f cetida, valerian, and castoreum are the most famous ; but probably few would at 
the present day claim that they possess any specific virtues. Perhaps the prepara- 
tions of valerian are the most useful where there is hysterical excitement, as 
evinced by convulsions or palpitation. Bromide of potassium, arsenic, and other 
medicines which ordinarily exert a favorable influence upon the nerves, seldom 
accomplish any permanent good in hysteria, although often prescribed. We must 
utter an urgent warning against narcotics, especially morphine, since they do little 
good and there is great danger of developing the morphine habit in such patients. 

If hysteria be complicated by some actual organic disease, the latter, of course, 
demands special treatment. Great benefit is hoped for by many from the cure of 
any uterine complaint which may be present. Cases are actually known where 
grave hysterical disturbance has vanished upon dilatation of a constricted cervical 
canal or rectification of a displacement; but there are numerous other instances 
on record where gynaecological treatment has proved entirely unavailing. There 
is hardly a doubt that, in the successful cases, the main benefit was due to the 
mental influence of the treatment. In general we would utter an urgent warning 
against needless gynaecological examinations and treatment in hysterical subjects. 
The patient's condition is often merely made worse by such procedures. 

In general, we may certainly maintain that all methods of treatment of hys- 
teria are efficient only when associated with the necessary psychical factor ; that 
is, the patient's belief in the efficacy of the remedy, or, as we are accustomed to 
say at present, with suggestion. Hence any prescription, no matter how sense- 
less it seems, may have the greatest effect as soon as the patient " believes in it " 
— that is, as soon as the psychical action of this belief is manifest. Hence it 
follows that in hysteria, as a rule, treatment either produces rapidly a brilliant 
success or it has no effect at all. 

We must here mention two methods of treatment which have lately been much 
discussed — metallotherapy and treatment by hypnosis. 

In regard to metallotherapy a French physician, named Burq, discovered years 
ago that by laying plates of metal upon a cutaneous surface affected by hysterical 
anaesthesia a remarkable result is sometimes produced. Almost at once sensation 
is restored to the immediate region, and often to a much larger area. Most of 
the cases have been those of hysterical hemianaesthesia. It is not every kind of 
metal which will prove effective, nor will the same kind affect all patients. It is 



1192 



DISEASES OE THE NERVOUS SYSTEM 



said that iron is most frequently efficient ; but sometimes copper, zinc, or gold is 
required. The process of determining the metal essential to each individual case 
Burq called " metalloscopy " ; and he stated that this metal would also have the 
same effect if given internally! In 1876 a committee appointed by the Paris 
Societe de Biologie tested these statements, at least with regard to the external 
application of metals — the idea of their internal administration having been 
pretty much abandoned — and confirmed them. Charcot also discovered many 
remarkable facts of a similar nature, which likewise soon received universal sub- 
stantiation. The most remarkable of these, phenomena is known as transfer. 
The return of sensation to the anaesthetic area, as a result of applying a metal 
plate, is accompanied by a simultaneous development of anaesthesia upon the 
opposite, previously normal side, in an exactly corresponding place. Sometimes 
sensation oscillates from one side to the other and back again, so that now one 
half of the body and now the other is alternately sensitive or anaesthetic. If the 
metal be placed at the start upon the normal skin, that part becomes anaesthetic, 
while the corresponding part upon the opposite side of the body regains its former 
normal condition. 

It has also been discovered that other hysterical symptoms exhibit analogous 
phenomena. Transfer can sometimes be observed in hysterical amblyopia, achro- 
matopsia, deafness, loss of smell and taste, contractures, and paralysis. Such 
transfers may be induced by various means other than metal plates. These are 
classed as aesthesiogenous remedies, and include large magnets, feeble galvanic 
currents, and static electricity. Vibrating tuning forks and sinapisms have also 
produced similar results. Hence it seems to us to be an indubitable conclusion 
that the whole group of symptoms just described has no peculiar position. 
These symptoms are simply the results of suggestion, produced in this case again 
by ideas. The similarity of the test as performed by the physician produces the 
similarity of the symptoms that ensue. 

Of late the treatment of hysteria by hypnosis has acquired a far greater prac- 
tical significance than metallotherapy ; it is a mode of treatment which has been 
employed most extensively by the " school of ISTancy " (Bernheim) and its ad- 
herents. If, during hypnosis, morbid states can be produced by suggestion, it 
naturally follows that morbid states can also be cured by suggestion. If by many 
well-known successes the hypnotizing physician has at the outset acquired the 
patient's confidence, as relics win the confidence of believers, the most beautiful 
results can of course be attained by hypnosis. There is no special peculiar princi- 
ple in the hypnotic treatment. Any other efficient mode of treating hysteria 
rests on the same conditions and presumptions. Hypnosis has only the one great 
consequence, that it is artificially produced as a severe abnormal mental state in 
a patient who previously had not spontaneously fallen into this state. In that 
lies the sequel, which of course need not always be permanent, but which often 
enough has been most severe: the attempt to hypnotize a patient who is sufferings 
from a slight hysterical affection has not infrequently been followed by the onset 
of a severe hysterical attack. The mischance will seldom happen to the physi- 
cians and magnetizers who practice hypnotism as a specialty, because their 
psychical influence on their patients is usually greater from the outset; but we 
should consider it a misfortune if hypnosis should come into too general use. 
That in this way apparently the most wonderful cures can often be obtained, is 
perfectly well established and not at all surprising ; but the same cures can also 
be obtained in other ways, without running the risk of producing first that of 
which you would cure your patient, for to hypnotize means to make temporarily 
hysterical (see page 1185). Furthermore, it is not hard to prophesy that, as the 
knowledge of the peculiar nature of hypnosis becomes general, it will lose its halo 
with the patient, and with that it will lose its healing power. 



NEUKASTHENIA 



1193 



CHAPTEE X 

NEURASTHENIA 

{Nervous Debility. Nervousness) 

Concept of the Disease and ^Etiology.— The name of neurasthenia is given 
to a nervous symptom-complex which comes on in a great variety of ways. Its 
cause is not to be looked for in an organic disease but in a merely functional dis- 
turbance of the nervous substance. The nature of this functional disturbance is 
ordinarily characterized by the two symptoms of " abnormal irritability " and " ab- 
normal exhaustibility " ; but the phenomena of neurasthenia and its allied morbid 
states are by no means wholly exhausted by the combined concept of " irritable 
weakness." We may also add that the entire nervous system does not by any 
means take part in this abnormal functioning. On the contrary, the more care- 
fully we study and analyze the symptoms of neurasthenia, the conviction is forced 
upon us here, just as in hysteria, that in neurasthenia we have to do essentially 
only with an abnormal mental condition of the sick person, and that the countless 
physical complaints and symptoms of the neurasthenic are ultimately to be re- 
ferred in the main to a disturbed ideational life. 

Nervousness and neurasthenia are brief practical terms applied to certain 
forms of an abnormal mental constitution. In by far the greatest number of all 
cases this abnormal mental constitution, or at least its basis, is congenital. Neu- 
rasthenia of course does not always show itself in childhood, although it does often 
enough. It does not always develop to the same degree, varying according to the 
action which various external influences exert in making it more or less promi- 
nent. We can only rarely, however, wholly dispense with the ultimate assumption 
of a definite congenital " nervous " predisposition. Of course we must admit that 
neurasthenic conditions of exhaustion and irritation may also occur under the 
influence of persistent mental over-exertion or persistent and severe mental 
irritation in persons who were previously " perfectly well " ; but in general we 
are usually inclined to attribute to these factors just mentioned merely the 
role of exciting causes; for every nervous system does not succumb to the same 
burden; one endures it without permanent harm, while another breaks down 
under it. 

The congenital factor in the onset of neurasthenia is shown especially by a 
careful regard of hereditary conditions. Nervousness, neurasthenia, hysteria, 
degenerative insanity — these are closely associated morbid conditions, at the basis 
of which lies the inherited abnormal mental constitution, and these conditions 
are, therefore, unfortunately linked together in many families. Where the laity, 
from a natural dread of the worst forms, are disposed to believe in a funda- 
mental distinction, the medical eye sees only quantitative differences in a long 
series of psychical conditions, which, without definite boundaries, join the nor- 
mal psychical life on the one side and on the other pass into pronounced in- 
sanity. 

It is our task here to describe merely the mild neurasthenic states, which far 
exceed in frequency all other nervous diseases. If it has been imagined that 
neurasthenia is a modern disease, this idea is incorrect. It is as old as our definite 
knowledge of the diseases of mankind, and if the increasing frequency of neu- 
rasthenia is often ascribed to the restless haste, the unrest and the excitement 
of " modern " life, a glance at the history of past centuries with their horrors and 
their disorders of war will render such a hypothesis extremely doubtful. The 
name " neurasthenia " is the only thing that is new or modern. This, and the 
better insight into the nature of the disease, we owe to the American neurologist 



1194 



DISEASES OF THE NEKVOUS SYSTEM 



Beard (1880).* It is also true that all the exciting causes above mentioned are 
still active in their full force to-day, and that it can not therefore amaze us if we 
observe neurasthenia with especial frequency in business men, whose bold specu- 
lations are attended by the excitements of hope and fear; in politicians, whose 
minds are constantly stirred by the eager strife of parties ; or in those artists and 
scholars whose never quiet ambition forces them into restless competition. 
Neurasthenia develops often enough, however, in persons disposed to it from 
the first through a congenital defect, without any special exciting cause. We 
can readily understand that a disease, which plays its part chiefly in the idea- 
tional life of those affected by it, should be materially influenced by the degree 
of education of its victims ; that is, by the richness and activity of their ideational 
life ; but it is incorrect to call neurasthenia a disease chiefly of the " educated " 
or of the " higher classes." Neurasthenic conditions occur very frequently in the 
uneducated and in the lower classes, although they may manifest themselves in a 
somewhat different fashion. 

The Symptoms of Neurasthenia. 1. The Mental Symptoms —One of the 
most important changes in the ideational life of the neurasthenic is the frequent 
and ready appearance of ideas of an anxious character. So far as these ideas 
refer to the patient's own corporeity, they have been called from old times hypo- 
chondriacal. Sometimes they seem to arise of themselves, at other times they 
are produced by readily recognized causes (reading of histories of patients or of 
medical works, cases of sickness and death in the neighborhood, etc.). These 
ideas may constantly arise into consciousness often in quite a fixed and definite 
form, and then dominate more or less all the rest of the ideational life. A large 
number of neurasthenics are dominated by the thought that they are threatened 
or already attacked by a serious organic disease. One constantly fears an im- 
pending attack of apoplexy, another heart disease, a third beginning consumption, 
a fourth believes he has noticed positive signs of disease of the spinal cord, cancer 
of the stomach, etc. The anxious ideas, however, may also take other forms ; they 
sometimes refer to the patient's nearest relatives rather than to himself. Women 
are sometimes tormented by the constant dread that their husbands or children 
may fall sick. The ideas may also relate to external processes, with which the 
anxious ideas are easily and incessantly associated. The so-called agoraphobia 
(anxious ideas on entering a large open space), the dread of a crowd, of a railway 
journey, of society, the fear of sitting under the chandelier in a theatre, the fear 
of fire, and many other symptoms of a similar character, are often observed in 
neurasthenics. 

Not infrequently such ideas of an anxious nature come on suddenly with es- 
pecial severity and lead to actual attacks of anxious distress with pronounced 
physical symptoms as a consequence. Such attacks may come on at night during 
sleep, drive the patient from his bed, and put him into a state of the greatest 
unrest and excitement. 

We can readily understand that the ease with which these ideas of an anxious 
nature arise may keep the patient to some degree in a state of constant irritation. 
Hence such patients often complain : " I am always so restless — every trifle vexes 
me — everything, no matter how small, irritates me." Only when their thoughts 
are taken up by something else do they become quiet and behave in a way that 
seems perfectly normal. 

These anxious ideas are by far the most frequent, but they are not the only 
form of morbid ideas which are observed in neurasthenia. In so far as such ideas 
constantly arise in consciousness independently of external events and constantly 



* [The disease had previously (1867) been described under the same name by Van Deusen, of 
Michigan, and the name itself is found in the first edition of Dunglison's Dictionary in 1833. — K.] 



NEURASTHENIA 



1195 



take possession of the patient, so to speak, we give them the general and fit name 
of imperative ideas. The following are some of the especially frequent 
forms of imperative ideas : . Many patients are distressed by the constant recur- 
rence of wholly superfluous questions : Why is this so, why is it not so ? What 
would happen if this or that should ensue? etc. (Grubelsucht, metaphysical or 
reasoning insanity, folie raisonnante). Other patients distress themselves with 
constant doubts, with the constant feeling of uncertainty whether this or that 
has been done correctly, whether they have not written something wrong, have not 
forgotten something, etc. (insanity of doubt). [Other patients are impelled to 
repeat certain words, or to perform acts a certain number of times. — K.] These 
and other imperative ideas, which occur in a pronounced fashion only in the 
severe forms of neurasthenia, form the transition to the special forms of neuras- 
thenic insanity. 

Although the morbid ideational life in most cases gives the mental constitu- 
tion of the neurasthenic the characteristics of excitement and restlessness, there 
may be also a pronounced inhibition of the rest of the ideational life and conse- 
quently a depressed, melancholy disposition. The mental dispositions may some- 
times vary in different forms. If there is in general an increased liveliness of the 
ideational life, the frequent and rapid transition from being " exalted to the 
clouds " to being " worried to death " may be especially striking. 

The worst result of the disturbed ideational life, however, is the disturbance 
and inhibition of all other trains of ideas by the constant intrusion of the morbid 
ideas into consciousness. This is the chief reason why the neurasthenic is so 
often incapable of any persistent, methodical mental work, or at least why he 
can perform it only with the greatest effort. Sensations of bodily weakness 
(vide infra) are often added to the feeling of mental fatigue, among them being 
the inability to read or write continuously, sometimes associated with unpleasant 
subjective sensations of weakness or pressure in the eyes (" nervous asthenopia ")• 
Of course in these disturbances of the power of mental work we must always make 
a sharp distinction between a congenital, primary, functional weakness and an 
impediment to mental work due merely to secondary causes. 

[The special morbid fears like agoraphobia and the questionings and doubts 
are rarely met with in neurasthenia, and are usually indicative of a pronounced 
neuropathic taint of a degenerative type. They may exist without neurasthenia. 
Anxiety, mental depression, and a tendency to worry are much commoner and are 
of less serious import. AEany neurasthenics, however, show hardly a trace of 
these mental disturbances, beyond a normal depression over their inability to per- 
form the ordinary duties of life or their failure to regain their health. Their 
chief symptoms consist of inability to make any long-continued physical or 
mental effort and of physical weakness. As a result of over-exertion various 
physical symptoms — headache, insomnia, backache, anorexia, indigestion, etc. — 
ensue, without any marked mental symptoms. Neurasthenia seems, therefore, to 
be rather a condition of pathological fatigue, upon which the various mental 
symptoms above described may develop secondarily. — K.] 

2. The Physical Symptoms. — Although the mental symptoms of neurasthenia 
are recognized only by the experienced physician as the special center of the dis- 
ease, the neurasthenic himself, as a rule, claims to suffer from countless subjec- 
tive symptoms, which may occur in almost every organ. By far the largest part 
of all these countless subjective sensations are in our opinion merely the result 
of the primary disturbance of the ideational life. We admit merely to the second 
place the possibility that there are independent functional nervous disturbances 
in other parts as well as the mental anomaly, and that these may lead to special 
bodily symptoms ; but it is evident that most of these subjective symptoms have a 
psychogenic origin, since they almost always conform absolutely to the character 



1196 DISEASES OE THE NEEVOUS SYSTEM 



of the existing hypochondriacal ideas, and since they disappear entirely as soon 
as we succeed in driving these ideas out of consciousness. 

In order to review the commonest neurasthenic symptoms we may very well 
classify them according to the organs to which the patient's fears generally refer 
them. The idea of a dreaded organic disease actually provokes the corresponding 
subjective sensations. Thus the " imaginary " diseases develop. If the patient's 
thoughts are occupied chiefly with the dreaded advent of a spinal disease, many 
symptoms apparently spinal ensue, especially pain in the back and unpleasant 
sensations along the spine, pain and paresthesia in the legs, etc. The more the 
patient knows about actual diseases by experience or reading, the more manifold 
become his symptoms. Neurasthenic physicians are therefore the worst pa- 
tients. — As we speak of a " spinal neurasthenia," so we can also speak of a 
" cardiac neurasthenia," a " gastric neurasthenia," etc. The cardiac neuras- 
thenics, who live in constant anxiety about heart disease and its consequences, 
complain of palpitation, pressure, pain and " fluttering " in the cardiac region, 
vertigo, and distress for breath. Patients with gastric neurasthenia (" nervous 
dyspepsia," q. v.) have a feeling of pain and pressure in the stomach after taking 
any food, and therefore are afraid to eat anything that is at all indigestible, suffer 
from unconscious voluntary eructations, etc. 

The long series of physical neurasthenic symptoms is by no means exhausted, 
however, with such subjective symptoms provoked by definite anxious ideas (or 
by "auto-suggestion," as the modern technical term is). In almost all cases a 
large number of physical symptoms are apparent, which we regard as the necessary 
(that is, the physiological) result of the general mental irritation. As in every 
healthy man every great psychical excitement is followed by a number of physical 
symptoms, it is plain that the abnormal state of excitement of the neurasthenic, 
coming on without sufficient external cause, may often have somatic results even 
in increased degree. Among these we may reckon first a large number of so- 
called " cerebral symptoms," such as headache, vertigo, and pressure and disturb- 
ance in the head, to which may of course be added many cerebral symptoms due to 
auto-suggestion. Among these belongs also the neurasthenic insomnia, one of 
the commonest and most important symptoms and a direct result of the mental 
irritation itself. In many cases the insomnia forms the center of the neuras- 
thenic symptom-complex. We may then say that the fear of insomnia is the chief 
reason for the actual insomnia. Many vaso-motor symptoms are also a direct 
result of the general psychical irritation — palpitation, a rapid pulse, redness or 
pallor of the face and hands, increased sweating or persistent coldness of the 
hands and feet, etc. We may also add tremor and the not infrequent increase 
of the tendon reflexes. Finally, the loss of appetite which many patients show, 
the habitual constipation, and in other cases the tendency to diarrhoea, are cer- 
tainly often most closely related to the psychical processes. 

The liveliness of the motor innervations also depends in the main upon the 
general psychical state. While many neurasthenics, impelled by constant rest- 
lessness, exhaust themselves in long and useless walks, there is in others a great 
physical weakness, which is due to inadequate cerebral volitional innervation of 
the muscles, so far as it is not dependent upon actual functional abnormality or 
impaired general nutrition. Such patients are soon tired on walking, they can 
not work persistently, they sometimes feel so weak that they will scarcely leave 
their rooms, and they spend most of their time in lying on the bed or the sofa. 

It is hard to decide whether neurasthenia exerts a direct influence upon the 
general bodily nutrition. We find neurasthenia in both full-blooded, corpulent 
persons and those who are frail and anaemic. Neurasthenia, however, very often 
exerts an indirect influence upon the patient's nutrition, since loss of appetite 
or fear of taking food gradually results in marked emaciation. We may mention 



NEURASTHENIA 



1197 



that large amounts of phosphates are often found in the urine, the reason for 
which is still uncertain. [In most cases of neurasthenia there is defective 
metabolism. The urine is scanty, the uric acid is increased relatively to the urea, 
and in sexual neurasthenia there may be an excess of indican. Many neuras- 
thenics, however, drink very little water. — K.] 

We must also devote a few words to a form of neurasthenia which is of great 
practical importance — sexual neurasthenia. It usually develops in persons who 
have practiced masturbation in their youth, and, by reading or their own reflec- 
tion, have fallen into the most exaggerated anxiety as to the supposed evil conse- 
quences of this vice. Such pitiable patients usually fear that they are affected 
past help with some disease of the brain or spinal cord, and suffer accord- 
ingly from a host of corresponding subjective symptoms; but the very common 
" psychical impotence " is still more significant. This is a sexual impotence which 
is the result of anxious ideas which disturb the sexual act and make it impossible. 
Other sexual disturbances are usually added to these, which are at least in part 
a direct result of the physiological hyperexcitation which has occurred in youth 
(frequent pollutions, urethrorrhcea, etc.). In sexual neurasthenia, therefore, the 
whole host of general neurasthenic symptoms above described are naturally 
grouped about this nucleus. 

As has been indicated above, we are not justified in regarding all the physical 
symptoms occurring in neurasthenia as secondary psychogenic symptoms. Since 
neurasthenia is due to a general constitutional abnormal disposition of the 
nervous system, it is not strange if functional disturbances in other parts of the 
nervous system should occur along with the abnormal symptoms in the patient's 
ideational life. Thus neurasthenia may be associated with true neuralgia, or 
with migraine or other forms of headache. It is therefore an important and often 
a difficult task for the physician to analyze the whole aspect of the disease in the 
individual case, to recognize the purely psychogenous symptoms as such, and to 
separate from them any co-existing physical nervous symptoms. This distinction 
is of great importance, especially in regard to the treatment to be advised. [It 
may also be important to determine how far the neurasthenic condition may be 
the result of some pre-existing physical condition, which, by the attendant suffer- 
ing, as of habitual headache, may have led to the general nervous exhaus- 
tion— K] 

General Course and Prognosis of Neurasthenia. — The course of neurasthenia 
is governed in the main by the degree of general nervous predisposition that 
exists and the severity of the unfavorable influences that act upon the patient 
from without. If we are dealing with a patient who was previously in normal 
mental health and in whom a neurasthenic state of irritation or exhaustion has 
come on merely as an effect of unusual mental excitement or effort, such conditions 
of " acute neurasthenia " may wholly or mainly disappear under proper treatment 
and the removal of the injurious external influences. The condition is different 
in cases where the neurasthenic tendency has appeared quite early in the patient's 
whole mental nature. Here also we may often notice, of course, great variations 
in the prominence of the morbid symptoms; but an actual recovery is scarcely 
possible, since it would be equivalent to a complete change in the whole mental 
individuality; but in later life there may sometimes occur, even in such cases, a 
striking retrogression in the morbid symptoms. In the milder cases there is 
little outward evidence of derangement; the patient endeavors to hide his 
troubles, as his indefinite symptoms seldom gain much sympathy, and are appar- 
ently contradicted by his well-nourished and healthy appearance. In the severe 
cases, however, the patient's vigor is so much impaired that the disease acquires 
a grave aspect even for others than the patient, and fills them, as well as him, 
with infinite anxiety. The disease is never actually dangerous, and its exist- 



1198 



DISEASES OF THE NERVOUS SYSTEM 



ence only exceptionally prepares the way for more severe secondary nervous dis- 
ease. Thus it happens that many neurasthenics, especially when external con- 
ditions are favorable, lead a comparatively endurable life and work hard and 
profitably in their calling. 

Diagnosis. — Neurasthenia can usually be detected without difficulty, but tlw 
establishment of the diagnosis requires the exclusion of organic lesions of the 
nervous system. Every case, therefore, must be submitted to a thorough and 
careful examination. Grave cerebral diseases, such as incipient tumors or gen- 
eral paralysis, have been repeatedly mistaken for neurasthenia. One important 
point in diagnosis is always the aetiology, including both the outward circum- 
stances and the presence or absence of a constitutional predisposition to nervous 
diseases. 

We can not draw an absolutely sharp boundary, naturally, between neuras- 
thenia, nervousness, and hysteria. In all these three conditions we are dealing, 
as has been said, with an abnormal nervous constitution, which is congenital or 
which has at least developed from outward circumstances on the basis of a con- 
genital predisposition. This constitution is manifest in the first place in the 
purely psychical domain, and, in the second, in the relations between the mental 
and the corporeal life. If the abnormal state shows itself merely in slight mentnl 
irritability, sensitiveness with a tendency to anxious ideas and unfounded fears, 
and thus to the development of all sorts of subjective abnormal sensations re- 
ferred, however, to the corporeity, we call it nervousness. If there is also asso- 
ciated a marked weakening of the capacity for mental effort and, in consequence 
of the defective or much inhibited mental energy, for physical effort as well — 
symptoms which, as a rule, are associated with increased anxiety and with con- 
sequent subjective sensations — we have pronounced neurasthenia. If, however 
the relation between the mental processes and the corporeity has become so vac- 
illating that there is a complete loosening of these relations (paralysis, anaes- 
thesia), or that wholly abnormal states of mental irritation (spasms, attacks) have 
developed in consequence of the loss of all healthy mental inhibition, we have 
before us pronounced hysteria. The basis of all these three states is — figuratively 
expressed — the lack of all determined order and fixity in the course of all those 
processes which we include under the name of psychical processes in the broadest 
sense of the word. 

Treatment. — As in hysteria, so also in neurasthenia, psychical or moral treat- 
ment is of prime importance ; but here it must be a different kind from that neces- 
sary in hysterical cases. The neurasthenic requires sympathy. As soon as we 
recognize by means of a careful inquiry the hypochondriacal anxiety which is 
usually present, this is to be removed, as far as possible, by soothing persuasion on 
the basis of the thorough physical examination which has been made. The neuras- 
thenic must be frequently examined and constantly encouraged and soothed. 
Herein, especially, is shown the physician's skill and personal influence. Every 
examination, which ends with the physician's assurance that he has found nothing 
to give occasion for any serious anxiety, has an extremely soothing and beneficial 
effect upon the patient. In so far as hypochondriasis is a prominent symptom, 
this moral influence may alone restore the patient to health. We should also pay 
attention to the patient's mental life otherwise. If the patient has been exposed 
to great strain and much excitement, we should of course procure a change. In 
such cases as these we prescribe mental rest, recreation, and abstention from work 
or any strenuous activity. Nothing, however, would be more improper than to try 
to make this prescription universal. On the contrary, it is absolutely necessary 
to prescribe resumption of regular and methodical work and occupation for many 
patients who, as a result of their mental disposition, do nothing but give way to 
their hypochondriacal broodings the whole day long. In this way alone can the 



NEURASTHENIA 



1199 



thoughts of such patients be diverted, and the patients themselves be gradually 
brought back to take pleasure in their life and occupation. Of course we must 
beware of any over-exertion. 

Besides the psychical or moral treatment, which must always take the first 
place, we must consider all the means at our command for " strengthening " the 
nervous system. In this respect there can be no doubt that the favorable results 
from physical methods of treatment in neurasthenia are to be referred in great, if 
not the greatest, part to their indirect psychical (" suggestive ") influences. All 
methods of treatment must therefore be used methodically and continued long 
enough for the patient to remain for some time under the permanent personal 
influence of the physician. In this way alone can the patient have that 
mental schooling which he needs to make him conquer his own disease. What 
has been said explains why treatment in a sanitarium is so often desirable or 
even necessary for a neurasthenic. 

Certain prescriptions as to diet are of importance in the physical treatment 
of neurasthenics. These are governed by the needs of the individual case. 

For a corpulent patient treatment calculated to diminish obesity will some- 
times be followed by decided improvement in the general condition and in bodily 
vigor. In those frequent instances where the patient is pale and thin, and very 
likely oppressed by nervous dyspepsia (see page 463), we should, on the other hand, 
make vigorous efforts to improve nutrition.* Definite instructions must be given 
in order that the patient may ingest a proper amount of food. Milk, butter, fresh 
meat, eggs, simple puddings, artificial foods, etc., are appropriate articles of diet. 
Often both the weight and strength improve rapidly. Any large amount of 
alcohol or of tobacco should be forbidden. Nothing is worse than to prescribe 
strong wine for a neurasthenic to " strengthen " him. We have countless times 
won a patient's gratitude by releasing him from such a prescription, which in his 
own experience he had found disagreeable (causing heat in the head, vertigo, etc.). 
Tea and coffee may be taken in moderation, if the patient is accustomed to their 
use. In regard to bodily exercise, we must again be guided by the condition of 
the individual. We would most earnestly warn the physician against the error, 
frequently committed, of driving weakly and debilitated persons to take long 
walks. For such, bodily rest is much more desirable; and fresh air may be en- 
joyed at the same time, if the patient sits or lies out of doors or drives. The 
sluggish and corpulent, on the other hand, often require persistent exercise. 
It is a good plan in many instances to employ the Swedish movement cure, or 
similar gymnastic exercises. [In many cases the treatment must be directed 
primarily toward increasing the nutrition of the patient and building up the gen- 
eral strength in every possible way — forced feeding, cod-liver oil, tonics, etc. To 
this we must add rest and a change of occupation or at least diversion. These 
are often more important than the psychical treatment, especially in the cases of 
pathological fatigue, where the morbid ideas are few or absent. — K.] 

Of other other general remedies electricity and hydropathy are at present most 
in use. Electricity is warmly praised by many patients. The galvanic current is 
generally employed, and is applied either over the sympathetic nerve or along the 
spinal cord. Its use demands great caution. The current should not be too strong, 
and there should be no abrupt changes in it. Galvanism applied to the head is sel- 
dom well borne. Another very valuable mode of treatment was first practiced by 

* Playfair, Weir Mitchell, and certain other neurologists, have built up a special "method" of 
treating neurasthenia and allied conditions of nervous exhaustion ; this consists in " over-feeding" the 
patient— that is, in introducing as large an amount of nourishment as possible into the system at the 
same time that complete bodily and mental rest is secured. Faradic electricity and massage are also 
daily employed. This mode of procedure is certainly excellent in many cases, but it must not be 
regarded as universally applicable. There are cases of neurasthenia for which it is not suitable. 



1200 



DISEASES OE THE NERVOUS SYSTEM 



Beard and Rockwell, and consists of general faradization. The patient is almost 
completely stripped, and places both feet upon a large, flat electrode, while the 
various parts of the body are stroked with another large sponge electrode; in 
place of this second electrode the " electrical hand " of the physician may be em- 
ployed. The physician takes the second electrode in his left hand and allows the 
current to pass through his own body. Various institutions have lately begun 
to employ electrical baths; these also often seem to produce good results. In 
addition to peripheral galvanization and faradization of the nerves and muscles, 
it is advantageous to employ the faradic wire-brush, particularly on the back 
of the neck, along the spinal column, and over the shoulders and thighs. It is 
hard to say whether all these methods of electrical treatment have any specific 
action. The greatest part of the benefit obtained is undoubtedly of a suggestive 
nature ; but there are few other methods by which such a suggestive effect can be 
so easily produced as by electricity, and therefore it is hard to dispense with it 
in the treatment of neurasthenics, in spite of what has just been said, since we 
often have to change our methods of treatment in so chronic a disease. 

The hydro-therapeutic treatment may be quite well carried out at the patient's 
home, but a severe case will be better off in some well-conducted institution. Cold 
sponging, douches, hip-baths, lukewarm baths (or swimming), are all employed. 
Douches must not be applied to the head. If there is sexual disturbance, hip- 
baths of cold water are advisable. They should not be taken at night. Douching 
of the genitals and loins is also excellent. We can not here give a detailed de- 
scription of the different hydro-therapeutic methods. The efficacy of hydro- 
therapy is due in part to its physical influence on the patient, which is undoubt- 
edly favorable, but also, of course, in large part to suggestion, just as with all 
other forms of treatment. Subsequently sea-bathing will prove extremely benefi- 
cial for many patients. We would recommend the seashore especially for emaci- 
ated and anaemic subjects, who are frequently greatly benefited by the improved 
appetite and rest thus obtained. If the patient be well nourished, on the other 
hand, a journey on foot through the mountains, if made cautiously, may be very 
valuable. Massage is also much used as a general means of strengthening in 
nervous conditions. We can judge of its value from what has been already said. 
It is prescribed most advantageously in those forms of nervous trouble which are 
associated with painful sensations in the spine, the extremities, etc. Massage 
displays an excellent direct effect when there is habitual constipation. 

In neurasthenia, internal remedies should be given only as indicated by the 
symptoms or in the way of suggestion. If there is anaemia, iron, quinine, or 
Eowler's solution is prescribed; if there is dyspepsia, some stomachic, such as 
dilute hydrochloric acid, pepsin, or some bitter. The constipation (see page 495) 
should be overcome mainly by diet, and laxatives should be given only in case of 
necessity. When there are vaso-motor symptoms (a feeling of heat, congestion, 
palpitation), we often prescribe ergotine, four to six one-grain (gramme 0.05) 
pills a day. In all states of nervous irritation bromide preparations are much 
used, a powder of potassic and sodic bromides, or bromine water. In nervous 
headaches, and also in other nervous states, antipyrine often has a good effect. 
Antifebrine and phenacetine, and many similar recent remedies, act in the same 
way. 

The treatment of the insomnia which results from neurasthenia deserves a 
brief mention. It is usually a difficult problem. Since the insomnia is in most 
cases merely the result of the mental excitation, especially the onset of anxious 
ideas, the suggestive action of all the remedies that can be thought of plays of 
course the chief part, and the physician should take advantage of this circum- 
stance. We must utter an urgent warning against the misuse of the stronger 
narcotics (chloral and morphine). The attempt should always first be made to 



THE SO-CALLED TRAUMATIC NEUROSES 



1201 



secure sleep by a rational general treatment, or by some less injurious remedies. 
Often a warm bath for half an hour at bedtime soothes the patient and brings him 
sleep ; and in other cases a wet cloth laid upon the head or back of the neck pro- 
duces the same favorable result. Patients often report that general faradization 
at bedtime is an excellent soporific. Sometimes a moderate dose of alcohol may 
be tried as a true hypnotic. A glass of beer at bedtime often has a particularly 
good effect. If none of these means avail, our next resort should be the bromide of 
potassium. Very likely small doses of this have only a subjective effect, but there 
can be no doubt that a large dose, about a drachm (grammes 3-5) in a glass 
of water, does have a direct tendency to produce sleep. We may also mention 
as the best of the other hypnotics, sulphonal, twenty to thirty grains (grammes 
1.5-2) in a large amount of water, in soup, [hot milk,] or tea, two or three hours 
before bedtime. Trional is equally to be recommended. These and other reme- 
dies, however, seldom give great satisfaction, and we must therefore rely mainly 
on general treatment. 



CHAPTER XI 

THE SO-CALLED TRAUMATIC NEUROSES (ACCIDENT NEUROSES) 

As an appendix to the last two chapters on hysteria and neurasthenia, we must 
now — -more from practical than from scientific reasons — speak in particular of a 
series of morbid states which are at any rate most closely related to the above- 
mentioned affections, but which yet show certain peculiarities. The morbid 
states in question develop as the result of various sorts of physical injuries 
(trauma, accidents). They were first noticed after railway accidents (the so- 
called " railway spine " and " railway brain " of English and American neu- 
rologists), and it was formerly the belief that the coarse material concussion of 
the central nervous system* was to be regarded as the cause of the subsequent 
nervous symptoms. Later the name of " traumatic neurosis " was often used for 
these morbid states. By this we would imply that the nervous symptoms pro- 
duced by the trauma do not depend upon coarse material injuries of the nervous 
system, but upon finer changes not yet made out anatomically. Soon, however, it 
was shown that in at least the great majority of these cases the material injury 
itself plays no other part than that of the exciting cause of a purely psychical 
change in the person affected by the injury. The material trauma is, as we ex- 
press it, associated with a " psychical trauma." Among these we may reckon not 
merely the fright associated with the accident but the whole series of new ideas 
occasioned by the accident and entering most vividly into the consciousness of the 
injured person — anxiety about the further course of the injury, about the restora- 
tion of the capacity to work and earn a living, and also about obtaining any proba- 
ble damages, etc. Sordid mental motives also are sometimes mixed with the 
others in consciousness, the desire for indemnification in money, for a better way 
of living, etc. From what has been said in the two previous chapters we can 
easily understand that this primary change in the ideational life of the injured 
person may be followed by a considerable number of apparently physical dis- 
turbances. 

The type of disease thus arising is peculiarly characteristic. Sometimes the 
original trauma (fall, blow, etc.) is so severe that directly after it the well-known 
symptoms of cerebral or spinal concussion (loss of consciousness, general motor 
paralysis, etc.) may ensue with more or less severity. In other cases, however, 
the intensity of the trauma or the special seat of its action (fall on the sacrum, 
76 



1202 



DISEASES OF THE NERVOUS SYSTEM 




'V 



back, or side, injury of a limb, etc.) is such that there can be no question of a 
material cerebral concussion. Not infrequently there may be some organic in- 
juries at first (contusion, haemorrhage, fracture), but these of themselves are 
capable of perfect recovery. 

The characteristic feature is that after the severe or slight initial material 
results of the injury have run their full course, there is not a complete cure, as 
might have been expected. The patient recovers, tries to get about again, and 
the improvement goes on up to a certain point; but, nevertheless, a number of 
symptoms remain which do not disappear, and which diminish or wholly destroy 

the victim's* capacity for work. 
If We now examine such patients 
we find no signs of material in- 
jury either in the nervous sys- 
tem or in any other internal 
organ. What at once strikes 
us is a peculiar psychical change. 
The patients are dull, depressed, 
disinclined to any occupation, 
wholly without energy, and they 
have no more pleasure in inter- 
course with their families and 
friends. They brood constantly 
over their accident and its re- 
sults. In very many cases the 
gloomy and listless disposition 
is mirrored in the patient's 
whole appearance, and especially 
in his facial expression. A prac- 
ticed observer can often recog- 
nize the genuine " accident 
case " at the first glance (see 
Eig. 185). The sleep is dis- 
turbed and often rendered un- 
easy by dreams. Of subjective 
symptoms we must mention 
especially pains in the part 
which was hurt; these are com- 
monest in the back, the sacral re- 
gion, the sides of the chest, the 
hips, etc. Patients also com- 
plain of headache, vertigo, dull- 
ness, dim vision, tinnitus, spots 
before the eyes, loss of appetite, 
etc. Objective examination often shows a general motor weakness. Many pa- 
tients can walk quite well alone, but they are soon fatigued; others walk only 
slowly and stiffly with support, complaining of pain in the back on walking, and 
therefore holding the hand on the back, etc. The nutrition of the muscles is 
usually good. The electrical excitability of nerves and muscles is completely 
normal. The reflexes are sometimes lively and sometimes weak, but never so 
much changed as we find them in actual organic diseases. Examination of the 
sensibility may reveal very marked changes, which do not occur in all cases. This 
examination must always extend to all the sensory organs. The skin over almost 
the entire body is often very insensitive to painful irritations, pin-pricks, the 
electric current, etc. There is analgesia. In some places we find complete anses- 




Fig. 185. — Accident case, with hysterical paresis and tremor 
of the right arm. .(Personal observation.) 



THE SO-CALLED TRAUMATIC XEUEOSES 



1203 



thesia, which may affect an entire extremity or only circnmscribed parts of the 
extremities and the trunk. The boundary between the anaesthetic and the nor- 
mally sensitive parts is indistinct or quite sharply defined, and the arrangement 
is often very peculiar, in a way that can never occur in organic nervous diseases. 
Examination of the eyes sometimes shows loss of visual acuteness, limitation of 
the visual field, and imperfect color perception. Very often the hearing is poor 
on one or both sides. The smell is often much blunted, and the taste completely 
lost, so that even quinine, vinegar, and substances of equally strong taste no 
longer excite any sensation of taste. 

Besides the symptoms of impairment of sensation and motion just described, 
we often find also symptoms of sensory and motor irritation. Pain in the head, 
spots before the eyes, and tinnitus have been mentioned above. Hyperesthesia of 
the skin is more characteristic — tenderness of the vertebral column, and particu- 
larly great tenderness of such parts of the body as were most affected by the origi- 
nal injury. Among the symptoms of motor irritation we may mention muscular 
contraction and muscular rigidity, again most common in the limbs most affected 
by the injury. A marked tremor is also very common. 

Almost always the subjective symptoms are referred definitely to the spot 
which was first injured. If the injury has affected the head, the chief com- 
plaint is there; if one side of the trunk or one limb has been affected, most 
of the symptoms are manifested there; but of course the symptoms often ex- 
tend beyond the part originally injured. If, for example, one shoulder receives 
a blow, the whole side, including the leg, etc., is often weak and painful. Gen- 
eral nervous symptoms, especially the subjective feelings of vertigo and pres- 
sure in the head, are found in the majority of cases, even after peripheral in- 
juries. 

If we ask after the cause and the special nature of this peculiar affection, char- 
acterized chiefly by psychical disturbances and in the second place by subjective 
sensations of pain, sensory anaesthesia, and motor weakness, the purely material 
effects of the injury are in most cases not to be considered, as we have said. Al- 
though we at present believe that there are morbid states which we must actually 
regard as traumatic neuroses in the stricter sense of the word, and as permanent 
functional disturbances resulting from an actual material cerebral concussion, the 
assumption does not hold for the vast majority of all " traumatic neuroses,' 5 for 
the neurosis is certainly produced by the ensemble of psychical effects, associated 
with the trauma (accident), which have been described in detail above. The per- 
plexity and frequent contentions about sick funds, insurance societies, and claims 
for damages, do their part in keeping the patient disturbed. 

In laborers, who have accident insurance, and in whom the " traumatic neuro- 
ses " are far most frequently observed, we often find a peculiar obstinacy in their 
claims and their opinions in regard to a presumed right of damages after every 
accident. We may therefore assert that the traumatic neuroses have become 
decidedly more common as a result of the accident legislation. 

[In America claims for' " damages " against corporations are much more im- 
portant factors in the aetiology of the traumatic neuroses than any claim for insur- 
ance. The various psychical influences associated with the litigation consequent 
upon such claims have given rise to the term " litigation neuroses." Although it 
is undoubtedly true that litigation aggravates, and sometimes perhaps originates, 
nervous conditions, it is equally true that we often see precisely similar condi- 
tions developing after an accident in which there was no possibility of making 
any claim for damages or insurance, and where the other psychical factors above 
referred to had only a slight influence. Furthermore, on considering a large 
number of cases, there seems to be some relation between the severity of the 
physical injury and the severity of the subsequent nervous conditions, even in 



1204 



DISEASES OF THE NERVOUS SYSTEM 



the cases of genuine hysteria, although hysteria may at times develop after a very 
slight physical injury. The pain and other physical effects of the injury may, 
of course, if long continued, so far affect the general condition as greatly to ag- 
gravate the nervous sequela?, but the influence of the actual material concussion 
is often under-estimated, and the " accident case " often receives less consideration 
than he really deserves. — K.] 

Various factors therefore act in producing a condition which has the closest 
points of contact with general nervousness, neurasthenia, hypochondria, and hys- 
teria. It would therefore be proper, now that our views as to the nature of the 
traumatic neuroses — a term, by the way, which we have always used merely in 
a symptomatic significance, and therefore justifiably — have become clear, to use 
this term merely as a symptomatic appellative and replace it by the terms " trau- 
matic neurasthenia," " traumatic hysteria," etc. On the other hand, we must not 
forget that the neurasthenic and hysterical affections following accidents often 
have a certain peculiar stamp, a common type which we do not often find in 
ordinary hysteria and neurasthenia. The chief characteristics are the patient's 
peculiar psychical state, manifestly conditioned by the special external circum- 
stances, his lack of courage and energy, his depression, the tendency to complain 
and be querulous, and also the great obstinacy with which these conditions persist 
and often resist any attempts at treatment. We know many cases where such 
patients, in spite of the fulfillment of every desire, have lived for years in a state 
of permanent neurasthenia, incapable of anything, and finally have fallen into a 
state of pronounced mental dullness. We may therefore still use the name " trau- 
matic neurosis," or, better, " accident neurosis " or " accident psychosis," for such 
cases from practical reasons, if we only associate the correct meaning with it. 
In all those cases, however, where there are pronounced objective symptoms of hys- 
teria (anaesthesia, paralysis, contractures at the seat of the injury), we should 
speak merely of hysteria, with the appropriate adjective, " traumatic " hysteria. 

In the great majority of cases it is not at all difficult to recognize positively 
the " traumatic neuroses." The existence of gross material injuries can, as a 
rule, be easily excluded. It may be harder to decide whether there is real disease 
or simulation. In such cases we can not decide by single criteria — as has been 
supposed — but ultimately only by careful observation of the constitutional state 
(if possible, in a hospital) and by consideration of the general conditions (the pa- 
tient's behavior, previous life, external circumstances, etc.). From our own 
experience we must in general state that conscious and intentional complete 
simulation is not very common, although, of course, it occurs often enough. Ex- 
aggeration and apparent simulation are of course very common, since the pa- 
tients report symptoms, which careful investigation shows to be absent or at 
least not to be constant. Such a condition, however, is no proof of conscious 
simulation, since we see it every day in all the psycho-neuroses (hysteria, neu- 
rasthenia). A hysterical woman who claims that she can not leave her bed, and 
then walks very well when led by the physician; another who says she can not 
bear the slightest touch on her back, and then hardly feels the strongest pressure 
when her attention is diverted ; a third who claims to have' pain in the stomach 
after a swallow of tea, and soon after eats a beefsteak with relish — would not be 
called a " simulator " by any physician. A similar thing occurs of course in the 
accident neuroses, because they are precisely analogous conditions. It is of 
course very hard to decide the question, which is often of such practical im- 
portance, how far such neurasthenic-hypochondriacal patients have a claim for 
damages and pecuniary assistance. In such cases we are decidedly of the opinion 
that the examining physician should not be too generous, since it is necessary 
from a therapeutic point of view to cure the patient of his delusion that he has 
a serious acquired disease. We should therefore always try in the first place to 



THE SC-CALLED TRAUMATIC NEUROSES 



1205 



bring about an amelioration or a recovery from the condition, and of course the 
chief stress is to be laid upon the proper psychical influence to be exerted on the 
patient; but we must also consider all the other methods of treatment (baths, 
sponging, electricity, gymnastics), with which we have become acquainted in the 
two preceding chapters. In this way we sometimes succeed undoubtedly in bring- 
ing about improvement and even recovery, but the outlook for the permanent 
success of the treatment is not in our experience very good. The accident 
neuroses apparently have an especially unfavorable prognosis, although, as 
we know, the same is unfortunately often enough the case in non-traumatic states 
of severe neurasthenia and hypochondria. In the accident cases, however, we 
often notice from the outset that they do not wish to be treated or cured. The in- 
curability of their condition has become a matter of conviction to them, and their 
only interest is to obtain as large an accident annuity as possible. In most cases, 
at least, we should therefore advise against any continuous medical treatment, un- 
less we have the impression that the patient will submit willingly and trustingly 
to the physician's directions. It seems to us of the greatest practical importance to 
" strangle " the traumatic neuroses " in the embryo," if possible, on their first 
development. ~Not infrequently we have seen accident cases who began to com- 
plain constantly of all possible nervous troubles after some slight external injury 
was evidently wholly cured. In such cases we should cut short such complaints as 
completely as possible from the outset and make the patient understand that he 
is now actually and completely well. The granting of a high accident annuity at 
first is therefore quite incorrect in such cases and makes recovery much harder, 
while the immediate and complete refusal is of the best influence. The patients 
are forced to resume their work and to forget their imagined symptoms. If a trau- 
matic neurasthenia has continued for years, it is usually very hard to convince the 
patient that his complaints have no objective foundation. 

[In many cases the patient is actually injured by resuming work too early. 
It is sometimes of decided advantage, especially in the early stages of the trouble, 
to prescribe a thorough " rest cure," with isolation, massage, forced feeding, etc., 
as prescribed by Weir Mitchell. The worries of litigation should be eliminated, 
if possible, by an early settlement of the case. It must be borne in mind that the 
various therapeutic procedures, which are often advisable in neurasthenic and 
hysterical conditions, such as massage, electricity, gymnastics, good nursing, 
travel, etc., are extremely expensive and often impracticable for those in poor 
circumstances. This is of importance when the physician is called upon to de- 
termine the amount of the damages or the accident annuity. — K.] 



APPENDIX I 



SUMMARY OF THE SYMPTOMS AND TREATMENT IN CASES OF 

POISONING 

1. Sulphuric Acid. — Mucous membrane of mouth, throat, oesophagus, and 
stomach deeply corroded. In the worst cases rapid death ushered in by convul- 
sions and asphyxia, or more rarely consequent upon perforation of the stomach. 
Usually the case is more protracted. The mouth and throat are whitened, or in 
severe cases blackened. They are soon attacked by an intense ulcerative inflam- 
mation. Deglutition is extremely painful, and there are most distressing chok- 
ing and retching. The vomitus contains black lumps. Profuse salivation. Pain 
along the oesophagus. Abdomen usually distended and very tender on pressure. 
There may be intestinal discharges of a bloody character, resembling dysentery. 
Urine is generally scanty, and often contains albumen and blood. Collapse. 
Small and rapid pulse. 

In mild cases, slow recovery, the necrosed tissues gradually sloughing off. 
Cicatricial stricture of the oesophagus frequently ensues and it may prove fatal. 
ISTeuralgia, hyperesthesia, and various other nervous disturbances may also occur 
as sequelae. 

In fatal cases, the autopsy discloses necrosis, ulceration, and inflammation in 
the upper portion of the digestive tract. The lining of the stomach is usually 
coal-black. Well-marked parenchymatous degeneration of the liver and kidneys. 
Perhaps nephritis. In later stages, extensive cicatrices. 

Treatment : If used at all, the stomach-pump must be introduced very cau- 
tiously,- for fear of causing perforation. The best remedy to give at once is sev- 
eral teaspoonfuls of magnesia in water, or a few drops of liquor sodae in mucilage. 
Later, the symptoms are to be combated with bits of ice, disinfecting mouth- 
washes and gargles, tonics, and cautious feeding with milk, eggs, etc. If stricture 
of the oesophagus develops afterward, an endeavor should be made to dilate it 
with bougies. 

2. Hydrochloric and Nitric Acids. — Symptoms similar to those of sulphuric 
acid. The most prominent symptoms are the local ones, intense stomatitis, phar- 
yngitis, etc. There is usually albuminuria, with casts and blood in the urine. 
ISTitric acid sometimes stains the corroded spots, especially the angles of the 
mouth, yellowish; and the vomitus may have the same tinge (xanthoproteic acid). 
In poisoning from fuming nitric acid the inhaled vapors cause pulmonary symp- 
toms. Prognosis and treatment as in case of sulphuric acid. 

3. Nitrous and Sulphurous Acid Fumes. — Intense local inflammation of the 
air-passages. Violent dyspnoea, cough, abundant bloody or yellowish expectora- 
tion. There may also be grave nervous disturbance and collapse. Treatment : 
Symptomatic: sinapisms, narcotics, expectorants, and inhalations. 

4. Oxalic Acid. — Local corrosive action similar to that of the other acids, only 
less severe. In severe cases collapse from cardiac paralysis. Apt to occasion cer- 
tain nervous symptoms — formication, anaesthesia of the finger-tips, tonic and 

1206 



APPENDIX I 



1207 



clonic convulsions, trismus, and tetanus; later paresis. There is sometimes 
sugar in the urine, and nephritis may develop. Anuria is frequent, and is due to 
plugging of the tubules by calcic oxalate crystals. The treatment should be 
symptomatic, and should also include the administration of preparations of cal- 
cium — liquor calcis, calcii carbonas, or even egg-shells — to form insoluble calcic 
oxalate. Magnesia is also useful. 

5. Ammonia. — The fumes affect the air-passages chiefly; the solution, the 
upper part of the digestive tract. The specific local effect is the production of an 
intense croupous inflammation of the mucous membrane. Accordingly, the 
symptoms are salivation, dysphagia, vomiting of strongly alkaline matter, and 
diarrhoea, or cough, dyspnoea, etc. In severe cases there is collapse, with rapid 
pulse, and such nervous symptoms as pain, paresthesia, vertigo, convulsions, etc. 
Treatment : In fresh cases the stomach-pump. The cautious use of acids — for 
instance, acetic or citric. Also, symptomatically, emulsions of oil, bits of ice, 
and narcotics. 

6. Caustic Potash or Soda. — Symptoms and treatment as in case of ammonia. 
In contrast to acid poisoning, it is to be noted that alkalies do not withdraw water 
and precipitate albumen, but dissolve it. The corroded spots are therefore not 
dry and brittle, but softened (" colliquation "). 

7. Potassic Nitrate. — Vomiting and diarrhoea. Severe abdominal pain. Col- 
lapse, with cold skin and rapid, thready pulse. Occasionally the pulse is slow. 
JSTervous disturbances, such as painful muscular contractions, and, in severe cases, 
convulsions and coma. Treatment : Symptomatic; opium and other narcotics, 
stimulants (camphor, ether), and bits of ice. 

8. Chlorine Gas. — Violent convulsive cough. Bloody expectoration. Spasm 
of the glottis. Dyspnoea. Darting pains through the chest. Sneezing and pro- 
fuse flow of tears. In severe cases pneumonia. Treatment : Fresh air. Inhala- 
tion of warm aqueous vapor, or of ammonia to form ammonic chloride. Chloro- 
form may also be tried, and narcotics. 

9. Iodine. — 1. Acute iodism, as seen, for instance, after the injection of large 
amounts of tincture of iodine into ovarian cysts : collapse, with pallor and cya- 
nosis, and small and very rapid pulse. Vomiting. Often marked dyspnoea. 
Suppression of urine. Sometimes hsemoglobinuria. Later, the skin becomes very 
red. There is albuminuria; also sore throat, coryza, conjunctivitis, severe frontal 
headache, and cutaneous eruptions. 2. Chronic iodism, caused, for example, by 
long-continued internal administration of potassic iodide : coryza, conjunctivitis, 
sore throat. Gastric symptoms. Vertigo, headache, and similar nervous phe- 
nomena of a mild character. Acne or erythema, sometimes in the form of ery- 
thema nodosum. Treatment: In acute cases, white of egg and stimulants. 
Other than this, treatment must be symptomatic. Prophylaxis demands caution 
in the internal administration of iodine or its compounds. According to Ehrlich, 
the symptoms of iodism often disappear rapidly after the exhibition of about a 
drachm and a half (grammes 6) of sulpho-nitro-salicylic acid (sulphanilic acid). 

10. Bromine. — 1. Acute poisoning from the fumes of bromine excites the same 
■symptoms as does chlorine gas. 2. Bromism, resulting from the long-continued 
use of potassic bromide, causes languor, debility, mental apathy, and impaired 
intellectual vigor. The reflexes are diminished, particularly the reflex irritability 
of the soft palate and pharynx. Anorexia. Diarrhoea. Impotence. Almost 
invariably a characteristic acne, the onset of which may be delayed by giving 
arsenic at the same time. 

11. Lead. — (a) Acute lead poisoning produces severe gastro-enteritis. The 
loest antidote is sulphate of sodium or magnesium; or phosphates, white of egg, 
-and milk. In fresh cases the stomach-pump, or emetics and purgatives. Other 
than this, symptomatic treatment. 



120S 



APPENDIX I 



(b) Chronic lead poisoning : Seen in type-setters, type-founders, painters, 
potters, and others. General symptoms : Lead line on the gums, lead anaemia, 
and lead cachexia. Important groups of symptoms are: 1. Lead colic: Violent 
colicky pains, radiating from the umbilicus. Usually constipation, exceptionally 
diarrhoea. Abdomen concave and hard. Vomiting. Hard, slow pulse. Tempera- 
ture usually normal. Urine sometimes contains a trace of albumen. Duration, 
one or two weeks. Treatment : If severe pain, opium and hot compresses. Atro- 
pine may also be tried. For constipation, enemata and gentle laxatives. Warm 
baths. 2. Lead paralysis {vide page 873) : Paralysis of the laryngeal muscles 
due to lead poisoning has been reported. 3. Saturnine encephalopathy : Sudden 
development of grave cerebral symptoms ; convulsions, coma, delirium, great men- 
tal uneasiness, and excruciating headache. Saturnine amaurosis. In severe 
cases, death. Cerebral lesions are very rarely found post mortem. Treatment 
is symptomatic. Lukewarm baths, with douching, narcotics, and stimulants. 
Later, potassic iodide. 4. Lead arthralgia: Most frequently attacks the knee. 
Also seen in the joints of the upper extremities. Sometimes associated with 
painful muscular contractions. Objective lesions are rarely seen. The treatment 
consists of warm baths and the administration of potassic iodide. It should be 
remembered that chronic lead poisoning may occasion gout and chronic inter- 
stitial nephritis. The reader is referred to the chapter describing these dis- 
eases. 

12. Copper (Blue Vitriol, Verdigris). — (a) Acute copper poisoning: Copper 
taste. Vomiting of greenish matter, colic, tenesmus, and bloody stools. Also 
nervous symptoms, headache, vertigo, anaesthesia, paralysis, delirium. Collapse. 
Dyspnoea. Treatment: White of egg, milk, wood charcoal. Magnesia is also 
valuable. Yellow potassic ferrocyanide, milk sugar, (b) Chronic copper poison- 
ing is rare. It occasions gastro-intestinal disturbance, colic, and a reddish or 
greenish discoloration of the hair. 

13. Zinc (Zinc Sulphate and Chloride). — In acute poisoning, symptoms of 
severe gastro-enteritis, especially vomiting. Also albuminuria. Treatment r 
Albumen, tannin, and alkaline carbonates. Chronic poisoning (zinc fumes !) r 
Fever, distress, vertigo, vomiting, metallic taste. General anaemia and emaci- 
ation. 

14. Mercury. — (a) Acute poisoning from corrosive sublimate: The mucous 
membrane of the mouth, throat, oesophagus, stomach, and intestines is deeply 
corroded. Metallic taste. Vomiting. Diarrhoea with painful tenesmus. Ischu- 
ria or complete anuria. Collapse. Generally quickly fatal. Treatment : Milk r 
white of egg, reduced iron, narcotics, (b) Chronic mercurial poisoning : Seen in 
the makers of thermometers, scientific instruments, and mirrors. Barely occa- 
sioned by the prolonged use of antisyphilitic remedies. The symptoms are 
anaemia, emaciation, with great muscular weakness, and gastro-intestinal disturb- 
ance. In the therapeutic use of mercury, besides the rarer mercurial enteritis, 
mercurial stomatitis is the most important toxic symptom ; onset of foul-smelling 
necrosis of mucous membrane, with ulceration of mucous membrane of cheeks, 
jaws, gums, etc. Treatment : Immediate discontinuance of medication; potassic 
chlorate as mouth-wash and gargle. 

Mercurial Tremor. — Tremor is common in chronic mercurial poisoning and is 
of special interest. It is usually preceded by a stage of pronounced mental irri- 
tability ("mercurial erethism and often some mental excitement, fright, etc., 
is the exciting cause of the tremor. The tremor itself is a pronounced intention 
tremor — that is, it is usually not present when the body is kept quiet, but it comes 
on with all movements, like the tremor in multiple sclerosis. The finer the 
movements the patient tries to make the more marked is the tremor. Mental 
excitement usually increases the tremor considerably. In severe cases the tremor 



APPENDIX I 



1209 



is so great that the patients can not leave their beds. In rare cases there is also 
paralysis. 

Treatment : Dietetic and hygienic. Iodide of potassium, hyoscine, and some- 
times galvanism, are also useful. 

15. Phosphorus. — (1) Acute phosphorus poisoning, as from matches: Violent 
epigastric pain, vomiting — the vomitus smells of phosphorus, and it may be phos- 
phorescent. After these initial symptoms usually comes a period of comparative 
comfort, lasting two or three days. Then appear grave symptoms: jaundice, 
severe pain in the hepatic region and whole abdomen, hepatic enlargement, fever, 
feeble and rapid pulse, sometimes gastric or intestinal haemorrhage, cutaneous 
ecchymoses, hematuria, epistaxis, or metrorrhagia. The intellect usually re- 
mains clear, except that just before death there may be drowsiness or convulsions. 
The urine contains albumen, blood, casts, bile-pigment, and sometimes leucine 
and tyrosine. No urea is excreted. Death occurs usually at the end of one or 
two weeks, but is may be more speedy. In mild cases the above symptoms are not 
strongly marked, and recovery may ensue. A very grave prognosis should be made 
in every case at the start. Post-mortem appearances in acute phosphorus poison- 
ing : Jaundice. Dark blood. Numerous internal ecchymoses — for example, in 
the serous and mucous membranes and kidneys. Patty degeneration of most of 
the internal organs, including the liver, heart, muscles, and kidneys. Treatment : 
In fresh cases, washing out of the stomach. Laxatives. As an emetic, sulphate 
of copper. The best antidote is old oil of turpentine (30^0 drops in mucilage). 
Oily substances should be avoided, as phosphorus is soluble in oil. Narcotics and 
other symptomatic remedies may also be indicated. (2) Chronic phosphorus 
poisoning: Necrosis of the lower jaw, less often of the upper jaw, extending 
from caries of the teeth. Necrosis of the bone with exuberant growth of osteo- 
phytes. 

16. Arsenic (Arsenious Acid, Schweinfurth Green, Scheele's Green, Arsen- 
ical Wall-paper). — (1) Acute arsenic poisoning: Symptoms of intense gastro-en- 
teritis, suggesting cholera. Violent vomiting. Rice-water stools. Severe abdom- 
inal pain. Nervous symptoms : Vertigo, headache, f aintness, twitchings. Car- 
diac weakness. Cyanosis. Collapse. Not infrequently a cutaneous eruption 
resembling urticaria or eczema. Sometimes albumen and blood are present in the 
urine. Severe cases are fatal in one or two days. With regard to arsenical 
paralysis, vide page 875. Treatment : At first the stomach-pump or emetics — for 
example, sulphate of zinc. The best antidotes are freshly prepared ferric hydrate 
in water, two to four tablespoonfuls every fifteen to thirty minutes ; ferrum oxy- 
datum saccharatum solubile (P. G.), in teaspoonful doses; magnesia; and, best 
of all, the compound of magnesia and ferric hydrate known as " antidotum 
arsenici" (P. G.), of which a tablespoonful may be given every fifteen to thirty 
minutes. (2) Chronic arsenic poisoning : Acquired in arsenic works and glass 
factories, or from arsenical fabrics, papers, and flowers. Conjunctivitis, chronic 
gastro-intestinal catarrh, eczema, and cutaneous ulcerations. Ansemia and ca- 
chexia, falling out of the hair, loss of sleep. Treatment is purely symptomatic, 
except as regards prophylaxis. In poisoning with arseniuretted hydrogen, haemo- 
globinuria and jaundice occur, Avith severe nervous symptoms. 

17. Alcohol. — (1) Acute alcoholic poisoning: Unconsciousness; anaesthesia; 
pupils either dilated or contracted, usually not reacting to light; pulse small, 
sometimes slow; skin cold and clammy; vomiting; stertorous respiration. There 
may be delirium and clonic convulsions instead of coma. Such cases last three or 
four days. Death has been repeatedly observed. Treatment: Bathing and 
douching. Stimulants. 

(2) Chronic alcoholism, (a) Physical and mental de~bility: Chronic catarrh 
of the throat, larynx, stomach, and intestines. Alcoholic tremor. Numerous 



1210 



APPENDIX I 



organic diseases, including cirrhosis of the liver, contracted kidney, heart-disease, 
cerebral disease, and neuritis. 

(b) Delirium tremens: Usually a sudden onset, as in connection with some 
acute disease or after a surgical injury. Disordered intellect. Great restlessness, 
hallucination (vermin, etc.), excitement, and loss of sleep. Treatment : Bathing 
and douching. Injections of strychnine. The use of chloral and other narcotics 
should be cautious. Physical restraint should be avoided if possible. The patient 
may often be allowed to go about the room as he likes, if only he be watched. 
Alcohol should be given if collapse be threatened. 

[(c) Alcoholic insanity: Marked mental confusion with loss of memory of 
recent events, failure to appreciate time or place, occasional hallucinations. In 
some cases marked depression or excitement, in other cases more systematized 
delusions, of persecution, marital infidelity, etc. In more severe cases pronounced 
mental failure. Conditions of physical weakness often associated (neuritis? 
vide supra, polyneuritic psychoses, page 894). Treatment : Abstinence from alco- 
hol, strychnine, forced feeding, free elimination. — K.] 

18. Chloroform. — Unconsciousness. Loss of sensibility and reflexes. Slow 
pulse. Pupils dilated. Failure of respiration, and finally of the heart. Danger of 
heart failure, especially in persons with weak hearts. Treatment : Artificial res- 
piration. Injections of strychnine. Stimulants. Counter-irritation. 

19. Iodoform. — (Repeatedly seen from the use of iodoform on wounds.) First 
of all, nervous symptoms : headache, vertigo, sleeplessness. Peculiar psychoses, 
maniacal attacks, delusions of persecution, refusal of food. In severe cases con- 
vulsions, deep coma. Very small, rapid pulse. Treatment : Symptomatic, by 
stimulants, baths, etc. Alkalies and atropine are recommended, but their action 
is doubtful. 

20. Carbonic-oxide Gas (Illuminating Gas). — At first, vertigo, headache, 
throbbing in the temples, ringing in the ears, and spots before the eyes. The 
patient gradually becomes unconscious. Skin pale and cyanotic. Respiration in- 
termittent. Subnormal temperature. The urine may contain albumen and sugar. 
The carbonic oxide may be demonstrated in the blood by means of the spectro- 
scope. Its color is clear cherry-red (CO-haemoglobine). Subsequently paralysis, 
disturbances of sensation and of speech. Treatment : Fresh air, artificial respi- 
ration, stimulants, transfusion. 

21. Sulphuretted Hydrogen. — Headache, vomiting, diarrhoea. In severe 
cases, unconsciousness, dyspnoea, cyanosis, convulsions, and death. The blood is 
thin, fluid, and black (sulph-haemoglobine). Treatment : Artificial respiration, 
fresh air, and the cautious inhalation of chlorine gas. 

22. Bisulphide of Carbon. — (Workers in rubber factories.) Vomiting. Se- 
vere nervous symptoms. Incontinence of urine, atrophic paralyses, anaesthesia, 
mental disturbances, especially loss of memory, spasmodic conditions, etc. The 
red blood-corpuscles are destroyed ; the black blood contains many flakes of pig- 
ment. Treatment: Symptomatic. 

23. Hydrocyanic Acid (Potassic Cyanide; Bitter Almonds). — Characteristic 
odor of bitter almonds. In severe cases death may occur in a few minutes. If 
the course be more protracted, convulsive and extremely slow respiration, the 
expiratory act being much prolonged; the eyeballs protrude, and the pupils are 
somewhat enlarged and do not react to light. Cardiac weakness, cyanosis, uncon- 
sciousness. Twitching of the muscles. Trismus. Treatment: Merely symptom- 
atic. Emetics, artificial respiration, cool douches, stimulants. Atropine may be 
tried ; also, hydrated ferric oxide and chlorine water. 

24. Nitrobenzine (Nitrobenzole, Oil of Mirbane). — Strong odor of bitter al- 
monds. At first, dizziness. The skin soon assumes a bluish hue, rapidly increasing 
to the deepest cyanosis. Increasing anxiety, sense of suffocation, and gradual 



APPENDIX I 



1211 



loss of consciousness. In severe cases, death, ushered in by convulsions. In 
milder cases, gradual recovery. Treatment: Stomach-pump. Artificial respira- 
tion. Stimulants. In the Leipsic clinique, transfusion has worked admirably in 
two cases. The symptoms caused by aniline a:id the aniline dyes closely resemble 
poisoning from nitrobenzole. 

25. Carbolic Acid, also Lysol and the like. — Corrosion of mouth, throat, and 
stomach. In mild cases, vertigo, headache, and collapse ; in severe cases, coma, 
preceded in rare instances by symptoms of cerebral irritation. Contracted pupils. 
Vomiting. Pulse slow at first, then rapid. The urine has a dark, olive-green 
color. Sometimes hsemoglobinuria and nephritis. Carbolic acid is very readily 
absorbed from the rectum, so that great caution should be employed in its use 
as an injection. Treatment: Stomach-pump. Slaked lime and water. Large 
doses of sulphate of sodium are especially to be recommended. [Alcohol is an 
antidote. Administer three or four ounces of whisky at once, then wash out the 
stomach with water containing sulphate of sodium. In desperate cases, vene- 
section followed by infusion of normal salt solution has been successful. — V.] 

26. Atropine (Belladonna). — Dryness of the mouth and throat. Excessive 
thirst. Dizziness and headache. Peculiar mental disturbances: hallucinations 
are particularly frequent. Pupils very widely dilated. Cutaneous erythema 
resembling that of scarlet fever. In severe cases, pulse enormously accelerated, 
with violent pulsation in the arteries. Convulsions may occur. Nervous symp- 
toms persist for some time. Treatment : The following physiological antidotes 
should be tried: physostigmine (eserine), pilocarpine, and morphine. 

27. Digitalis. — Vomiting. Diarrhoea. Pulse very slow (forty beats per min- 
ute, or less). Dyspnoea. Symptoms of collapse. Cold extremities, muscular 
tremor. Somnolence. In the worst cases, sopor and death. Even the milder 
cases are protracted. Treatment : Emetics, stomach-pump. Tannin. Camphor, 
strong cafe noir, ether, ammonia. Counter-irritation. 

28. Nicotine (Smoking; Tobacco Juice; Tobacco Enemata). — 1. Acute: 
Pulse small and slow, syncope, sense of oppression, salivation, vomiting. In se- 
vere cases, loss of consciousness, tetanic spasms, both pulse and respiration inter- 
mittent. 2. Chronic (from excessive use of tobacco) : Palpitation, irregular ac- 
tion of the heart, paroxysms of asthma and angina pectoris. Tremor, muscular 
weakness. Loss of sleep. Sometimes there are symptoms of ataxia ("nicotine 
tabes" seen in cigar makers). Amblyopia, scintillating scotoma. Gastric dis- 
turbance, chronic catarrh of the pharynx and larynx. Treatment : In acute cases, 
stimulants. Chronic poisoning necessitates the giving up of tobacco. Further 
treatment is symptomatic. 

29. Strychnine. — Violent tetanic reflex convulsions. Exaggeration of the cu- 
taneous and tendon reflexes. Trismus. Opisthotonos. Pulse small and very rapid. 
The convulsions come in paroxysms, with intervals between them. The intellect 
is usually perfectly clear. Recovery occurs only in mild cases. Treatment: 
Emetics, stomach-pump. Tannin. Tincture of iodine. Castor-oil. The convul- 
sions are to be combated by morphine, chloroform, chloral, or potassic bromide. 
Curare has also been tried. 

30. Coniine (Hemlock). — In severe cases convulsions, then general paralysis, 
especially of the respiratory muscles, loss of consciousness, and death. Pupils 
dilated. In milder cases confusion, muscular weakness, vomiting, and diarrhoea. 
Treatment : Emetics, tannin, stimulants. 

31. Morphine (Opium). — 1. Acute: Begins with fatigue, headache, darken- 
ing of the visual field, nausea, vomiting. Then coma comes on with slow, ster- 
torous,, sometimes irregular respiration. Muscles completely lax. Pupils usually 
very small. Pulse often slow, but in other cases rapid and small. Toward the 
end of life Cheyne-Stokes's respiration. In milder cases only vomiting, stupor, 



1212 



APPENDIX I 



headache, etc. Treatment : Sulphate of zinc, or some other emetic; stomach- 
pump. [One-per-cent. solution of permanganate of potassium. — V.] Tan- 
nin. Cafe noir. Atropine may be tried as a physiological antidote. Stimu- 
lants (camphor, ether) are best, also cold baths with shower-baths; arti- 
ficial respiration. 2. Chronic (morphine habit) : Emaciation, anaemia, headache, 
vertigo, wakefulness. Tremor. Mental disturbance. Unconquerable longing for 
morphine ; and, if this be denied, the appearance of grave symptoms. To break 
up the morphine habit is almost impossible except in hospitals and special asy- 
lums. The withdrawal of the drug is abrupt according to the practice of some, 
and gradual according to others. For particulars consult monographs. 

32. Ergot (Ergotine). — 1. Acute: At first nausea, vomiting, colic, and diar- 
rhoea. Then vertigo, headache, and muscular weakness. Pulse slow. In severe 
cases, sopor, disturbance of respiration, and sometimes death. Treatment : Emet- 
ics and purgatives. Tannin. Ether, camphor, and cafe noir as stimulants. 2. 
Chronic ergotism: Gastric symptoms, vertigo, languor, cardiac weakness. The 
nervous disturbances are, however, of especial importance. Of these, pallesthesia 
has long been recognized. Recently attention has been attracted to the great 
resemblance of the nervous symptoms to those of tabes dorsalis; and there is, 
moreover, an anatomical change in the posterior columns of the cord. Convul- 
sions and psychical phenomena are also observed. A second form of chronic 
ergotism is called gangrenous ergotism. It results in dry gangrene of the hands 
and feet. A line of demarcation forms and the gangrenous parts slough off. 
The process may be attended by fever and pyaemia. The probable explanation is 
that the minute blood-vessels become spasmodically contracted and thrombi form 
under the influence of the poison. The different symptoms are due in part to the 
different constituents of the ergot. The best known are sphacelinic acid, which is 
probably the cause of gangrenous ergotism and ergotine tabes ; cornutine, which 
causes severe convulsive symptoms (convulsive ergotism) and uterine contrac- 
tions; and finally ergotinic acid. The treatment of chronic ergotism is purely 
symptomatic. 

33. Poisonous Mushrooms. — 1. Poisoning from morels: Fresh morels ("mor- 
cheln " or " lorcheln ") contain a poison which is readily soluble in hot water, and 
which evaporates completely if the morels be dried. Morels that have been dried 
or parboiled are therefore perfectly harmless, but the fresh ones are poisonous. 
The symptoms are nausea, vomiting, diarrhoea, headache, coma, and, above 
all, hemoglobinemia and hemoglobinuria (q. v.), associated with which is a 
hematogenous icterus. In severe cases death occurs, ushered in by convulsions. 
Treatment is symptomatic, and includes the administration of emetics, purga- 
tives, and stimulants. 2. Poisoning from the red agaric (amanita muscaria). 
This contains the poisonous alkaloid muscarine. Gastric symptoms and diar- 
rhoea. Mental excitement, delirium, tetanic and epileptiform convulsions. A 
rapid pulse, small pupils, disturbed vision from spasm of accommodation, sweat- 
ing, salivation, and in most of the severe cases sopor and death. Treatment : 
Emetics, etc. Atropine, which acts as a physiological antidote to muscarine. 
Also tannin, and stimulants. 3. Poisoning from bulbous mushrooms {ama- 
nita phalloides), confused with young button mushrooms (champignons). Di- 
gestive disturbances, later jaundice, somnolence, coma. The autopsy shows fatty 
degeneration of the liver, kidneys, and stomach, as in phosphorus poisoning. 

34. Poisoning from Sausages (Botulismus). — This sometimes occurs as the 
result of eating partially decayed sausages. The symptoms are pain in the stom- 
ach, nausea, vomiting, colic, and diarrhoea. There are also marked feebleness, 
precordial anxiety, and dyspnoea ; vertigo, headache, somnolence ; and very often 
disturbance of vision (amblyopia, spots before the eyes), and, what is surprising, 
ptosis. In severe cases, dysphagia, as a result of more or less complete paralysis 



APPEXDIX I 



1213 



of the tongue and the constrictors of the pharynx. The mouth is dry. The heart 
is feeble; this and the general prostration and malnutrition may prove fatal. 
The cases are usually protracted, rarely being very acute. The active principles 
(alkaloids of putrefaction) have lately become known in part. In sausage and 
also in meat poisoning the most important substance is ptomato-atropine, a sub- 
stance which acts almost exactly like atropine. Treatment : Emetics, purgatives 
(calomel), stimulants, and, if indicated, artificial feeding. 

35. Poisoning from Meat. — In repeated instances severe symptoms have been 
occasioned by eating tainted meat, or possibly that obtained from animals which 
had been diseased. These symptoms are certainly due to the products of putre- 
faction, substances which act partly like muscarine, partly like atropine, neurine, 
methylguanidine, etc. The special poison is not yet fully known. Probably 
there are several poisons, either chemical or organic and infectious. The usual 
symptoms are vomiting and diarrhoea. The case may closely simulate cholera. In 
most instances certain nervous phenomena are also observed — wakefulness, de- 
lirium, headache, and changes in the pupils. There may be roseola, wheals or 
erythema. Frequently there is a high fever, but sometimes the temperature is 
subnormal. The pulse is small and slightly accelerated, although it may occa- 
sionally be slower than normal. There is a sense of thoracic oppression. The 
cases are often protracted. Tendency to relapses. Death may occur. Post mor- 
tem, there is usually found an intense and often hsemorrhagic enteritis with sec- 
ondary changes in the spleen, kidneys, lungs, and other organs. Treatment : 
Symptomatic : calomel, emulsions, stimulants, and baths. Pood should be given 
cautiously. 

36. Poisoning from Fish. — The eating of tainted fish has likewise caused 
grave disturbance. The symptoms vary. Usually there are pain in the stomach, 
precordial anxiety, vertigo, dryness of the throat, aphonia, and labored respira- 
tion. There may also be disturbance of vision, amblyopia, and colored vision, or 
paralysis of the motores oculi and of accommodation. In severe cases there may 
be dysphagia and general paresis. Sometimes dyspnoea and cardiac weakness are 
observed. The cases are frequently Tery tedious. Here, too, there are many 
active poisonous products of putrefaction, among them one which acts like mus- 
carine. Treatment similar to that recommended in the two preceding paragraphs. 

37. Poisoning from Mussels (Mytilus Edulis). — This is also common. A 
drawing feeling in the neck, a blunt feeling in the teeth, crawling and burning in 
the arms and legs, dullness in the head, mental excitability, feeling as if every- 
thing were light, as if the patient must fly ; in the later stages dilated, immobile 
pupils, difficult speech, paresis and ataxia of the muscles ; also nausea, skin erup- 
tions (urticaria), fall of temperature. In severe cases death may ensue in a few 
hours. At the autopsy we find severe enteritis, enlargement of the spleen, and 
often a peculiar speckling of the liver. The poison of mussels has been isolated, 
and it is called mytilotoxine. 

38. Poisoning from Cheese. — Vomiting, colicky pains, diarrhoea, vertigo, sense 
of thoracic oppression, headache, languor, and disturbance of vision. Treatment 
as in paragraphs 35 and 36. 



APPENDIX II 



TABLE OF WEIGHTS AND MEASURES 



Table of Relation of U. S. Fluid to Metric Measure 



Minims. 


Cubic 
Centimetres. 


Minims. 


Cubic 
Centimetres. 


Fluid 
Drachms. 


Cubic 
Centimetres. 


Fluid 
Ounces. 


Cubic 
Centimetres. 


1 


= .06 


30 


= 1.85 


4 


= 14.79 


4 


= 118.24 


2 _ 


= .12 


40 


= 2.46 


6 


= 22.18 


6 


= 177.39 


5 
'10 


= .31 
= .62 


Fluid 
Drachms. 


Cubic 
Centimetres. 


Fluid 
Ounces. 


Cubic 
Centimetres. 


8 
12 


= 236.53 
= 354.82 


15 


= .92 


1 


= 3.70 


1 


= 29.57 


16 


= 473.11 


16* 


= 1.00 


2 


= 7.39 


2 


= 59.10 






20 


= 1.23 


3 


= 11.09 


3 


= 88.67 







Table of Relation of Troy Weight to Grammes 

* 



Grains. 




Grammes. 


Grains. 


Grammes. 


Drachms. 


Grammes. 


Ounces. 




Grammes. 


L 

8 




.008 


8 


= .52 


1 = 


3.89 


1 




31.1 


i 




.011 


10 


= .65 


H 


5.83 


n 




46.6 


i 




.016 


15 


= .97 


2 = 


7.77 


2 




62.2 


i 




.032 


15.43 


= 1.00 


3 = 


11.66 


3 




93.3 


1 




.065 


20 


= 1.29 


4 = 


15.55 


4 




124.4 


2 




.13 


30 


= 1.94 


6 = 


23.3 


6 




186.6 


4 




.26 


40 


= 2.59 






8 




248.8 


5 




.32 


61.73 


4.00 












6 




.39 

















Table of Comparison between Centigrade and Fahrenheit Scales 
Degrees Centigrade. Degrees Fahrenheit. Degrees Centigrade. Degrees Fahrenheit. 



25 




77 


36 




96.8 


26 




78.8 


37 




98.6 


27 




80.6 


38 




100.4 


28 




82.4 


39 




102.2 


29 




84.2 


40 




104 


30 




86 


41 




105.8 


31 




87.8 


42 




107.6 


32 




89.6 


43 




109.4 


33 




91.4 


44 




111.2 


34 




93.2 


45 




113 


35 




95 









1214 



APPENDIX II 



1215 



The Metric System in Medicine 

Old Style, 
m j or gr. j 
f 3 j or 3 j 
f 3 j or Id 

The decimal Zine, instead of points, makes errors impossible. As .06 (drug) is 
less than a grain, while 4. and 32. (vehicle) are more than the drachm and ounce, 
there is no danger of giving too large doses of strong drugs. 

C. c. (cubic centimetres), used for grms. (grammes), causes an error of five per 
cent, (excess). 

A teaspoonful is usually five grammes ; a tablespoonful, twenty grammes. 



Metric. 
06 grin. 

4 ' 
32 



INDEX 



Abasia, 1178, 1189. 

Abdomen, in cholera, 8S; in peritonitis, 524; 

in typhoid, 10. ■ 
Abdominal typhus, 1. 
Abducens nerve, paralysis of, 856. 
Abnormalities in size and position of the 

stomach, 460; gastroptosis, 462; idiopathic 

dilatation, 460; motor efficiency in, 461; 

neurasthenic symptoms, 463; palpation in, 

461; treatment, 461. 
Abortion, in acute yellow atrophy of the liver, 

568; in small-pox, 58; in typhoid, 8. 
Abortive typhoid. 20. 

Abscess, cerebral, 1106; from foetid bron- 
chitis, 169; embolic in the lungs, 274, 275; 
gastric, 432; hepatic, 577 (see also Sup- 
purative Hepatitis); in acute peritonitis, 
527, 528; in erysipelas, 65; in glanders, 126; 
in glossitis, 388; in laryngeal perichondritis, 
145; in pericarditis, 306; in peripleuritis, 
295; in plague, 109; in septic and pysemic 
diseases, 118; in small-pox, 58; in suppura- 
tive parotitis, 391; in typhlitis and peri- 
typhlitis, 485; of the brain, 1106; para- 
nephritic, 641; peritoneal, 434; pulmonary, 
from pneumonia, 221, 222; renal, 641, 642, 
655; retropharyngeal, 403; subphrenic, 438; 
tonsillar and peritonsillar, 396; worm, 516. 

Absorptive powers of the stomach, tests of, 
421. 

Accessory nerve, spasm of, 878. 

Accident neuroses. See Traumatic Neuroses. 

Acetonsemia. See Diabetic Coma. 

Acetone test, 754. 

Achillodynia, 821. 

Achlorhydria, 452. 

Acholia, 569. 

.Achromatopsia, hysterical, 1176. 

Achylia gastrica. See Anomalies of Secre- 
tion of Gastric Juice. 
Acid dyspepsia, 455. 
Acid fumes, 1206. 

Acid perspiration in articular rheumatism, 
680. 

Acoustic tract, 1089. 

Acromegaly, 902; tumor of brain in, 903; in 

diabetes mellitus, 750. 
Acroparesthesia, 822. 

Actinomycosis of the thoracic cavity, 302; 
77 



diagnosis and treatment, 303; haemorrhage 
in, 303; infection. 303. 

Acute bulbar myelitis, 1051. 

Acute febrile jaundice, 542. 

Acute yellow atrophy of the liver, 565; in 
typhoid, 12. 

Addison's disease, 650; aetiology and patho- 
logical anatomy of, 650; anaemia in, 652; 
course and termination of, 653; pigmen- 
tation in, 651; symptomatology, 652; 
treatment, 653; tuberculosis of adrenals, 
651. 

Adenia. See Pseudo-leukemia. 

Adenitis, inguinal, 108. 

Adenitis, in plague, 109. 

Adenoid growths in pharynx, 401. 

Adiposis dolorosa, 902. 

JEgophony, in pleurisy, 287. 

Agaric, red. See Mushroom Poisoning. 

Agaricine in night-sweats, 260. 

Agoraphobia, 1194. 

Agraphia, 1081. 

Akinesia algera, 1178. 

Albuminuria, 589. 

Albuminuria, in croupous pneumonia, 215; 
in small-pox, 58; in typhoid, 19. 

Alcohol, in chronic gastritis, 425, 430; in cir- 
rhosis of the liver, 556; in nephritis, 606, 
613. 

Alcohol poisoning, 1209. 

Alcoholic insanity, 1210: paralysis, 893; poly- 
neuritis, 889-893. 

Alcoholic stimulants, in croupous pneumonia, 
225; in interstitial myocarditis, 344-346; in 
pulmonary tuberculosis, 257; in yellow fever, 
106. 

Alcoholism, chronic, 1209; effect of, in pri- 
mary weakness of myocardium, 352: in 
arterio-sclerosis, 370; in contracted kidney, 
626; in diabetes mellitus, 750, 751. 

Alexia, 1081. 

Alkaline carbonates in gastric ulcer. 441. 
Allochiria, 791. 
Allorhythmia, 328. 
Alopecia in small-pox. 56. 

Alveolar ectasis. See Pulmonary Emphy- 
sema. 

Amanita. See Mushroom Poisoning. 
Amaurosis, uraemie, 599. 

1217 



1218 



INDEX 



Amblyopia in chronic nephritis, 622. 
Amimia, 1080. 
Ammonia poisoning, 1207. 
Ammonic urate crystals, 669. 
Amnesia, 1078; agraphic, 1081. 
Amoeba coli in dysentery, 81-84. 
Amphoric respiration in tuberculosis, 243. 
Amusia, 1081. 

Amyl nitrite, in cardiac neuroses, 356; in 
epilepsy, 1151, 1152; in interstitial myocar- 
ditis, 345. 

Amyloid diseases in phthisis, 250. 

Amyloid kidney, 635; aetiology of, 635; clini- 
cal history, 637; degeneration in other 
organs in, 639; dropsy in, 638; pathological 
anatomy, 636; predisposing conditions, 636; 
prognosis, diagnosis, and treatment, 639; 
urine in, 637, 638, 640. 

Amyloid liver, 580; diagnosis, 580; fatty liver, 
580. 

Amyotrophic lateral sclerosis, 986; aetiology 
and pathological anatomy of, 986; atrophy 
of muscle in, 987, 988; clinical history, 988; 
diagnosis, prognosis, and treatment, 990; 
gait in, 989; respiratory disturbances, 990; 
tendon reflexes in, 989. 

Anaemia, 708; baths in, 719; blood in, 716; 
cardiac murmurs in, 713, 715; classification 
and aetiology of, 708; clinical history of 
chlorosis, 714; diagnosis and prognosis, 716; 
fatty degeneration in, 714; from arsenic, 
711; pernicious form, 710 (see also 719); 
pulse in, 713; relation to iron supply, 710; 
symptomatology of, 711; treatment, 717; 
urine in, 714. 

Anaemia, cerebral, 1066; in Addison's disease, 
652; in gastric ulcer, 436; in pulmonary 
tuberculosis, 247. 

Anaemia, progressive pernicious, 719; blood 
in, 724; bone-marrow in, 721, 723; definition 
and aetiology, 719; diagnosis, 725; digestive 
organs in, 723; fever in, 725; general course, 
duration, and prognosis, 725; haemorrhages 
in, 721; retinal, 722; pathology, 720; re- 
spiratory symptoms, 722; symptoms, 721; 
treatment, 726. 

Anaesthesia, cutaneous, causes of, 799; treat- 
ment, 803. 

Anaesthesia, hysterical, 1175-1177. 

Anaesthesia of the trigeminus, 802 (see also 
Diseases of the Nervous System). 

Analgesia, in hysteria, 1175; in syringomyelia, 
1031. 

Anasarca, in scarlet fever, 43; in cirrhosis of 
the liver, 559. 

Anchylosis in arthritis deformans, 689. 

Anchylostoma, 720; duodenale (see Intes- 
tinal Parasites), 518. 

Aneurism, cardiac, 341; dissecting, 380; mil- 
iary, in cerebral haemorrhage, 1090. 

Aneurism of the abdominal aorta, 379. 

Aneurism, of thoracic aorta, 374; aetiology and 
pathological anatomy of, 374; auscultation 
in, 376; cardiac hypertrophy in, 376; clinical 
symptoms, 375; course and termination of, 
377; diagnosis and treatment, 378; dyspnoea 
in, 377; galvano-puncture in, 379; haemor- 
rhages in, 377; physical signs, 375; Roentgen 



rays, use in, 376; sequelae, 376; syphilis as- 
cause of, 374; venous signs, 377. 

Aneurism, of the trunk of innominate, 379; of: 
the other vessels, 380. 

Angina Ludovici, 392. 

Angina pectoris, 327, 343, 355. 

Angioneurotic oedema, 900. 

Ankle clonus, 948, 1099, 1179. 

Anorexia, in achylia gastrica, etc., 452, 454; in 
acute gastric catarrh, 423; in cholera, 87, 
88; in chronic gastritis, 428, 432; in diph- 
theria, 70; in erysipelas, 64; in relapsing 
fever, 34; in small-pox, 55. 

Anosmia and hyperosniia, 827. 

Anthracosis pulmonum, 271. 

Anthrax, 127; bacillus anthracis, 127, 128, 130;. 
clinical history, 129; convulsions in, 129; 
fever in, 129; infection, 128; inoculation, 
127-130; intestinal, 129; in animals, 127, 128; 
malignant pustule, 129; pathology, diagno- 
sis, and treatment, 130; pulmonary, 130. 

Antipyrine, in articular rheumatism, 686; in 
erysipelas, 67; in migraine, 907; in neu- 
ralgia, 809; in scarlet fever, 47; in septic 
and pyaemic diseases, 122; in small-pox, 62; 
in typhoid, 26. 

Antitoxine, in diphtheria, 74; in plague, 111. 

Anuria, in acute nephritis, 609; in cholera, 89; 
in jaundice, 542. 

Aorta, narrowing of, 380; rupture of, 380; dis- 
secting aneurism, 380; haemorrhage in, 380. 

Aortic stenosis, 320. 

Apex catarrh, 161. 

Aphasia and allied conditions, 1077; agraphia, 
alexia, and amnesia, 1081; amimia, 1080; 
amnesic, 1077 ; anatomical changes occur- 
ring in, 1081; ataxic, 1078; Dejerine's views 
on, 10S2; monophasia and paraphasia, 1079; 
from cerebral embolism, 1105; in haemor- 
rhagic polymeningitis, 1054. 

Aphonia, hysterical, 152, 1178; in laryngeal 
catarrh, 141; in paralysis of the laryngeal 
muscles, 151; in tuberculosis of the larynx, 
148. 

Aphthae, Bednar's, 385. See also Aphthous 
Stomatitis. 

Aphthous stomatitis, 385; Bednar's aphthae, 
385; relation to thrush, 385; treatment, 
385; ulceration in, 385, 386. 

Aplasia of the lungs in kyphoscoliosis. See 
Pulmonary Atelectasis. 

Apoplectic cyst, 1091. 

Apoplexy, meningeal, 919; spinal, 929. 

Appendicitis, 482. 

Arc de cercle, 1183. 

Arhythmic pulse, 314| 328, 342. 

Arsenic, in anaemia and chlorosis, 711, 719; in 
arthritis deformans, 693; in chorea, 1155; 
in leukaemia, 732; in malaria, 101; in 
pulmonary tuberculosis, 254; in pseudo- 
leukaemia, 735. 

Arsenical paralysis, 875; poisoning, 1209; re- 
semblance to cholera, 91. 

Arterio-sclerosis, 370; aetiology of, 370; alco- 
holism in, 370; atheroma, 370; atheroma- 
tous ulcers, 371; cardiac hypertrophy in, 372, 
373; cerebral haemorrhage in, 373; clinical 
symptoms, 372; gangrene in, 373, 374; in-- 



INDEX 



1219 



termittent claudication in, 373; pathological 
anatomy' of , 371; predisposition, 370; pulse, 
372; treatment and prophylaxis, 374; with 
nephritis, 370; in myocarditis, 341. 

Arthralgia in lead poisoning, 1208. 

Arthritis deformans, 688; in acute articular 
rheumatism, 676. 

Arthrogryposis, 881. 

Arthropathy, in tabes dorsalis, 974; in syringo- 
myelia, 1031. 
Articular neuroses, 821. 

Ascaris lumbricoides. See Intestinal Para- 

SITES. 

Ascending spinal paralysis, acute (so-called), 
1021; diagnosis and prognosis, 1023; general 
symptomatology, 1022; pathological anat- 
omy and pathogenesis, 1023; treatment, 1024. 

Ascites, 533; chylous, 534; differential diag- 
nosis, 534; percussion in, 533, 534; respira- 
tion in, 533; tapping in, 535; treatment, 534; 
in cirrhosis of the liver, 558, 560, 562. 

Asiatic cholera, 85. 

Asphyxia stage of cholera, 91. 

Aspiration in pleurisy, 293. 

Associated movements, in encephalitis of 
children, 1112; in hemiplegia, 1100, 1112; in 
paralysis, 837. 

Astasia, 1178. 

Asthenia in Addison's disease, 652. 

Asthenic bulbar paralysis, 1046. 

Asthenic pneumonia, 220, 223. 

Asthenopia, neurasthenic, 1195. 

Asthma, bronchial, 181; Curschmann's spirals 
in, 184; diagnosis, 185; definition and cause 
of, 181; dyspnoea in, 181, 183; expectoration 
in, 184; iodide of potassium in, 186; pro- 
dromata, 183; reflex, 182; symptoms and 
course, 183; treatment, 186. 

Asthma, humidum, 164; hysterical, 185; 
nephritic, 630; thymic, see Spasm of the 
Glottis. 

Asthma crystals, 184; in chronic bronchitis, 163. 

Asthmatic bronchiolitis, see Asthma; pneu- 
monia, 220, 223. 

Ataxia, 837 ; acute, curable, see Multiple 
Neuritis; alcoholic, 893, 894; after small- 
pox, 58; cerebellar, 1086; forced movements 
and positions in cerebellar, 1087; hereditary 
cerebellar, 984; hereditary juvenile, 9S1; 
locomotor, see Tabes Dorsalis; in multiple 
sclerosis, 955; in myelitis, 947; in poly- 
neuritis, 890, 892. 

Ataxic aphasia, 1078. 

Ataxic paraplegia, 1011. 

Atelectasis, lobular, 233; pulmonary, 195. 

Atheroma of the vessels. See Arterioscle- 
rosis. 

Athetosis, 836, 1161: movements of, 1161; 

symptomatic and idiopathic forms, 1162. 
Athrepsia in intestinal catarrh of children, 

479. 

Atony of the stomach, 460. 

Atrophy, granular, of the kidney, 625; neu- 
rotic muscular, 996; of facial muscles, 1003; 
of interossei, 868; of lips, 1040; of the liver, 
579; of liver (acute yellow), 565; of mucous 
membranes in chronic bronchitis, 163; of 
muscles in progressive bulbar paralysis, 



1040; of pancreas, 585; of small muscles of 
hand, 992; spinal progressive muscular, 990. 

Atropine for salivation, 1044; in acid dys- 
pepsia, 459; in neuralgia, 809; in paralysis 
agitans, 1160; poisoning, 1211. 

Aura, epileptic, 1143. 

Babinski reflex, 839, 940, 989, 1096. 

Bacilli anthracis, 127, 128, 130; icteroides, 104; 
of cholera, 85; of glanders, 125; of influenza, 
77; of tuberculosis, 227, 228, 231, 232, 234, 
240, 489; pestis bubonicse, 107, 108; smegma, 
633; typhoid, 1. 

Bacillus of tetanus, 1165. 

Bacteria, diphtheritic, 68, 69, 71, 73; in acute 
catarrh of trachea and bronchi, 157-159; in 
catarrhal pneumonia, 200; in cystitis, 668, 
669; in endocarditis, 304; in foetid bron- 
chitis, 167; in peritonitis, 521; in pleurisy, 
281, 290; in pulmonary gangrene, 268; in 
purulent nephritis, 640; in sore throat, 394; 
in suppurative hepatitis, 553, 554; in variola. 
54. 

Bacterium coli commune, 544, 548. 
Balanitis in diabetes mellitus, 757. 
Balneo-therapeutics in typhoid, 24, 25. 
Barlow's disease, 743. 
Basilar artery, thrombosis of, 1050. 
Basilar meningitis. See Tubercular Menin- 
gitis. 

Basedow's disease. See Exophthalmic 
Goitre. 

Baths, in acute nephritis, 615, 617; in anaemia 
and chlorosis, 719: in arthritis deformans, 
693, 694; in bronchial catarrh, 161, 162; in 
cardiac hypertrophy, 350; in catarrhal pneu- 
monia, 204; in cerebro-spinal meningitis, 116; 
in croupous pneumonia, 224, 226; in heart 
disease, 335; in muscular rheumatism, 697; 
in myelitis, 952; in polyneuritis, 892; in pul- 
monary atelectasis, 197; in scarlet fever, 47; 
in small-pox, 61, 62; in tabes dorsalis, 980; 
in typhoid, 24; in typhus, 33; in yellow 
fever, 106. 

Bednar's aphthae, 385. 

Bedsores, in cerebral haemorrhage, 1100; in 

small-pox, 58; in typhoid, 23. 
Belladonna poisoning, 1211; in enuresis, 674. 
Bell's palsy. See Facial Paralysis. 
Benzine in trichinosis, 134. 
Beri-beri. See Endemic Multiple Neuritis. 
Bile ducts, cancer of, 572; diseases of, 536. 
Bilharzia haematobia, 646. 

Biliary calculi, 543; aetiology of, 543; anatomi- 
cal and clinical results of, 545; bacterium 
coli commune, 544; biliary colic, 546; 
causes of colic in, 547; changes in gall blad- 
der, 547; chemical and physical properties 
of, 545; cholelithiasis, 544; composition 
of. 543; diagnosis, 549; hepatic calculi, 
545; narcotics in, 551, 552; occurrence, 545; 
predisposition, 544; prognosis, 550: sequelae, 
549; sex, influence of, 544: treatment, 551. 

Biliary and hypertrophic cirrhosis of the liver, 
562. 

Bilious pneumonia, 210. 

Bisulphide of carbon poisoning, 1210. 

Bitter almond poisoning, 1210. 



1220 



INDEX 



Black death. See Plague. 

Black small-pox, 59. 

Black vomit in yellow fever, 105, 106. 

Bladder, cancer of, 672; diseases of, 654; irri- 
gation of, in cystitis, 671, 672. 

Bladder, new growths in, 672; cancer of, 672; 
cystoscopy in, 672; papilloma of, 672. 

Bleeders. See Hemophilia. 

Blennorrhcea, bronchial, 164. 

Blepharospasm, 877. 

Blood and tissue metamorphosis, diseases 
affecting, 708. 

Blood changes, in cholera, 90: in typhoid, 18; 
corpuscles in urine, 594; -fluke, 646; in 
anaemia and chlorosis, 716, 724; in gastric 
contents, 422; in haeinoglobinaeniia, 737; in 
leukaemia, 729; in malarial diseases, 94; in 
relapsing fever, 33; in septic and pyaemic 
diseases, 120; in trichinosis, 133. 

Blue vitriol poisoning, 1208. 

Bone-marrow, in leukaemia, 728; in pernicious 
anaemia, 721. 

Bones, affection of, in typhoid, 19. 

Borborygmi in intestinal catarrh, 470. 

Bothriocephalus latus, 511. 

Bottger's test for sugar, 753. 

Botulismus, 1212. 

Bradycardia from scarlet fever, 45. 

Brain, abscess of, 1106 (see also Brain, In- 
flammation or). 

Brain, disturbances of circulation in, 1066; 
anaemia, 1066; hyperaemia, 1067; syncope, 
1066. 

Brain, embolism and thrombosis, 1103; 
aetiology and pathology, 1103: aphasia in, 
1105; clinical history, 1104; diagnosis, 1106. 

Brain, haemorrhage of, 1089; aetiology, 1089; 
acute malignant decubitus, 1100; apoplectic 
cyst, 1091; associated movements, 1100; 
clinical history, 1091; diagnosis, 1101; func- 
tional disturbances, 1094, 1095; hemiplegia 
in, 1095, 1097, 1098, 1100; miliary aneurisms 
in, 1090; muscular atrophy in, 1101; pa- 
thology of, 1091; prodromata, 1092; prog- 
nosis and treatment, 1102; reflexes in, 1096; 
symptoms, 1094, 1095; urine in. 1094. 

Brain, haemorrhage of, in arterio-sclerosis, 
373. 

Brain, hydatids of, 1124. 

Brain, hyperaemia Of, 1066. 

Brain, idiopathic softening of, 1110. 

Brain, inflammation of, 1106; aetiology, 1106; 
aphasic disturbances, 1109; clinical history. 
1108; diagnosis, 1109; general and focal 
symptoms, 1108; infection, 1106; pathology 
of, 1107; treatment, 1110. (See also acute 
and chronic encephalitis, 1110: acute en- 
cephalitis of children, 1111: cerebral paraly- 
sis of children, 1111; curable form of en- 
cephalitis, 1110; diffuse cerebral sclerosis, 
1110; idiopathic softening of the brain, 1110.) 

Brain, lesions in, topical diagnosis of, 1068. 

Brain, multiple sclerosis of, 954. 

Brain, sclerosis of, diffuse, 1110. 

Brain, symptoms in tabes dorsalis, 976. 

Brain, syphilis of, 1125: aetiology of, 1125; 
arteries in, 1126, 1127; basal cerebral syph- 
ilis. 1127; clinical history. 1127; complica- 



tions, 1128; diagnosis, prognosis, and treat- 
ment, 1128; formation of syphiloma, 1127; 
pathology of, 1126; symptoms, 1127. 

Brain, tumors of, 1115; aetiology, 1115: 
cysticerci in, 1125; epileptiform convul- 
sions, 1118; general course and diagnosis, 
1122; general symptoms, 1117; glioma, 
1116; gumma and solitary tubercle, 1116; 
hydatids of the brain, 1124; location of 
tumor and focal symptoms, 1119-1122; 
optic neuritis, 1118; prognosis, 1123: 
psammoma, 1116; sarcoma and carcinoma, 
1116; treatment, 1124; tubercular growths 
in, 1124; varieties of, 1116. 

Brand's method in typhoid, 24. 

Bright*s disease. See Nephritis. 

Bromide of sodium in gastroxynsis, 460. 

Bromides, in chorea, 1156; in epilepsy, 1149. 

Bromine poisoning, 1207.' 

Bromism, 1207. 

Bronchial dilatation. See Bronchiectasis, 
176. 

Bronchial rales, 159. 
Bronchial stenosis, 181. 

Bronchiectasis, 167; cylindrical, 176; expecto- 
ration in, 178: pulmonary haemorrhages in, 
179; rales in. 177; relation to tuberculosis, 
178, 179; saccular, 177; terminal phalanges 
thickened in, 179; treatment, 179. 

Bronchiolitis, exudative. See Asthma. 

Bronchitis, acute, 156: aetiology, 156; bac- 
teria in, 157, 159; baths, 161; bronchial 
catarrh, 156; capillary bronchitis, 160; 
catarrh of the finer bronchi, 160; cough in, 
158; diagnosis and treatment, 161; expecto- 
ration of, 158; fever in, 159; infectious 
causes and irritating inhalations, 157: 
milder forms of, 159; pains in, 158; physical 
examination in, 158; predisposition to, 157; 
rales and rhonci in, 159; respiration in, 160; 
secondary bronchitis, 157; severer febrile 
forms of, 159: symptoms, 157; tracheitis, 157. 

Bronchitis, chronic, 162; aetiology of, 162: 
asthma humidum, 164; atrophy of mucous 
membranes in, 163; bronchial blennorrhcea 
in. 164; chronic bronchial catarrh, 162; 
course of the disease, 164; diagnosis, prog- 
nosis, and treatment, 165; dry chronic 
catarrh in, 164: emphysema of lungs in, 
162; expectoration of, 163, 164; in renal dis- 
eases, 162; noxious inhalations, effect of, 
162; pathological anatomy of, 163: physical 
examination in. 163: rales in, 163; serous 
bronchorrhcea, 164. 

Bronchitis, croupous, 170; aetiology of, 170: 
casts of bronchi, 171: chronic form of, 171; 
dyspnoea in, 170, 171; in typhoid. 170: 
pathological anatomy of, 171; prognosis, 171; 
spirals in sputum, 171; symptoms and 
course, 170: treatment, 172. 

Bronchitis. fibrinous. See Bronchitis, 
Croupous. 

Bronchitis, foetid, 167; aetiology of, 167; ana- 
tomical changes, symptoms and course of, 
167; bacteria of, 167: bronchiectasis, 167; 
Dittrich's plugs, 168; expectoration. 167: 
fatty acid crystals, 16S; fever in, 167; gan- 
grene in, 168, 169; inhalations in. 170: pueu- 



INDEX 



1221 



monia, 168; sputum of, 16S; symptoms, diag- 
nosis, prognosis, and treatment, 169. 

Bronchitis, in glanders, 126; in erysipelas, 66; 
in relapsing fever, 34; secondary, 157. 

Bronchitis, putrid. See Bronchitis. 

Broncho-pneumonia. See Pneumonia, Ca- 
tarrhal. 

Bronchophony, in catarrhal pneumonia, 203- 
212; in pleurisy, 287. 

Bronchorrhoea, serous, 164. 

Bronzed skin. See Addison's Disease. 

Brown induration of the lungs, 275; cells of 
heart disease, 176; dyspnoea in, 276; sputum 
in, 276. 

Bruit. See Murmurs. 

Bubonic plague. See Plague. 

Bulbar paralysis, acute and apoplectiform, 
1048; chronic and asthenic, 1045. 

Bulbar paralysis, progressive, 1039; aetiology 
and clinical history of, 1039; diagnosis, 1043; [ 
muscular atrophy in, 1040; pathology of, 
1042; prognosis and treatment, 1044; saliva- 
tion in, 1041. 

Bulbous pulse, 332. 

Butyl chloral in neuralgia of trigeminus, 813. 

Cachexia, chronic malarial, 99; in dysentery, 

83; strumipriva, 901, 913. 
Caecum, inflammation of. See Typhlitis 

and Perityphlitis. 
Caffeine in valvular heart disease, 337. 
Caisson disease, 932. 

Calculi, biliary, 543; faecal, 483; intestinal, 
500; pancreatic, 587; renal, 567, 568. 

Calomel, in cardiac dropsy, 338; in cholera 
morbus, 477; in dysentery, 83: in intestinal 
catarrh, 481; in relapsing fever, 38; in tuber- 
cular meningitis, 1064; in typhoid fever, 23. 

Camp fever, 31. 

Camphorated oil in typhoid, 28. 

Cancer, colloid, 445; of the intestines, 491; of 

the small intestines, 492. 
Cancer of the caecum, 492. 

Cancer, of the colon, 492; of the kidney, 644; 
of the larynx, 156. 

Cancer of the liver and bile ducts, 572; 
aetiology and pathology of, 572; clinical his- 
tory, 573; diagnosis, 573, 574; histological 
structure of, 573; jaundice in, 574; melanotic 
sarcoma, 574; palpation and percussion in, 
573; relation to biliary calculi, 573; syphilitic 
growths, 574; tumors in, 573. 

Cancer of the lungs, 276; expectoration of, 
277; sequelae, 278. 

Cancer of the oesophagus. 412; aetiology and 
pathology of, 412; clinical history, 414; gan- 
grene, pulmonary, in, 413. 414: prognosis and 
treatment, 414: symptoms and complica- 
tions, 413; termination, 414; ulceration of, 
413. 

Cancer of the pancreas, 5S6. 

Cancer of the peritoneum, 535; colloid cancer 
of, 535, 536; diagnosis, 536; inflammation in, 
536; miliary carcinosis, 535; symptoms and 
treatment, 536. 

Cancer of the pleura, 300. 

Cancer of the stomach, 444; aetiology of, 444; 
blood in, 448; diagnosis, 449; gastric con- 



tents in, 447; hepatic growths in, 448; palpa- 
tion and percussion in, 446; pathology of, 
445; sarcinae in, 446; treatment, 451; ulcera- 
tion in, 445. 

Cancer of the vertebrae, 941. 

Cancrum oris. See Noma. 

Cantharides as cause of cystitis, 668. 

Capillary bronchitis, 160; congestion in yellow 
fever, 105, 106. 

Carbolic acid, in erysipelas, 67; in foetid bron- 
chitis. 170: in scarlet fever, 47; in typhoid, 
28; poisoning, 1211. 

Carbolic mask, 170, 270. 

Carbon in the lungs. 271. 

Carbonates of lithia and soda in nephro- 
lithiasis, 661. 

Carbonic oxide gas poisoning. 1210. 

Cardiac neuroses, 355; angina pectoris, 355, 
356; cardiac neuralgia, 355; nervous palpita- 
tion, 356; prognosis and treatment, 357; 
pulse in, 355; stenocardia, 355; tachycardia, 
357. 

Cardialgia, in gastritis, 426; in gastric ulcer, 
435. 

Caries of vertebrae, 934. 

Casts of the bronchi in croupous bronchitis, 

171, 210. 
Casts, urinary, 592, 593. 

Catalepsy, 1170; anaesthesia in, 1171: progno- 
sis and treatment, 1171; relation to hys- 
teria, 1171. 

Catarrh, of bronchi, 156; gastric, 422; intes- 
tinal. 468: laryngeal, 140; of trachea. 156; 
vesical, see Cystitis. 

Catarrhal inflammation of the mouth, 383. 

Catarrhal jaundice. 536. 

Catarrhal pneumonia, 199. 

Catarrhal sore throat, 395. 

Catarrhal stomatitis, 382. 

Caustic potash or soda poisoning, 1207. 

Cephalalgia. See Habitual Headache. 

Cephalic cry of children in tubercular menin- 
gitis, 1063. 

Cephalic tetanus, 1167. 

Cerebellar ataxia, hereditary, 984: and ver- 
tigo, 1086. 

Cerebellum, 1086; forced movements and posi- 
tions, 1087. 

Cerebellum, tumors of. 1121. 

Cerebral diseases, localization of, 1068. 

Cerebro-spinal fever. See Meningitis, Cere- 
brospinal. 

Cervico-brachial neuralgia, 814. 

Cestodes, 508. 

Chalicosis pulmonum, 271. 

Charbon. See Malignant Pustule. 

Charcot's crystals, 184: in leukaemia, 72S. 

Cheese, poisoning from, 1213. 

Cheyne-Stokes, breathing in heart disease, 
333. 

Chicken-pox. See Varicella. 
Cinchonism in malarial diseases, 102. 
Chloral amide in heart diseases, 338, 356. 
Chloral hydrate in heart disease. 338. 
Chlorate of potassium, in cystitis. 671: in 

genito-urinary tuberculosis. 664. 
Chlorine gas poisoning. 1207. 
Chloroform in hydrophobia, 124. 



1222 



INDEX 



Chloroform poisoning, 1210. 
Chlorosis, 70S. 

Choked disk, in cerebral syphilis, 1127: in 
chronic hydrocephalus, 1138; in tumor of 
brain, 1118. 

Cholsemia, 569. 

Cholelithiasis. See Biliaey Calculi. 

Cholera, 85; abdomen in, 88; absorption im- 
paired, 93; anorexia in, 87, 88; blood in, 90; 
catarrhal inflammation in, 90, 91, sicca, 88; 
typhoid, 89; choleraic diarrhoea, S7; choler- 
ine, 87; circulatory system in, 88; clinical 
history, 87; comma bacillus, 85; complica- 
tions, 91; dejections of, 88; diagnosis, prog- 
nosis, prophylaxis, and treatment, 91: diet, 
92; disinfection in, 91, 92; history, 85; 
immunity, 87; in animals, 86; infection, 86; 
mortality, 91; muscular cramp in, 89: nerv- 
ous symptoms, 89; pathology and patho- 
genesis, 90; Peyer's patches in. 90; predis- 
posing causes, 87; relation to ground water, 
87; temperature in, 88; urine in. 87, 89. 

Cholera infantum. See Cholera Morbus. 

Cholera morbus, 475; diagnosis, 476; fever in, 
476; infection, 475; symptoms, 475: tem- 
perature in, 476; treatment, 477. 

Cholera nostras. See Cholera Morbus. 

Cholera sicca, 88. 

Cholitis, chronic, from dysentery, 83. 
Chorditis, tuberosa, 143. 

Chorea, 1152; aetiology,. 1152; causation, 1152; 
chronic hereditary, 1156; clinical history, 
1153: diagnosis, prognosis, and treatment, 
1154; electrical, 1156; hydrotherapeutics and 
electricity in, 1156; motor disturbances. 1153, 
1154; nature of the disease, 1155: tendency 
to valvular cardiac disease, 1154. 

Chorea, chronic hereditary. 1156; Hunting- 
ton's, 1156. 

Chorea, post-hemiplegic, 1100. 

Chyluria, 646. 

Cicatricial contraction of the stomach, 434- 
438. 

Cirrhosis, biliary, 562. 

Cirrhosis of the liver, 555: aetiology and 
pathology of, 555: ascites in, 558, 560, 562; 
cerebral symptoms, 560; clinical history, 557; 
diagnosis and prognosis, 560: diet in, 561; 
haemorrhage in, 558; influence of alcohol in, 
556: intestinal symptoms, 55S; spleen in, 
558: treatment, 561; venous stasis in. 557. 

Clap-threads in cystitis, 670. 

Claudication, intermittent, in sclerosis, 373. 

Clownismus, 1184. 

Coagulation necrosis in small-pox. 57. 

Coccygodynia, 820. 

Colchicum in gout, 779. 

Cold in the head. See Coryza. 

Cold pack in measles, 52; in typhoid. 26. 

Cold-water treatment in epilepsy, 1150. 

Colic, hepatic, see Biliary Calculi: in 

dysentery, 82; mucous, 474. 
Colon, cancer of, 492; clinical symptoms, 491; 

shape of faeces in, 492; ulceration in, 491. 
Coma, in cholera, 90; diabetic, 578, 579; 

uraemic, 597. 
Comma bacillus, 85. 
Compensated pyloric stenosis, 439. 



Compression of the lungs. See Pulmonary 

Atelectasis. 
Compression of medulla, 1052. 
Compression of spinal cord, 934. 
Condurango in chronic gastritis, 431. 
Coniine poisoning, 1211. 

Conjunctivitis, in scrofula, 787; from measles, 
50. 

Constipation, habitual. 495: dejections in, 497: 
injections, 497, 498; relation to neuras- 
thenia. 496: treatment, 497. 

Constitutional diseases, 708. 

Consumption, of the larynx, see Tubercu- 
losis op the Larynx; pulmonary, see 
Tuberculosis. 

Contagious carbuncle. See Malignant Pus- 
tule. 

Contractures, hysterical, 1179; law of, 844. 
Convulsions, epileptic vs. hysterical, 1188; 

epileptiform, from cerebral tumor, 1118; 

hysterical vs. epileptic, 1188; infantile, 1151; 

in cholera, 90; in hydrophobia, 123, 124; in 

malarial diseases, 98; in plague, 109. 
Copper poisoning, 1208. 
Coprolalia in hysteria, 1187. 
Corpora amylacea in tabes dorsalis, 964. 
Corpulence. See Obesity. 
Corrigan's pulse, 319. 
Corrosive sublimate poisoning, 1208. 
Corset liver, 581. 

Cortex cerebri, motor region of, 1069. 
Coryza, 135; dyspnoea in, 136; hay fever, 135; 

headache, 136; infection, 135; treatment. 

136; cause of erysipelas, 64; diphtheritic. 70: 

in influenza, 78. 
Cough in bronchitis, 158; in tuberculosis. 

237. 

Cramps, muscular, in cholera, 89, 90. 

Creasote in foetid bronchitis, 170; in intes- 
tinal catarrh, 481; in tuberculosis of lungs. 
254. 

Cretinism, 901. 

Croup. See Diphtheria. 

Curare in hydrophobia, 124. 

Curschmann's spirals, 184. 

Cyanosis in valvular heart disease, 323, 330. 

Cynanche contagiosa, see Diphtheria; gan- 
grenosa, 392. 

Cysticercus cellulosse. 509; in the brain. 1225: 
racemosus, 510. 

Cystitis, 667; aetiology of, 667; bacteria in. 668. 
669; cantharides in. 668; clinical symptoms. 
668; infection. 667; pathological anatomy, 
668: treatment and prophylaxis, 670: urine 
in, 669. 

Cystitis in typhoid, 19.' 

Cystoscopy, 672. 

Cysts, apoplectic, 1091; echinococcus, 27S: 
echinococcus of the kidney, 646; in larynx. 
. 155: pancreatic, 586. 

Dandy fever. See Dengue. 

Decubitus, acute malignant, 1100. 

Degeneration, fatty, in anaemia. 714. 

Degeneration of muscles and nerves, anatomi- 
cal changes in, 849; reaction of. 848-850. 

Delirium, in cholera. 90: in croupous pneu- 
monia, 215; in erysipelas. 65: in small-pox. 



INDEX 



1223 



o5; in tubercular meningitis, 1061; tremens, 
1210. 

Delivery paralyses, 869. 

Dementia, paralytic and paretic, 1129. 

Dengue, 102; aetiology and pathology of, 103; 
diagnosis, prognosis, and treatment, 103; 
prodromata, symptoms and course of, 103. 

Dentition, anomalies of, 392; nervous disturb- 
ances in, 393. 

Desquamation, in measles, 49; in scarlet fever, 
42, 44. 

Diabetes insipidus, 767; clinical history, 768; 
diagnosis, 769; definition and aetiology, 767; 
post-mortem appearances, 769; treatment, 
770; urine in, 768. 

Diabetes mellitus, 748; abnormal appetite in, 
755; acromegaly in, 750; alcoholism, 750; 
circulatory symptoms in, 756; clinical his- 
tory, 751; coma in, 758; constitutional 
symptoms in, 755; cutaneous affections in, 
757; definition and aetiology of, 748; diag- 
nosis and treatment, 763; diet in, 763; 
digestive symptoms in, 755; exercise in, 766; 
genito-urinary symptoms in, 756; glycosuria 
in, 749; hereditary influence, 750; kidneys 
and liver in, 760; nature of, 762; nervous 
system in, 757; organs of special sense in, 
757; oxybutyric acid in, 754; pathological 
anatomy and histo-chemistry of, 759; pruri- 
tus in, 757; pulse in, 756; respiratory symp- 
toms in, 756; sources of sugar and variations 
in, 754; sugar tests in, 752; urine in, 752; 
varieties, course, and prognosis of, 760. 

Diabetes mellitus, effect on gastric juice, 453; 
relation to pulmonary gangrene, 267. 

Diaphoresis in acute nephritis, 615. 

Diaphragm, clonic spasm of, 882; paralysis of, 
871. 

Diarrhoea, in intestinal catarrh, 469; in 
intestinal tuberculosis, 489; in pulmonary 
tuberculosis, 249; in typhoid, 10, 28; in 
whooping-cough, 174; septic, 121. 

Dicrotism in typhoid, 17. 

Diet, in cancer of the stomach, 451; in catar- 
rhal jaundice, 541; in cholera, 92; in chronic 
gastritis, 429; in cirrhosis of liver, 561; 
in croupous pneumonia, 226; in diabetes mel- 
litus, 763; in diphtheria, 75; in dysentery, 
83; in gastric ulcer, 441; in gout, 778; in 
interstitial myocarditis, 344; in intestinal 
catarrh, 474; in measles, 52; in nephro- 
lithiasis, 661; in pulmonary tuberculosis, 
257; in scarlet fever, 46; in symptomatic 
achylia, 455; in typhoid, 23. 

Digitalis, in croupous pneumonia, 225; in valv- 
ular heart disease, 335; poisoning, 1211. 

Diphtheria, 67; aetiology and general pa- 
thology of, 67; cardiac weakness in, 72; 
causes of, 68; clinical history. 69; con- 
tagiousness, 69; croup, 68; ascending croup, 
70; false croup, 141: diagnosis. 73: diph- 
theritic coryza, 70; diphtheritic paralysis, 
72; in animals, 69: incubation, 69; laryngeal, 
70; micro-organisms of, 68; nephritis in, 
72; nervous sequelae, 72; of the external 
genitals, 72; pharyngeal, 68; pneumonia 
(lobular), 72; prognosis and treatment, 74: 
prognosis of nervous sequelae, 73; prophy- 



laxis, 76; relation of filth to, 69; serum in- 
jection and treatment, 74; sopor, 71; source 
of infection, 69; temperature in, 70; toxines, 
69, 71, 73; tracheotomy in, 69, 74, 76. 

Diphtheritic ocular paralysis, 857. 

Diplegia facialis, 1045. 

Diplegia, infantile spastic, 1012. 

Diplococci, in cerebro-spinal meningitis, 111; 
diplococeus pneumoniae, 205, 206, 208, 210, 
215, 219. 

Diplococci, in influenza, 79; in pleurisy, 280; 

in sore throat, 394; in tuberculosis, 234. 
Diplococeus pneumoniae, 205. 
Disinfection, in cholera, 91; in plague, 108; 

in small-pox, 60; in typhoid, 28; in yellow 

fever, 106; of sputum in foetid bronchitis, 

170. 

Dittrich's plugs in foetid bronchitis, 168. 
Diuretics, in acute nephritis, 616; in pleurisy, 
292. 

Drinking water as cause of typhoid, 2. 

Dropsy, in pulmonary emphysema, 191; of 
renal disease, 594, 610, 617, 622, 638; tho- 
racic, 299. 

Drunkard's pneumonia, 218. 

Dubini's disease, 1157. 

Duodenum, cancer of, 493; perforating ulcer 
of, 488. 

Dura mater, haematoma of, 1053; aetiology and 
pathology of, 1053; aphasia in, 1054; diag- 
nosis and treatment, 1055; symptoms, 1054. 

Dust, diseases from inhalation of, 270. 

Dysentery, 81; aetiology of, 81; amoebae coli 
in, 81; bacteria, 82; clinical history, 82; 
complications, diagnosis, prognosis, treat- 
ment, and prophylaxis, 83; diet, 83; diph- 
theritic and catarrhal forms, 81; gangrenous 
form, 81; infection, 81; in animals, 81; sec- 
ondary, 82; tenesmus in, 82. 

Dyspepsia, chronic, of children, see Intes- 
tinal Cataeeh of; anaemic, 722; gouty, 
774; nervous, 463; with hyperacidity, 456; 
with hypersecretion of gastric juice, 457. 

Dysphagia in stenosis of the oesophagus, 409, 
410. 

Dyspnoea, from heart disease, 276; in anthrax, 
128; in aortic aneurism, 377; in bronchial 
asthma, 181, 183, 185; in cancer of the lungs, 
277; in chronic bronchitis, 163; in coryza, 
136; in croupous bronchitis, 170; in croupous 
pneumonia, 208; in diphtheria, 70; in hydro- 
thorax, 299; in mediastinal tumors, 301: in 
miliary tuberculosis, 262; oedema of the 
glottis, 146; in pericarditis, 361; in pleurisy, 
283, 293; in pulmonary emphysema, 190; 
in pulmonary gangrene, 268; in pulmonary 
oedema, 197; in pulmonary tuberculosis, 241; 
in retropharyngeal abscess, 403; in scar- 
let fever, 41; in spasm of the glottis, 154; in 
tabes dorsalis, 974; in tracheal stenosis, 180; 
in valvular heart disease, 326, 333. 339. 

Dystrophy, progressive muscular, 998; infan- 
tile, 1002; diagnosis and treatment of, 1005; 
infantile form of, 1002; juvenile form of, 
1003. 

Ecchymosis, cutaneous, in malarial diseases, 
•99; in purpura, 744: in small-pox. 59: in ty- 



1224 



INDEX 



phoid, 18; in acute yellow atrophy of liver, 
567. 

Echinococcus of the kidney, 646. 

Echinococcus of the liver, 575; clinical symp- 
toms, 576; complications, 576; diagnosis and 
treatment, 577; hepatic abscess, 577; hydatid 
cysts, 575; infection, 575; natural his- 
tory and pathology, 575; rupture, 576; sup- 
puration, 577; taenia echinococcus, 575. 

Echinococcus of the lungs, 276; multilocularis, 
577; expectoration, 278; symptoms of, 278. 

Echolalia in hysteria, 1187. 

Eclampsia infantum, 1151; in dentition, 393; 
uraemic, 599. 

Ectasis, alveolar. See Pulmonary Emphy- 
sema. 

Ehrlich's reaction in typhoid, 19; test (foot- 
note), 19. 

Elastic fibers in tuberculosis expectoration, 

240, 268. 
Electrical chorea, 1156. 

Electrical excitability in motor nerves and 
muscles, 842. 

Electricity, in cerebral haemorrhage, 1102; in 
cutaneous anaesthesia, 803; in enuresis, 674; 
in gastroptosis, 463; in hysteria, 1190; in 
hysterical aphonias, 153: in muscular 
rheumatism, 697; in myelitis, 952; in nerv- 
ous dyspepsia, 467; in neuralgia, 808; in 
neurasthenia, 1199; in progressive bulbar 
paralysis, 1044; in sciatica, 819; in tetany, 
1165. 

Embolic infarction in the kidneys, 643. 
Embolic processes in the lungs, 273; aetiology 

of, 273; expectoration of, 274; haemorrhagic 

infarction, 273; pathological anatomy and 

symptoms, 274. 
Embolic processes in valvular heart disease, 

331. 

Embolism and thrombosis of basilar artery, 
1050; cerebral, 1103. 

Emphysema, in rupture of oesophagus, 414; of 
lungs in chronic bronchitis, 162, 188; of lungs 
in croupous bronchitis, 171; pneumonia in, 
219; pulmonary, 187; pulmonary, after 
whooping-cough, 174, 189; pulmonary (vicari- 
ous), 181; vicarious, in pleurisy, 288. 

Empyema in septic and pyaemic diseases, 
120. 

Encephalitis, acute and chronic non-suppu- 
rative, 1110; acute haemorrhagic, 1113; cur- 
able form of, 1110. 

Encephalitis of children, acute, 1111; asso- 
ciated movements in, 1112. 

Encephalitis, suppurative, 1106. 

Enchondroma of lungs, 277. 

Endarteritis chronica deformans, see Ar- 
terio-sclerosis; syphilitic, 341. 

Endocarditis, acute, 304; abscesses, 306; 
aetiology of, 304; bacteria in, 304; diag- 
nosis, 307; diphtheritica, 305; embolism, 
305; fever in, 307; haemorrhages, 306; 
inoculation and infection, 304; malignant, 
non-septic form, 306; pathological anatomy 
of, 305; prognosis and treatment, 308; pulse, 
306; recurrent form and septic ulcerative 
form, 307; ulcerosa, 305; verrucosa, 305, 306. 

Endocarditis, chronic, see Valvular Disease 



op the Heart; septic ulcerative, 307; rheu- 
matic, 679: ulcerosa and verrucosa, see 
Endocarditis. 

Endothelioma of the lungs, 277. 

Enemata, in dysentery, 83; in intestinal ob- 
structions, 507; in jaundice, 541; of air, 507. 

Enteric fever. See Typhoid. 

Enteritis, see Intestinal Catarrh; mem- 
branous, 474. 

Enuresis nocturna, 673. 

Epilepsy, 1141; aetiology, 1141; causative fac- 
tors, 1142; clinical history, 1143; clonic 
spasms in, 1144: cortical origin of, 1148; 
diagnosis, 1148 (see also 1188); eclampsia 
infantum, 1151; epileptic aura, 1143; gen- 
eral course of, 1145; hereditary influence, 
1141; infantile convulsions, 1151; milder and 
rudimentary forms, 1144; pathology of, 1147; 
petit mal, 1144; prodromata, 1143; prog- 
nosis, 1147; reflex, 1142; relation to physical 
degeneracy, 1146; stages of the paroxysm, 
1143; traumatic form, 1142; treatment, 1149; 
treatment during paroxysm, 1150; urine in, 
1144. 

Epilepsy, Jacksonian, partial or cortical, 1072. 
Epistaxis, see Nosebleed; in malarial dis- 
eases, 99; in relapsing fever, 37; in typhoid, 8. 
Erethism, mercurial, 1208. 

Ergot, in caisson disease, 933; poisoning, 1212. 
Ergotine injections, in aortic aneurisms, 379; 

in pulmonary tuberculosis, 260; in typhoid, 

23. 

Ergotism, chronic, 1212. 

Eruptions, in small-pox, 55: in typhus, 32. 

Erysipelas, 63; clinical history of, 64; compli- 
cations, 66; contagiousness, 64; diagnosis, 
prognosis, and treatment, 66; erysipelas 
migrans, 65; fever in, 65; inoculation, 64; 
in drunkards, 66; in the newborn, 63; intes- 
tinal disturbances, 66; recurrence of, 64; 
skin in, 64; temperature in, 65. 

Erysipelas in small-pox, 58. 

Erythema of small-pox, 55. 

Erythromyelalgia, 900. 

Ethyl-chloride spray in intercostal neuralgia,. 
816. 

Eucalyptus oil in leukaemia, 733. 

Eustrongylus gigas, 647. 

Exalgine in chorea, 1156. 

Exfoliation in scarlet fever, 39. 

Exophthalmic goitre, 909; aetiology of, 909; 
course and diagnosis of, 913; pathological 
anatomy and pathogenesis, 912; pulse in, 
910: relation to mental excitement, 910; 
symptomatology, 910 ; treatment, 914; tremor 
in, 911. • 

Eyes, disturbances in tabes dorsalis, 972; dis- 
turbances in erysipelas, 66; strain of, in ha- 
bitual headache, 825; strain of, in migraine, 
905; symptoms in acute miliary tuberculosis, 
265: symptoms in tubercular meningitis, 
1061. 

Face-ache. Fothergill's. See Neuralgia of 

Trigeminus. 
Facial hemiatrophy, 908. 

Facial muscles and muscles of mastication- 
851. 



INDEX 



1225 



Facial paralysis. S5S; aetiology, 858; diagnosis, 
prognosis, and treatment, 862: symptoms 
and course of, 859: various forms of, 861. 

Facial spasm, clonic, 876. 

Facial tic. See Clonic Facial Spasm. 

Faecal calculi, 483. 

Faeces in diphtheria, 68. 

Fainting. See Cerebral An.emia. 

Falling sickness. See' Epilepsy. 

Famine fever, 31. 

Farcy. See Glanders. 

Fastigium in typhoid, 6, 21. 

Fat in urine, 594. 

Fatty acid crystals in sputum, 168. 

Febrile jaundice, acute, 542. 

Febris recurrens. See Relapsing Fever. 

Fehling's test for sugar, 753. 

Fermentation test for sugar, 753. 

Ferric hydrate in arsenic poisoning, 1209. 

Fever, anaemic, 436: and ague, see Malarial 
Diseases: break-bone. 102: intermittent, 
96; in acute articular rheumatism, 677; in 
acute catarrh of trachea and bronchi, 159; 
in laryngeal catarrh, 141; in catarrhal pneu- 
monia, 201, 216; in cerebro-spinal menin- 
gitis, 114; in cholera, 88: in diphtheria. 
70: in endocarditis, 307; in erysipelas, 65; 
in foetid bronchitis, 167: in glanders, 125, 
126; in influenza. 78: in malignant pus- 
tule, 129; in measles. 50: in plague, 108: in 
pleurisy, 284; in pulmonary tuberculosis, 
246. 253. 260; in purulent meningitis, 
1058: in rheumatism. 677: in septic and 
pya?mic diseases. 119: in small-pox, 55; in 
typhlitis and perityphlitis. 484: in typhoid. 
6, 15, 20, 24: in varicella. 62: splenic, see 
Malignant Pustule; thermic, see Insola- 
tion; typho-malarial. 100: yellow. 104. 

Fibrillary contractions in neurotic muscular 
atrophy, 997. 

Fibroid phthisis, 243. 

Fibroma of larynx. 155. 

Filaria sanguinis, 647. 

Filth, relation to diphtheria, 69; relation to 

plague, 107. 
Fish, poisoning from. 1213. 
Flajam's disease. See Exophthalmic 

Goitre. 

Fowler's solution, in chorea, 1155: in epilepsy. 
1149. 

Friedrich's disease (Hereditary Ataxia), 981; 
aetiology and pathological anatomy of, 981; 
clinical history, 982; diagnosis and treat- 
ment, 984; pathological anatomy. 983. 

Furunculosis. after influenza, 80: in diabetes 
mellitus, 757. 

Gait, ataxic. 966; cerebellar. 984, 10S6: in neu- 
ritis, 890: of osteomalacia. 705: spastic 
paretic, 1008. 

Gall-stones. 543: in diphtheria. 68. 

Galvano-puncture in aortic aneurism, 379. 

Gangrene, pulmonary. 221: pulmonary, in 
cancer of oesophagus. 413: self-induced. 
1180: symmetrical spontaneous. 900: in 
arterio-sclerosis, 373: in erysipelas, 65: in 
foetid bronchitis. 168: in plague. 109: in pneu- 
mothorax. 295; in small-pox, 58. 



Gangrene of the lungs, 266; aetiology of, 266; 
bacteria in, 268: clinical history, 268; diag- 
nosis and prognosis, 269; dyspnoea in, 268; 
elastic fibers, 268: expectoration, 268, 269; 
haemoptysis in, 268; pathological anatomy 
of. 267; pneumothorax from, 268; relation to^ 
diabetes mellitus, 267; treatment, 270. 

Gangrene of the tonsils in scarlet fever, 40. 
See also Noma. 

Garrod's thread-test for uric acid, 777. 

Gas in pneumothorax, composition of, 298. 

Gastralgia, in gastritis, 426: in gastric ulcer, 
435. 

Gastric catarrh, acute. 422. 

Gastric contents, blood in, 422; examination 
of. 415: tests for, 417. 

Gastric crisis in tabes dorsalis, 974. 

Gastric juice, anomalies of the secretion of, 
452: achylia gastrica and achlorhydria, 452 r 
anacidity of the stomach, 452; diagnosis, 
454: dyspepsia in, 454; hypersecretion and 
hyperacidity of, 455 et seq. ; in diabetes mel- 
litus, 453; treatment, 455. 

Gastric juice, constituents of. 417. 

Gastric juice, hypersecretion and hyperacidity 
of, 455 (see also Anomalies in the Secre- 
tion of): dyspepsia with, 456; gastric con- 
tents in, 458; periodical hypersecretion, 459: 
prognosis and treatment, 458; relation to 
gastric ulcer, 457; relation to migraine, 459; 
resemblance to gastric crisis, 459. 

Gastric neurasthenia. See Nervous Dys- 
pepsia. 

Gastric ulcer, 432; aetiology of, 432; cicatri- 
cial contraction of stomach in, 434: clinical 
history, 434; diagnosis, 440; diet, 443; fever 
in. 436; gastralgia in. 435; gastric contents 
in. 437; haematemesis in, 436; haemorrhage 
in. 434; in chlorotic patients, 433; pathologi- 
cal anatomy of, 434; perforation in, 438; 
prognosis and treatment. 441: pyloric ste- 
nosis in, 434, 438, 443; urine in, 436; vomiting 
in. 439. 

Gastritis, acute, aetiology and pathologi- 
cal anatomy of, 422; from alcohol. 423: in- 
fection and predisposition, 423: symptoms, 
423: toxic gastritis in, 423; treatment, 425 ; 
urine in, 424. 

Gastritis, chronic, 425; aetiology of, 425; 
alcohol in, 425: chronic catarrh of the 
stomach. 425: course of the disease, 428; 
diagnosis. 429: motor functions of stomach 
in. 428: nervous disturbances in. 42S: other 
symptoms. 42S; pathology of. 426: predisposi- 
tion. 425: symptoms on part of the stomach, 
426: treatment. 429: urine in, 42S. 

Gastritis, phlegmonous. 432: abscess in. 432. 

Gastro-duodenal catarrh. See Catarrhal 
Jaundice. 

Gastroptosis, 462. 

Gastroxynsis, 459. 

General paresis, 1129. 

General progressive paralysis of the insane, 
1129: aetiology. 1130: aphasic disturbances^ 
in. 1132: clinical history, 1131: cortical 
changes in. 1134: delusions. 1133: diagnosis, 
1135: early symptoms, 1133: literal ataxia 
in. 1131: nature of the disease and patho- 



1226 



INDEX 



logical anatomy. 1134; preliminary remarks, 
1129; prognosis and treatment, 1136; pulse 
and temperature, 1134; relation to syphilis, 
1130; speech and handwriting in, 1132. 

Genitals, neuralgia of, 820. 

Genito-urinary apparatus in typhoid, 19. 

Genito-urinary tuberculosis, 229, 250, 662. 

German measles. See Rotheln. 

Gigantism. 903. 

Gin-drinkers' liver. See Cirrhosis of Liver. 
Gingivitis, 382-384. 

Glanders, 125; abscesses in, 126; aetiology of, 
125; clinical history and diagnosis, 126; 
fever in, 125; infection, 125; inoculation, 126; 
in animals, 135; malleine in, 127; treatment, 
127; ulcers in, 125. 

Glioma, of brain, 1116; of spinal cord, 1024/ 

Gliosis, central, 1030. 

Globus hystericus, 415, 1186. 

Glossitis, acute parenchymatous, 388; disse- 
cans, 388. 

Glosso-labio-laryngeal paralysis. See Bulbar 
Paralysis, Progressive. 

Glottis, spasm of, 153; aetiology of, 153; rela- 
tion to rachitis, 153: symptomatology and 
treatment, 154. 

Gluteal nerves, paralyses of. 872. 

Glycosuria in pancreatic diseases, 586. See 
also Diaeetes Mellittts. 

Gmelin's test, 540. 

Goitre, exophthalmic, 909. 

Gonococci in cystitis, 668. 

Gonorrhoea, endocarditis in. 307. 

Gout, 770; aetiology of. 770; anatomical 
changes in, 775; chronic, 773; clinical 
history, 771; complications in, 775: diag- 
nosis in. 776: diet in, 778: gouty diseases of 
various organs. 773; gouty dyspepsia. 774; 
hereditary influence. 771: kidneys in, 775; 
nature of. 775: nephritis in, 776: prodromata, 
772: prognosis and treatment. 777: uric acid 
in. 772. 

Gout in contracted kidney. 626. 

Granular kidney. See Contracted Kidney. 

Graves's disease. See Exophthalmic Goitre. 

Green sickness. See Chlorosis. 

Grippe. See Influenza. 

Guaiac-turpentine test for blood, 422, 445, 492. 
Guaiacol in pulmonary tuberculosis, 254. 
Guarana, in headache, 826; in migraine, 908. 
Giinzburg's test, 417. 

Gymnastics in cardiac hypertrophy, 350. 

Haematemesis, in gastric ulcer, 435, 440; in 

hypertrophic cirrhosis of liver, 564. 
Haematidrosis, 904. 

Haematoidine crystals in croupous pneumonia, 
222. 

Haematomyelia, 929. 
Haematothorax, 300. 

Haematuria in papilloma of the bladder. 673. 

Haemine crystals in gastric contents, 422. 

Haemoglobinaernia and haemoglobinuria, 736; 
blood in, 737; definition and aetiology. 736; 
influence of cold in. 737: origin of, 736; 
paroxysmal type, 737; pathology and symp- 
toms, 736; prognosis, 738: urine in. 737. 

"Haemophilia, 746: clinical history. 747: defini- 



tion and aetiology, 746; prognosis and treat- 
ment, 748. 

Haemoptysis, hysterical, 1179; in pulmonary 
cancer, 277; in pulmonary gangrene, 268: in 
tuberculosis, 236, 259. 

Haemorrhages, cerebral, 1089; conjunctival, 
in whooping-cough, 173; in aortic aneurism, 
377; in aortic rupture, 380; in cirrhosis of 
the liver, 558; in gastric ulcer, 434: in 
leukaemia. 731; in pernicious anaemia, 721; 
in plague, 109; in pulmonary tuberculosis, 
238, 253; in septic and pyaemic diseases, 120: 
in yellow fever, 105. 

Haemorrhages into medulla oblongata and 
pons, 1048; paralysis in, 1049. 

Haemorrhages, into pancreas, 585; into spinal 
cord, 929: into spinal meninges. 919; pul- 
monary, in bronchiectasis, 179; pulmonary, 
in cancer, 277; renal, in endocarditis. 307; 
retinal, in septic and pyaemic diseases, 121. 

Haemorrhagic encephalitis in adults, acute, 
1113. 

Haemorrhagic pachymeningitis, 1053. 
Haemorrhagic infarction of the lungs. See 

Embolic Processes in. 
Haemorrhagic pericarditis, 360. 
Haemorrhoids, 493; haemorrhage in, 494, 495; 

nmcous, 494: predisposition, 494: treatment, 

494. 

Hair, loss of. in typhoid, 19. 

Handwriting in general paralysis, 1132. 

Hay fever (footnote), 135. 

Head, deformed, in rachitis, 702. 

Headache, habitual, 824: predisposition and 
causes, 824: relation to eye-strain, 825; 
treatment, 825. 

Headache, in cerebral tumors, 1117; in coryza, 
136: in erysipelas. 64: in gastroxynsis. 459: 
in plague. 108: in purulent meningitis, 1057: 
in small-pox. 55: in tubercular meningitis, 
1061: in typhoid, 15; in yellow fever, 105. 

Heart, aneurism of, 341: complications in 
croupous pneumonia, 214: disease, cells of, 
276; disease, compensation in, 311, 316, 326, 
334; diseases of, 304: diseases of. congenital, 
323: diseases of. valvular. 308: failure in 
diphtheria. 71: failure in nephritis, 602. 

Heart, congenital lesions of. 324. 

Heart, congestion of liver. 330; mental dis- 
orders in, 332; musical murmur, 317, 318; 
oedema in, 330-338: pericarditis, 329. 

Heart, constitutional symptoms. 332 ; fever, 
332. 

Heart, Corrigan's pulse, 319: cyanosis in, 323- 
330: diastolic rnurrnur. 315. 317. 318; dilata- 
tion of left ventricle, 317: dyspnoea, in, 326, 
333. 339: embolic processes, 331: fatty de- 
generation. 329: general course and prog- 
nosis. 333: general pathology, 310. 

Heart, fatty. 353: aetiology and pathological 
anatomy of. 353; clinical symptoms. 354: 
relation to fatty degeneration. 353: treat- 
ment, 355. 

Heart, fatty degeneration of. 329: fibrinous 
degeneration of the myocardium, see Myo- 
carditis. Interstitial. 

Heart, hypertrophy of. 345; aetiology and gen- 
eral pathology, 345: clinical history. 347: 



INDEX 



1227 



diagnosis and treatment, 348; effect of alco- 
holic stimulants, 346; influence of amount of 
fluid, 348; massage, passive movements, 
gymnastics, and baths, 350; nephritis in, 
348; pulse in, 347; strengthening of cardiac 
muscle, 349. 
Heart, hypertrophy of, 315, 317, 320; origin of 
murmur, 315; hypertrophy of left ventricle, 
320. 

Heart, insufficiency of mitral valve, 311; 

auscultation in, 313; inspection, palpation, 

and percussion, 313. 
Heart, insufficiency of pulmonary valves, 316; 

insufficiency of semilunar valves, 316. 
Heart, insufficiency of tricuspid valves, 322; 

hypertrophy in, 322; pulse in, 322; systolic 

murmur in, 322. 
Heart, mechanical strain of, see Idiopathic 

Hypertrophy; nervous palpitation of, 356; 

neuralgia, 355; neuroses, 355; sounds in pul- 
monary emphysema, 192. 
Heart, pulmonary stenosis, 323; congenital, 

323. 

Heart, pulse, 313, 314, 319, 328; arhythmic, 

314, 315, 328; curve of, 319. 
Heart, relation to articular rheumatism, 308, 

327. 

Heart, sequelae and complications, 326. 

Heart, sequelae in heart itself, 327; allorhyth- 
mic pulse, 328; myocarditic nodules, 329; 
pericarditis, 329; pulsus bigeminus, 328. 

Heart, stenosis of aortic orifice, 320; ausculta- 
tion, inspection, palpation, and percussion, 
320. 

Heart, stenosis of tricuspid orifice, 322; rheu- 
matism in, 323. 

Heart, subjective symptoms, 326; palpitation, 
327; tachycardia, 327. 

Heart, symptoms in peripheral arteries, 318; 
symptoms of stasis in organs, 329. 

Heart, systolic murmur, 312, 319. 

Heart, treatment, 334; caffeine in, 337; digi- 
talis in, 335; morphine in, 339; prophylaxis, 
334; of ruptured compensation, 335: stro- 
phanthus, 338; symptomatic treatment, 338. 

Heart, urine in, 331. 

Heart, valvular disease of, 308; aetiology of, 
308; affections of the joints in, 332; angina 
pectoris, 327; baths in, 335; bulbous pulse in, 
322; Cheyne-Stokes breathing, 333: com- 
bined valvular disease, 325; comparison of 
physical signs in, 325; compensated heart 
disease, 311, 316, 326, 334; complications on 
part of nervous system, 332. 

Heat prostation, see Insolation; test for 
albumen, 590. 

Helminthiasis. See Intestinal Parasites. 

Hemianaesthesia, hysterical, 1176. 

Hemianopsia, 1075. 

Hemiatrophy, facial, 908. 

Hemicrania. See Migraine. 

Hemiplegia, cerebral, 1095, 1097; associated 
movements of, 1100. 

Hemiplegia, in heart disease, 332; in tabes 
dorsalis, 976; in whooping-cough, 173: in 
relation to cerebral lesions, 1085: spastic 
infantile, 1111. 

Hemiplegic gait, 1099. 



Hemlock poisoning. See Coniine. 
Hepatic calculi, 545; colic, see Biliary Cal- 
culi. 

Hepatitis, diffuse, interstitial. See Liver, 
Cirrhosis of. 

Hepatitis, suppurative, 553; aetiology of, 553; 
bacteria in, 533; clinical history, 554; fever 
in, 554; hepatic abscesses, 553; infection, 
553; pathology, 553; perforation in, 554; 
treatment, 555. 

Herniae, 500. 

Heroine in tuberculosis, 259. 
Herpes facialis, 114. 

Herpes, in croupous pneumonia, 208, 216, 219; 

in erysipelas, 66; in malarial disease, 98; in 

typhus, 32. 
Herpes labialis, 114; in influenza, 79. 
Hiccough. See Clonic Spasm of Diaphragm. 
Hobnailed liver. See Liver, Cirrhosis of. 
Hodgkin's disease. See Pseudo-leukemia. 
Hot-air treatment in arthritis deformans, 

694. 

Huntington's chorea, 1156. 

Hydatid cysts of the liver, 575. 

Hydatids of the brain, 1124. 

Hydrocephalus, chronic, 1137; aetiology and 
pathology, 1137; clinical history, 1137; diag- 
nosis and treatment, 1138: hydrocephalic 
fluid, 1137; in adults, 1138; motor disturb- 
ances in, 1138; physical signs, 1137; predis- 
posing causes, 1137. 

Hydrochloric acid poisoning, 1206. 

Hydrocyanic acid poisoning, 1210. 

Hydromyelus, 1029. 

Hydronephrosis, 665; aetiology of, 665; clinical 
symptoms, 665; diagnosis, 666; pathological 
anatomy, 665; treatment, 667; tumor in, 665; 
urine in, 666. 

Hydronephrosis from movable kidney, 649. 

Hydroperitoneum. See Ascites. 

Hydrophobia, 122; blood in. 124; chloroform 
in, 124; clinical history. 123; convulsions in, 
123; curare in, 124; diagnosis, treatment, 
and prophylaxis, 124; hysterical hydro- 
phobia, 124; immunity, 123; inoculation, 123; 
inoculation, Pasteur's, 124; paralysis in, 122; 
prodromata, 122; rabies in dogs, 122: tem- 
perature in, 123. 

Hydrophobic tetanus, 1167. 

Hydro-pneumothorax. See Pneumothorax. 

Hydrops articulorum intermittens, 904. 

Hydrorrhachis. See Spina Bifida. 

Hydrotherapy, in neurasthenia, 1200: in pul- 
monary tuberculosis, 259; in typhoid, 24. 

Hydrothorax, 299: dyspnoea of, 209: lymphat- 
ics in, 299. 

Hydrothorax, in acute nephritis. 614: in scar- 
let fever. 44. 

Hyoscine in paralysis agitans, 1160. 

Hyperaemia. cerebral, 1066: in erysipelas, 65: 
of the liver, 578. 

Hyperesthesia in typhoid, 17. 

Hyperchlorhydria, 456. 

Hyperosmia, 827. 

Hyperostosis cranii, 904. 

Hyperplasia from intestinal catarrh, 469. 

Hypertrophy, of the heart, 315. 341. 345: in 
aortic aneurism. 376: in arterio-sclerosis. 



1228 



INDEX 



372; associated with congenital smallness 
of the systemic arteries, 350. 

Hypertrophy of the tonsils, chronic, 399. 

Hypnotism in hysteria, 1185. 

Hypophysis cerebri in acromegaly and gigan- \ 
tism, 903. 

Hypoplasia of aorta. See 350. 

Hysteria, 1172: abasia aud astasia, 1178, 1189; ] 
achromatopsia in, 1176; aetiology and defini- 
tion, 1172; aphonia in, 1178; arc de cercle, 
1183; attacks, conditions of spasm, etc., 
1182; causes, 1173; clownismus, 1184; 
contractures, 1179; coprolalia and echo- 
lalia in, 1187; diagnosis. 1187: diagnosis, 
differential, 1188; general course of, 1187; 
globus hystericus, 1186; haemorrhages in, 
1179; hereditary predisposition, 1174; 
hypnotic symptoms and treatment, 1185, 
1191; hysterical paralysis, 1178; hysterical 
vs. epileptic convulsions, 1188; hysteroge- 
nous zones, 1186 (see also 1149); influence of 
sex, nationality, and race, 1174; ischuria and 
polyuria in, 1180; in children. 1174; mental 
and bodily constitution in, 1181; metallo- 
therapy, 1192; muscular sense in, 1176; 
psychical factors, 1173, 1181, 1191; reflexes 
in. 1175; respiration in, 1183: sensory 
anaesthesia and hypersesthesia, 1175; stig- 
mata, 1173; suggestion in. 1184. 1191; 
symptoms and manifestations of, 1175; 
symptoms in the internal organs, 1179; 
traumatic influences, 1173; treatment, 1189; 
vaso-motor and secretory disturbances, 1179. 

Hysterical asthma, 185; hydrophobia, 124. 

Hysterogenous zones, 1149, 1186. 

Icterus catarrhalis. See Catarrhal Jaun- 
dice. 

Icterus neonatorum, 570. 
Icterus in typhus, 33. 
Icteric casts, 540. 
Ileo-typhus, 1. 

Illuminating gas poisoning, 1210. 

Indican test (footnote), 504. 

Infantile convulsions, 1151. 

Infantile hemiplegia, spastic, 1111; spastic 
diplegia, 1012; spinal paralysis, 1014. 

Infarction, embolic, in the kidneys, 643. 

Inflammation of the pericardium, see Peri- 
carditis; of the soft palate and tonsils, see 
Sore Throat. 

Influenza, 77: aetiology of, 77; bacilli, 77; 
catarrhal form, 78; clinical history and 
symptoms, 77 ; complications and sequelae, 
79; diagnosis, prognosis, and treatment, 80; 
fever, 78: furunculosis, 80; herpes labi- 
alis in, 79; in animals, 77; nervous sequelae, 
80: otitis media, 79; pandemics of, 77; pneu- j 
monia in, 79: rheumatoid form, 78. 

Inhalations, carbolic mask. 170; cause of 
acute catarrh of bronchi and trachea, 157; 
in foetid bronchitis, 170; in pulmonary gan- 
grene, 270: in tuberculosis of larynx, 149. 

Inhalations of dust, diseases from. 270; 
anthracosis pulmonum, 271; black pigment 
and carbon in the lungs, 271; chalicosis, 271; 
sequelae, 272. 

Inhalations of oxygen in croupous pneumonia, | 



225; of steam in bronchial catarrh, 161; of" 

steam in laryngitis, 142; treatment of 

chronic bronchitis, 166. 
Inoculation of measles, 49. 
Insolation, 1113; aetiology and pathology, 1113; 

diagnosis, prognosis, and treatment, 1114; 

pathological anatomy, 1113; symptoms and 

course, 1114. 
Insufficiency of muscular fiber of stomach, 

460; of the pylorus, 439; valvular, 311, 316,. 

321, 323. 

Intention tremor, 836; in multiple sclerosis, 
955. 

Intercostal neuralgia, 815. 
Intermittent fever. See Malarial Diseases.. 
Intermittent tetanus. See Tetany. 
Intertrigo in obesity, 782. 

Intestinal catarrh, 468; aetiology of, 468; 
atrophy of mucous membrane in, 469; diar- 
rhoea in, 469; diet in, 474; different forms 
of, 470; hyperplasia in, 469; infection, 468; 
pathological anatomy, 468; stools, examina- 
tion of, 470: symptomatology of, 469; treat- 
ment, 473; ulceration in, 468. 

Intestinal catarrh of children, 477; arthrepsia 
in, 479; complications, 479; feeding in, 480 r 
pedatrophy, 479; prophylaxis, 482; stools 
in. 478, 481; tenesmus in, 478; treatment, 
481. 

Intestinal constriction, 500. 

Intestinal ecchymoses in septic and pyaemic 
diseases, 121. 

Intestinal mycosis, 129. 

Intestinal obstruction, 499. 

Intestinal parasites, 508; anchylostoma duo- 
denale, 518: ascaris lumbricoides, 515; blood 
in. 512; bothriocephalus latus, 511; cestodes, 
508; cysticercus cellulosae, 509; cysticercus 
racemosus, 510; oxyuris vermicularis, 516; 
round worms, 515; symptoms and diagnosis, 
512; taenia cucumerina, 511; taenia nana, 511 ; 
taenia solium, 508; tape-worms, 508; treat- 
ment, 513; trichocephalus dispar, 519. 

Intestinal puncture, 508. 

Intestines, cancer of, 491; congenital closure 
of, 499: invagination of, 501. 

Intestines, stricture and obstructions of, 499 r 
aetiology and pathological anatomy of, 499; 
clinical history, 502; compression from with- 
out, 501: congenital closure, 499; diagnosis, 
504; intestinal constriction, 500; intestinal 
obstruction, 499; intussusception, 501; patho- 
logical changes, 502; physical examination, 
502; puncture, 508; stercoraceous vomiting, 
503; treatment, 506; tumors and cicatricial 
strictures, 499: twists and knots of intes- 
tines, 500: ulceration in, 502; urine in, 504; 
varieties of, 504: volvulus, 500. 

Intestines, tuberculosis of, 488: volvulus, 500. 

Intussusception, 501. 

Inunction in glanders, 127; in myelitis, 952; 
in scarlet fever, 46. 

Iodide of potassium in arterio-sclerosis, 374; 
in asthma. 186: in cerebral syphilis, 1129; 
in interstitial myocarditis, 345; in lead 
paralysis, 874; in neuralgia, 808; in spinal 
syphilis, 1029; in syphilis of the liver, 572. 

Iodine, in contracted kidney, 635; in ery- 



INDEX 



1229 



sipelas, 67; in parotitis, 391: in peritonitis, 
532; in small-pox, 61; poisoning, 1207. 

Jodism, chronic, 1207. 

Iodoform poisoning, 1210. 

Iritis, from gout, 775; from measles, 50. 

Iron, in anaernia and chlorosis, 710, 718; in 
amyloid kidney, 639. 

Irrigation of the bladder in cystitis, 671, 672. 

Ischialgia. See Sciatica. 

Ischuria, hysterical, 1180. 

Jacksonian epilepsy, 1072. 

-Jaundice, acute febrile, 542; fever in, 543; 
haemorrhages in, 543; muscular pains in, 
542; treatment, 543; urine in, 542. 

Jaundice, catarrhal, 536; aetiology and patho- 
logical anatomy, 536; bile absorption in, 539; 
diagnosis and treatment, 541; diet, 541; 
epidemics of, 537 ; examination of liver in, 
540; faeces in, 539; infection, 537; pulse rate 
in, 538; symptoms and clinical course, 537; 
tympanites, 539; urine in, 539; xanthelasma, 
538. 

Jaundice, infectious, see Jaundice, Acute 
Febrile; in acute yellow atrophy of liver, 
566; in croupous pneumonia, 214; in heart 
disease, 330; in malarial diseases, 98; in 
yellow fever, 105; of the new-born, 570; per- 
nicious, 569; xanthelasma in, 538. 

Joints affected, in arthritis deformans, 690; 
in articular rheumatism, 678; in chronic 
rheumatism, 690-692; in glanders, 126; in 
gout, 773; in heart disease, 332; in septic and 
pyaemic diseases, 120; in syringomyelia, 1031; 
in tabes dorsalis, 974; in typhoid, 19. 

Juvenile muscular dystrophy, 1003. 

Karaala, for tape-worm, 514. 

Keratitis, in anaesthesia of the trigeminus, 
803; from gout, 775; from influenza, 79; 
from measles, 50. 

Kidney, contracted, 625; alcoholism in, 626; 
anatomical complications, 632; arterioscle- 
rosis in, 632; cardiac hypertrophy in, 629; 
clinical symptoms, 628; definition and 
aetiology of, 625; diagnosis, 633; dyspnoea in, 
630; general course, duration, and termina- 
tion, 633; gout, 626; haemorrhage in, 632; 
pathological anatomy, 627; treatment, 634; 
uric acid, 627; urine, 628. 

Kidney disease, pathology and preliminary 
remarks on, 588 (see also 564); albuminuria, 
589; blood-corpuscles in urine, 594; cardiac 
hypertrophy in, 602; casts and other abnor- 
mal morphological constituents of urine, 
592; changes in circulatory apparatus, 601; 
dropsy of renal diseases, 594; fat in urine, 
594; nephritic oedema, 596; toxines, 589. See 

alSO UltiEMIA. 

Kidneys, amyloid, 635. 

Kidneys, calculi of, in diphtheria, 68; calculus, 
see Nephrolithiasis. 

Kidneys, cancer of, 64; circulatory disturb- 
ances in, 643; congenital sarcoma of, 644. 

Kidneys, dilatation of pelvis. See Hydro- 
nephrosis. 

Kidneys, floating, 648; granular, 625. 

Kidneys, inflammation of pelvis, 654; ab- 



scesses, 655; aetiology, 654; clinical symp- 
toms, 655; nervous symptoms, 656; patho- 
logical anatomy of, 654; treatment, 657; 
urine in, 655, 656. 

Kidneys in diabetes mellitus, 760. 

Kidneys, movable, 648; aetiology, 648; hydro- 
nephrosis in, 649; hysteria and neurasthenia 
in, 650; symptoms, 649; treatment, 650. 

Kidneys, new growths in, 644; diagnosis, 
prognosis, and treatment, 645; haematuria 
in, 645; treatment, 645. 

Kidneys, parasites of, 646; chyluria, 647; 
distoma haematobium, 646; echinococcus of, 
646; echinococcus cysts, 646; filaria san- 
guinis, 647; strongylus, 647. 

Kidneys, tumors of, 644. 

Kousso for .tape-worm, 514. 

Kyphoscoliosis in croupous pneumonia, 220. 

Kyphosis, angular, in vertebral caries, 936; 
in osteomalacia, 705. 

Labyrinthine vertigo. See Meniere's Dis- 
ease. 

Laennec's cirrhosis. See Cirrhosis of Liver. 

Laryngeal catarrh, acute, 140. 

Laryngeal crises in tabes dorsalis, 974. 

Laryngeal perichondritis, 145; abscesses in, 
145; pathological anatomy of, 145; sympto- 
matology and diagnosis, 145; treatment, 146. 

Laryngeal phthisis. See Tuberculosis of 
Larynx. 

Laryngeal polypi, 155. 

Laryngismus stridulus. See Spasm of the 
Glottis. 

Laryngitis, acute, 140; aphonia in, 141; false 
croup in, 141; fever in. 141; irritants as cause 
of, 140; symptomatology of, 140; treatment, 
142. 

Laryngitis, chronic, 143; pachydermia laryn- 
gis, 143; symptomatology of, 143; treatment, 
144. 

Laryngitis from measles, 51. 

Larynx, new growths in, 155. 

Lateral sclerosis, primary, 1006. 

Laudanum in intestinal catarrh, 481. 

Lead arthralgia, 1208; colic, 1208; encepha- 
lopathy, 1208. 

Lead paralysis, 873 (see also 1208): prognosis 
and treatment of, 874; urine in, 874. 

Lead poisoning, 1207; chronic, 1208; in gout, 
771. 

Lepto-meningitis, acute, 915: chronic, 917; 
purulent cerebral, 1055. 

Leptothrix fibers in sputum, 168. 

Leucine and tyrosine in liver, 566. 

Leucocythaemia. See Leukaemia. 

Leucocytosis, in croupous pneumonia, 214; in 
erysipelas, 66. 

Leucoplacia. See Lingual Psoriasis. 

Leukaemia, 726; blood in, 729; Charcot's crys- 
tals, 728; clinical history, 731; definition and 
aetiology, 726; haemorrhages in. 731: v lymph 
glands in, 728; other organs in, 728; patho- 
logical anatomy, 727; priapism in, 731; prog- 
nosis, diagnosis, and treatment. 732: 
retinitis in, 730: spleen in. 727. 730, 732; 
symptoms in, 729. 

Lime in rachitis, 704. 



1230 



INDEX 



Lime-water in croupous bronchitis, 172. 
Lingual psoriasis, 388. 
Lingual spasm, 877. 
Lipoma of larynx, 155. 

Little's disease. See Infantile Spastic 
Diplegia. 

Liver, acute yellow atrophy of, 565; abortion 
in. 568; acholia and cholsemia, 569; aetiology 
and pathology of, 565; anaemia, hepatic, 578; 
clinical history, 566; cutaneous ecchymoses, 
567; diagnosis, 568; jaundice in, 566; leucine 
and tyrosine in. 566; nervous symptoms, 
566, 569; pernicious jaundice, 569; prodrom- 
ata, 566; splenic tumor in, 566; in typhoid, 
12: urine in, 566; vomiting in, 568. 

Liver, amyloid, 580; anomalies in shape and 
position, 581; atrophy, hypertrophy, and 
degeneration of, 579; biliary and hyper- 
trophic cirrhosis of, 562: cancer of, 572; 
circulatory disturbances in. 578; cirrhosis of, 
555: haemorrhages in. 564: primary hyper- 
trophic cirrhosis, 563: prognosis, 564; sec- 
ondary, 562; splenic tumor in, 563. 

Liver, circulatory disturbances in, 578. 

Liver, congestion of, 578; echinococcus of, 
575-577; fatty, 580; hypertrophic and biliary 
cirrhosis of, 562: in diabetes mellitus, 760; 
in heart disease, 330; in pleurisy, 286. 

Liver, secondary cirrhosis of, 562; syphilis of, 
571; waxy, 580. 

Lobar pneumonia. See Croupous Pneu- 
monia. 

Lobular atelectasis, 233. 

Localization of cerebral diseases, 1068; 
anatomical changes occurring in aphasia, 
1081; aphasia and allied conditions, 1077; 
central ganglia and optic thalamus, 1084; 
centers and disturbances of speech. 1077; 
centrum ovale, 1083; cerebellum, 1086; cor- 
pora quadrigemina and crura cerebri, 1085; 
course of conducting tracts, 1089; frontal 
convolutions, 1074; Jacksonian, partial or 
cortical epilepsy, 1072: motor region of 
cortex cerebri, 1069; occipital convolutions, 
1075; parietal convolutions. 1075; soul blind- 
ness and deafness, 1076; temporal convolu- 
tions. 1076. 

Localization, spinal, 920; reflexes in, 927. 

Lock-jaw. See Tetanus. 

Locomotor ataxia. See Tabes Dorsalis. 

Lower extremity, paralyses of. 871. 

Ludwig's angina, 392. 

Lumbago, 696. 

Lumbar puncture, in acute miliary tubercu- 
losis, 265: in cerebro-spinal meningitis, 115; 
in chronic hydrocephalus, 1138. 

Lumbo-abdominal neuralgia, 816. 

Lung fever. See Pneumonia, Croupous. 

Lungs, atelectasis of, 195; aetiology of, 195; 
baths in. 197; in kyphoscoliosis, 196; in 
the new-born, 195; symptoms, 196; treat- 
ment, 197. 

Lungs, brown induration of, 275: cancer of, 
276; echinococcus of, 276. 

Lungs, emphysema of, 187; alveolar ectasis, 
190; complications, 194: diagnosis, prog- 
nosis, and treatment, 194; dropsy in, 191; 
dyspnoea in, 190; expiratory pressure in. 



193; nature and aetiology of, 187; other symp- 
toms in lungs and other organs, 193; patho- 
logical anatomy, 189; physical examination,. 
191: symptoms and course, 190. 

Lungs, malignant lymphosarcoma of, 278. 

Lungs, oedema of, 197; aetiology and general 
pathology of, 197; dyspnoea in, 198; from 
paralysis of left ventricle, 198; rales in, 198; 
symptoms and treatment, 198. 

Lungs of heart disease, see Brown Indura- 
tion; sarcoma in, 277; syphilis of, 276-279; 
tumors of, 276. 

Lupus, tubercular, 229, 251. 

Lymph glands, in scrofula, 787; swollen, in 
glossitis, 388; swollen, in pulmonary cancer, 
278; swollen, in stomatitis, 384; swollen, in 
tuberculosis, 230, 236, 250; tumors of, 734. 

Lymph, stasis of, in vertebral caries, 936. 

Lymphatic leukaemia, 728. 

Lymphoma and lymphosarcoma. See 
Pseudo-leukemia. 

Lymphosarcoma, malignant, of the lungs, 278. 

Lyssa. See Hydrophobia. 

Maculae tendinae, in pericarditis, 360. 

Magnesium borocitrate in nephrolithiasis, 661. 

Malaria, 93; aetiology and pathological 
anatomy of, 93; blood in, 94: cardiac disturb- 
ances in. 98; cinchonism, 102: chronic 
malarial cachexia. 99; collections of pig- 
ment in viscera, 95; diagnosis and treatment, 
100; dropsy in, 99; epistaxis in, 99; geo- 
graphical distribution of, 93; intermit- 
tent fever, 96; in animals, 95; jaundice in, 
98, 99: manner of communication, 95; 
masked intermittent, 99; non-contagious, 93; 
periodicity, 98; pernicious intermittent 
fever, 98; Plasmodium malariae, 94, 95; 
quinine in. 97. 100: remittent forms. 99: 
skin in, 98: spleen in, 95, 98; temperature- 
curve of, 96; time of incubation, 96; typho- 
malarial fever, 100. 

Male fern for tape-worm, 513, 516. 

Malignant pustule. 127. See Anthrax. 

Malleine in glanders, 127. 

Malum cotunnii. See Sciatica. 

Marasmus, predisposing to erysipelas. 64. 

Massage in arthritis deformans, 693; in ar- 
ticular rheumatism, 686; in cardiac hyper- 
trophy, 350; in muscular rheumatism, 697; 
in sciatica, 820; of paralyzed limbs, 1102. 

Mastodynia, 816. 

Measles, 48; acquired resistance to. 48: black, 
50; catarrhal pneumonia in. 202; clinical his- 
tory, 49; complications of, 50: contagious- 
ness of, 48: diagnosis and prognosis of. 52; 
desquamation in, 49; epidemic nature of, 48: 
eruption of, 49; fever in, 50; haeinorrhagic, 
50; initial stage, 49; inoculation of, 49: in- 
testinal symptoms, 51; noma in, 51; pe- 
culiarities in the course of, 51; temperature- 
curve in. 49: treatment of, 52. 

Measles, German. 53. See Rotheln. 

Meat juice and meat peptones in typhoid, 24. 

Meat, poisoning from, 1213. 

Median paralysis, 868. 

Mediastino-pericarditis, 363. 

Mediastinum, tumors of, 301; diagnosis, prog- 



INDEX 



1231 



nosis, and treatment, 302; dyspnoea of, 301; 
vascular stasis in, 301. 

Medulla, compression of, 1052. 

Megaloblasts in blood, 724. 

Megrim. See Migraine. 

Melanine in malarial diseases, 94. 

Membranous enteritis, 474; course and treat- 
ment of, 475. 

Meniere's disease, 1139. 

Meninges, spinal, haemorrhage into, 919. 

Meningitis, basal gummatous, 1127; basilar, 
see Tubercular Meningitis. 

Meningitis, epidemic cerebro-spinal, 111; aeti- 
ology of, 111; cerebral symptoms, 113; clini- 
cal history, 112; contagiousness, 111; diag- 
nosis, 115; diplococci of, 111; fever in, 
114; herpes labialis in, 114; infection, 
111; in animals, 112; lumbar puncture 
in, 115; mortality in, 116; pathological 
anatomy, 112; prodromata, 112; prognosis 
and treatment, 116; reflexes, 114; secondary, 
116; sequelae, 115; tinnitus aurium, 113; 
urine in, 114. 

Meningitis, purulent, 1055; aetiology, 1055; 
clinical history, 1057; diagnosis, 1058; fever 
in, 1058; pathology, 1056; prognosis and 
treatment, 1059. 

Meningitis, spinal chronic gummatous, 1027; 
secondary, 116. 

Meningitis, tubercular, 1059; aetiology of, 1059; 
delirium in, 1061; diagnosis, 1063; eyes in, 
1061; in children, 1062; pathology and clini- 
cal history, 1060; prodromata, 1061; pulse 
and temperature in, 1062: relation to 
phthisis, 1059; treatment, 1064. 

Meningocele. See Spina Bifida. 

Menstruation, in chlorosis, 715; in epilepsy, 
1146: vicarious, 139. 

Mental disturbances, in anaemia, 712; in 
athetosis, 1162; in articular rheumatism, 
681; in cerebellar abscess, 1108; in cerebral 
embolism, 1105; in cerebral haemorrhage, 
1101; in cerebral syphilis, 1127; in cerebro- 
spinal meningitis, 113; in cholaemia, 569; in 
cholera, 88; in chorea, 1154; in convulsions, 
123, 1120, 1188; in epilepsy, 1141, 1145; in 
general paralysis of insane, 1131; in haema- 
toma of dura mater, 1054; in heart disease, 
332; in hydrocephalus, 1138: in hysteria, 
1181; in infantile paralysis, 1115; in neu- 
rasthenia, 1194; in neuralgia, 822; in peri- 
tonitis, 526; in poliomyelitis, 1016; in syn- 
cope, 1067; in tuberculosis, 263; in typhoid, 
15. 

Mercurial tremor, 836, 1208. 

Mercury, in hepatic syphilis, 572; in intestinal 
obstruction, 507; in myelitis, 592; in general 
paralysis, 1136; in peritonitis, 532; poison- 
ing, 1208; in syphilis, 1029, 1129; in tuber- 
cular meningitis, 1064. 

Metallic sound, in pericarditis, 360; in pneu- 
mothorax, 297. 

Metallotherapy in hysteria, 1191. 

Metatarsalgia, 821. 

Methyl-chloride spray, in intercostal neu- 
ralgia, 816; in sciatica, 819. 
Metrorrhagia in phosphorus poisoning, 1209. 
Microcytes in the blood, 448, 724. 



Migraine, 905; aetiology of, 905; diagnosis and 
treatment, 907; hereditary influence, 905;. 
prodromata, 906; relation to eye-strain, 905; 
relation to gastroxynsis, 459; symptoma- 
tology of, 906. 

Miliaria in typhoid, 18. 

Miliary tuberculosis, 261. 

Milk-cure in acute nephritis, 615. 

Millar's asthma. See Spasm of the Glottis.. 

Mitral insufficiency, 311; stenosis, 312. 

Mogigraphia, 882. 

Monophasia, 1079. 

Monoplegia, 831. 

Moore's test for sugar, 753. 

Morbilli. See Measles. 

Morbus maculosus Werlhofi. See Purpura. 

Morbus sacer. See Epilepsy. 

Morel poisoning. See Mushroom Poisoning.- 

Morphine, in cerebro-spinal meningitis, 116; 
in croupous pneumonia, 223; in heart dis- 
ease, 339; in neuralgia, 809; poisoning, 1211. 

Morvan's disease, 1031. 

Mosquitoes, relation to chyluria, 648; relation 
to malarial diseases, 95; relation to yellow 
fever, 104. 

Motility, disturbances of, 829. 

Motor ataxia in polyneuritis, 890. 

Motor disturbances of the stomach, 460; effi- 
ciency of the stomach, 461. 

Motor region of cortex cerebri, 1069; diseases 
in, 1072. 

Motor tabes, 1007. 

Motor tract, primary degeneration of, 985. 
Mucous colic, 474; haemorrhoids, 494. 
Muguet. See Thrush. 

Multiple sclerosis of brain and spinal cord, 
954; aetiology and pathology, 954; ataxia and 
tremors in, 955; clinical history of, 955; 
diagnosis, 958; prognosis and treatment, 959; 
pseudo-scleroses, 959; reflexes in, 956; un- 
usual forms of, 958. 

Mumps. See Parotitis. 

Murmurs, anaemic, 713, 715, 723, 731; cardiac, 

325, 362. 
Muscle changes in typhoid, 19. 
Muscles of head and trunk, 851. 
Muscles of mastication, paralysis of, 858. 
Muscular atrophy in progressive bulbar 

paralysis, 1040. 
Muscular atrophy, neurotic, 99. 
Muscular atrophy of small muscles of hand, 

992. 

Muscular atrophy, spinal progressive, 990; 
aetiology and clinical history, 992; atrophy 
of small muscles of the hand in, 992; cu- 
taneous sensibility in, 995; diagnosis, 995; 
duration, 994; electrical excitability of 
muscles in, 994; hereditary and generic influ- 
ences, 992; preliminary remarks and patho- 
logical anatomy, 990; prognosis and treat- 
ment, 966; reflexes in, 995; respiratory dis- 
turbances, 994. 

Muscular dystrophy, progressive, 998. 

Muscular sense, 794, 1176. 

Mushroom poisoning, 1212. 

Mussels, poisoning from, 1212. 

Mutism, hysterical, 1178. 

Myalgia. See Muscular Rheumatism. 



1232 



INDEX 



^Myasthenia, pseudo-paralytic, 1046. 
Mycosis, intestinal, 129. 

Myelitis, acute and chronic, 943; ataxia in, 
947; baths in, 952; cervical, dorsal, and lum- 
bar forms of, 950; definition and aetiology of, 
943; diagnosis, 951; disturbances of bladder 
and rectum, 949; disturbances of sensibility 
in, 987; individual symptoms of, 946; infec- 
tion, 944; motor irritation in, 946; motor 
paralysis in, 946; pathological anatomy, 944; 
reflexes in, 948; relation to syphilis, 943; 
treatment, 952; trophic disturbances, 949. 

Myelitis, acute bulbar, 1051. 

Myelitis, diffuse, 943; syphilitic, 1028; trans- 
verse, 943. 

Myelocele. See Spina Bifida. 

Myelocytes, 730. 

Myocarditic nodules, 329. 

Myocarditis, interstitial, 340; aetiology and 
pathological anatomy of, 340; angina pec- 
toris, 343; apoplectiform paralysis, 343; 
arterio-sclerosis in, 341; cardiac aneurism, 
341: clinical history, 342: diagnosis, prog- 
nosis, and treatment, 344; diet, 344; hyper- 
trophy of heart in, 341: pulse, 342; syph- 
ilitic endocarditis, 341. 

Myocardium, primary weakness of, 351; 
effect of alcoholism in, 352; prognosis and 
treatment, 353; pulse in, 352. 

Myoclonia, 1157. 

Myokymia in sciatica, 818. 

Myopathic muscular atrophy, 998; diagnosis 
of, 1006. 

Myositis. See Muscular Rheumatism. 
Myositis in trichinosis, 132. 
Myotonia, congenital, 1169. 
Myxcedema, 901. 
Myxcedematous infantilism, 902. 
Myxomata of larynx, 155. 

Nails, curved, in heart disease, 324; loss of, in 

typhoid, 19. 
Narcotics in cholelithiasis, 551. 
Nasal catarrh, 135, 137; in measles, 49. 
Nasal catarrh, acute, 136; chronic, 137. 
Nephritic oedema, 596. 

Nephritis, acute, 603; aetiology, 603; alco- 
holic nephritis, 606; anuria in, 609: baths 
in, 615; casts, 609; clinical history, 60S; 
course and different forms of, 612; diag- 
nosis, 613; diuretics in, 616; dropsy in, 611, 
617: milk cure, 615; oedema in, 610; patho- 
logical anatomy, 606; in pregnancy, 606, 613; 
primary idiopathic form, 612; prognosis, 614; 
prophylaxis, 614; relation to scarlet fever, 
604; relation to small-pox, 604; relation to 
cholera, 604; relation to erysipelas, 605; 
symptoms, 610; toxic nephritis, 605; treat- 
ment, 614: uraemia in, 617; urine in, 608; 
vomiting in, 611. 

Nephritis, alcoholic, 606, 613; choleraic, 89. 
"Nephritis, chronic and subchronic, 618; aeti- 
ology of, 618; cardiac hypertrophy, 621; 
clinical history, 621; course, duration, and 
termination of, 623: diagnosis, 622; different 
forms of, 622; dropsy in, 622; haemorrhagic 
form, 619; inflammatory fatty kidney, 620; 
oedema in, 621; pathological anatomy, 619; 



retinitis in, 622, 632; secondary contracted 
kidney, 620; treatment, 624; urine in, 621. 
Nephritis, chronic interstitial, 625; erysipel- 
atous, 66; in croupous pneumonia, 215: in 
diphtheria, 72; in gout, 776; in hyper- 
trophy of the heart, 348; in influenza, 79; 
in scarlet fever, 43; in septic and pyaemic 
diseases, 119; in typhoid (nephro-typhoid), 
19; of pregnancy, 606, 613; primary idio- 
pathic, 612. 

Nephritis and perinephritis, purulent, 640; 
abscesses in, 641; aetiology of, 640; bac- 
teria in, 640; clinical symptoms, 641; diag- 
nosis and treatment, 642; fever in, 642; in- 
fection. 640; pathology, 640. 

Nephritis, toxic, 605; tubercular, 250; with 
arterio-sclerosis, 370. 

Nephrolithiasis, 657 ; anatomical changes in, 
658; clinical symptoms, 659; colic in, 659- 
662; diagnosis, 660; diet in, 661; occurrence, 
chemical composition, and aetiology of renal 
concretions, 657; predisposing causes, 658; 
sequelae, 659; treatment, 661; urine in, 659. 

Nephrophthisis, 663. 

Nephro-typhoid, 19. 

Nerve-stretching, in sciatica, 820; in tabes, 
980. 

Nervous debility. See Neurasthenia. 

Nervous dyspepsia, 463 (see also 1181); diag- 
nosis, 465; nervous symptoms, 465; prog- 
nosis, 466; psychical influence, 464; treat- 
ment, 465. 

Nervous fever, 15. 

Nervous palpitation of the heart, 356. 

Nervousness. See Neurasthenia. 

Neuralgia, aetiology of, 804; articular, 821; 
cardiac, 355; cervico-brachial, 814; of geni- 
tals, 820; infection, 805; intercostal, 815; 
ischiatic, 817; of lumbar plexus, 816; in 
malarial diseases, 99; of mammary gland. 
816. 

Neuralgia, occipital, 813; of rectum, 820; 
symptomatology, 806; treatment, 807; in ty- 
phoid. 17. 

Neuralgia of the trigeminus, 810; aetiology of, 
810; diagnosis, prognosis, and treatment, 
812; symptoms and course of, 811. 

Neurasthenia. 1193; aetiology, 1193; agora- 
phobia in, 1194; asthenopia in, 1195; concept 
of the disease, 1193; congenital factors, 1193: 
diagnosis. 1198; general course and prog- 
nosis, 1197; insomnia in, 1200: mental symp- 
toms, 1194; physical symptoms, 1195; 
psychical factors in. 119S; sexual, 1197; 
treatment, 1198; urine in. 1196. 

Neurasthenia, gastric, see Nervous Dyspep- 
sia ; spinal, 933. 

Neuritis, degenerative, 885; diabetic, 887; en- 
demic, 985. 

Neuritis, multiple, 8S6 (see also Endemic); 
acute curable form, 892; alcoholic form of, 
889; ataxic form of, 892; diabetic, 887; diag- 
nosis, prognosis, and treatment, 892; distri- 
bution of, S91: mental disturbances in, 894; 
motor ataxia in, 890: pathological anatomy 
of. 888; primary, acute, and chronic forms, 
890; symptoms and course of, S90; toxic. 
887. 



INDEX 



1233 



Neuritis, multiple bulbar, 1051; optic, 1118; 
primary, secondary, and simple, 885. 

Neuro-fibromata, 897. 

Neuroma, multiple, S96. 

Neuroses, articular, 821; cardiac, 355. 

Neuroses of the oesophagus, 414; globus hys- 
tericus, 415; paralysis of the oesophagus, 
415; spasm of the oesophagus, 414; ulcera- 
tion in, 415. 

Neuroses, professional, 882; traumatic, 1201; 
vaso-motor and trophic, 898; without known 
anatomical basis, 1141. 

Neurotic muscular atrophy, 996; fibrillary con- 
tractions in, 997. 

New growths in the larynx, 155; benignant, 
155; carcinoma of, 155; fibroma, 155; laryn- 
geal cysts, 155; laryngeal polypi, 155; lipo- 
mata of, 155; malignant, 155; myxoma of, 
155; papilloma, 155; treatment, 156; tumors 
of, 155. 

New growths in the peripheral nerves, 896. 

New growths of the pleura, 300; endothelial 
carcinoma of, 300; prognosis, 301. 

New growths of the spinal cord, 1024; patho- 
logical anatomy of, 1024; symptoms and 
course, 1025. 

Nicotine poisoning, 1211. 

Nicotine tabes, 978. 

Nitrate of silver in chronic gastritis, 431. 
Nitrobenzine poisoning, 1210. 
Nitroglycerine in heart disease, 356. 
Nitrous acid fumes, 1206. 

Nocturnal incontinence of urine. See Enure- 
sis Nocturna. 

Nodular sclerosis. See Multiple Sclerosis. 

Noma, 389; fever in, 389; prognosis and treat- 
ment, 390. 

Noma in measles, 51. 

Normoblasts in blood, 724. 

Nosebleed, 139. 

Nutmeg liver, 578. 

Obesity, 779; alcoholic beverages in, 781; baths 
in, 786; cardiac disturbance in, 782; defini- 
tion and aetiology, 779; dyspnoea in, 782; 
intertrigo in, 782; muscular exercise in, 786; 
pathology of, 782; treatment, 784. 

Obturator nerve, paralysis of, 872. 

Occipital neuralgia, 813. 

Occupation paralyses, 870. 

Ocular muscles, paralyses of, 854; in cerebral 
lesions, 1085; in diphtheria, 72; in purulent 
meningitis, 1057; in tabes, 972; in tumors of 
the brain, 1128. 

Oedema, in valvular heart disease, 330; acute 
angioneurotic, 900; in plague, 109; in trichi- 
nosis, 133; in typhoid, IS; nephritic, 596, 610, 
621. 

CEdema of the glottis, 146. 
CEdema, pulmonary, 197. 
CEsophagismus, 414. 

(Esophagitis, corrosive, 405; purulent, 405. 
OEsophagus, cancer of, 412. 

CEsophagus, dilatation of, 406; aetiology and 
pathology of, 406; clinical history, 407; dif- 
fuse dilatation, 406; diverticula, 406; maras- 
mus in, 408; symptoms, 406; treatment, 408; 
ulceration in, 408. 

78 



CEsophagus, disease of, 404. 

CEsophagus, inflammation of, 404; aetiology 
and pathology of, 404; corrosive and puru- 
lent oesophagitis, 405; symptoms and treat- 
ment, 405; ulcers in, 405. 

CEsophagus, neuroses of, 414; paralysis of, 
415; rupture of, 414; spasm of, 414; stenosis 
of, 409. 

Oleoresina aspidii for intestinal parasites, 513. 

Oligocythaemia, 512-518. 

Oliguria in cholera, 89. 

Omalgia in muscular rheumatism, 695. 

Ophthalmoplegia, progressive, 1045. 

Opisthotonos in tetanus, 1166. 

Opium, in acute peritonitis, 528; in diabetes 
mellitus, 766; in dysentery, 84; in intestinal 
catarrh, 473; in intestinal obstruction, 507; 
in perityphlitis, 4S6; in tuberculosis of 
the intestine, 490; in typhoid, 27; poison- 
ing, see Morphine. 

Optic atrophy, in chronic hydrocephalus, 113S; 
in diabetes, 757; in general paralysis of the 
insane, 1133; in multiple sclerosis, 957; in 
tabes, 972. 

Optic neuritis, cerebral tumors, 111S: in puru- 
lent meningitis, 1058. 
Optic tract, 1089. 

Orchitis, in parotitis, 391; in typhoid, 20. 

Organo-therapy, in acromegaly, 903; in Addi- 
son's disease, 653; in myxoedema. 901. 

Orthopnoea in pleurisy, 286. 

Osteomalacia, 704; aetiology and pathology, 
704; clinical history, 705; diagnosis and 
treatment, 707; ovariotomy in, 707; relation 
to pregnancy and menstruation, 705. 

Osteomyelitis in septic and pyaemic diseases, 
117-120. 

Otitic abscess of the brain, 1110. 

Otitis, in influenza, 79; in measles, 51; in 

scarlet fever, 40; in typhoid, 13; in typhus, 

33. 

Ovaries in osteomalacia, 705. 
Oxalic-acid poisoning, 1206. 
Oxybutyric acid in diabetes mellitus, 754. 
Oxygen in pernicious anaemia, 726. 
Oxyuris vermicularis. See Intestinal Para- 
sites. 
Ozaena, 137, 138. 

Pachydermia laryngis, 143. 

Pachymeningitis cervicalis hypertrophica, 918; 

interna haemorrhagica, 1053; spinal, 915, 916, 

919. 

Pain, in chorea, 1154; in hysteria, 1178; paraly- 
sis agitans, 1159; rheumatoid, in paralysis of 
the insane, 1131. 

Pain, sense of, 793. 

Pains of tabes dorsalis, 965. 

Palisade-worm, 647. 

Palpitation in valvular heart disease, 327. 

Pancreas, diseases of, 585; atrophy of, 5S5; 
calculi, 587; cancer, 5S6; cysts, 586; diag- 
nosis, 5S6; glycosuria in, 5S6; haemorrhages 
into, 585; prognosis, 587: vomiting in. 585. 

Pancreatitis, 585. 

Papilloma of the bladder, 672. 

Papilloma of larynx, 155. 

Paradoxical contraction, 842 



1234 



INDEX 



Paralysis, 829; aetiology of, 832; acute bulbar, 
104S; of arm muscles, 869; arsenical, 875; 
ascending spinal, 1021; asthenic bulbar, 1046; 
of back and abdomen, 865; Bell's, 858; 
Brown-Sequard's, 1036; bulbar, 1049; cere- 
bral infantile, 1111; classification of, 829; of 
diaphragm, 871; diphtheritic, 72; electrical 
reactions in, 842; facial, 858; family periodic, 
1047; flaccid, 834; general, 1127; gluteal, 872; 
hysterical, 1178; in hydrophobia, 122; Lan- 
dry's, 1021; lead, 873, 1208; of leg muscles, 
871: median, 868; musculo-spiral, 866; ob- 
stetrical, 869; obturator, 872; occupation, 
S70; peripheral, 854; peroneal, 872; radial, 
866; reflex, 833; sciatic, 872; of shoulder, 863; 
spastic, 1007; spinal infantile, 1014; syph- 
ilitic spinal, 1028; of tibialis, 873; toxic, 832; 
trigeminal, 858; in typhoid, 17; ulnar, 868; 
vaso-motor, 898. 

Paralysis agitans, 1157; aetiology and clinical 
history, 1157; diagnosis and treatment, 1160; 
nature of the disease, 1160; propulsion and 
retropulsion in, 1159; temperature in, 1159; 
voice in, 1159. 

Paralysis, laryngeal, 150: of arytaenoideus, 
152; of crico-arytaenoid, 153; of dilators of 
the glottis, 151; prognosis, 152; of recurrent 
laryngeal, 151; of superior laryngeal, 150; of 
thyro-arytaenoid, 152; treatment, 153. 

Paralysis, ocular, 854; of abducens, 856; aeti- 
ology of, 854; of oculo-motor, 856; recurrent, 
857; strabismus in, 855: trochlear, 856. 

Paralytic dementia, 1129. 

Paramyoclonus, 1157. 

Paranephritic abscess, 641. 

Paraphasia, 1079. 

Paraplegia, 831; in acute ascending spinal 
paralysis, 1022; ataxic. 1011; congenital 
spastic, 1012; in hydrocephalus, 1138; in 
myelitis, 946. 

Parasites, intestinal, 508. 

Paretic dementia, 1129. 

Parkinson's disease. See Paralysis Agitans. 

Parotitis, 390; clinical history, 390; complica- 
tions, 391; idiopathic, 390; infection, 390: 
secondary suppurative form of, 391. 

Parotitis, in scarlet fever, 42: in typhoid, 13: 
in typhus, 33: in secondary suppurative, 391. 

Parry's disease. See Exophthalmic Goitre. 

Pedatrophy, 479. See also Intestinal, 
Catarrh of Children. 

Peliosis. See Purpura. 

Pelvis, deformed, in osteomalacia, 706. 

Peptonuria in croupous pneumonia, 215. 

Percussion, in acute peritonitis, 524; in 
ascites, 533; in pulmonary emphysema, 192; 
in tuberculosis, 245. 

Pericarditis, 359 (see also 329); adhesive peri- 
carditis, 364; aetiology of, 359; clinical symp- 
toms, 360; course, 367: diagnosis, 366; 
dyspnoea in, 361; effusion of, 360; explora- 
tory puncture in, 367; fever in, 361; friction 
in, 362, 366; hemorrhagic, 360; maculae 
tendinae, 360; mediastino-pericarditis, 363; 
obliteration of the pericardial cavity, 364; 
pathological anatomy, 360; percussion reso- 
nance in, 362; pericardial friction rub, 362, 
366; pericarditis externa, 363; physical signs, 



361; pleuro-pericarditis, 363; prognosis, 367; 
pseudo-cirrhosis of liver in, 365; pulse; 361; 
pulsus paradoxus, 363; relation to articular 
rheumatism, 359-367; relation to tubercu- 
losis, 359; sequelae, 363; special forms of, 
363; treatment, 367; tubercular pericarditis^ 
365. 

Pericarditis, purulent, 360. 

Pericarditis, rheumatic, 679. 

Pericardium, diseases of, 359. 

Perinephritis, 640. 

Periodic family paralysis, 1047. 

Peripheral nerves, new growths in, 896. 

Peripleuritis, 295. 

Peritoneal tuberculosis, 249. 

Peritoneum, cancer of, 535; colloid cancer of, 
536; miliary cancer of, 535. 

Peritonitis, acute, 520; abscesses in, 527; aeti- 
ology of, 520; bacteria in, 520; circum- 
scribed, 526; clinical history, 523; diagnosis, 
527; infection, 520; pathology of, 521: per- 
cussion in, 524; pulse in, 525; rheumatic, 521; 
symptoms, 523; treatment, 528; ulceration, 
522; vomiting in, 525. 

Peritonitis, chronic and tubercular, 529; aeti- 
ology of, 529; clinical history, 530; defor- 
mans, 530; diagnosis, 530; fever in, 531; in 
children, 531; palpation in, 530; pathology. 
529; treatment, 532; tubercles, 530. 

Peritonitis, from gastric ulcer, 438; from 
typhlitis and perityphlitis, 485; in relapsing 
fever. 37: in typhoid, 12; tubercular, 249, 
530. 

Perityphlitis, 482. 
Pernicious anaemia, 710. 

Pernicious intermittent fever. See Malarial 

Diseases. 
Peroneal paralysis, 872. 

Perturbatio critica, 32, 217; in relapsing fever, 
35. 

Pertussis, see Whooping-cough; after 

measles, 52. 
Pestis minor. See Plague. 
Petechiae, in plague, 110: in typhoid, 18; in 

typhus, 32. 
Petit mal. 1144. 

Peyer's patches, in cholera, 90; in typhoid, 9. 

Phalanges, terminal, thickened, in bronchi- 
ectasis, 179; in heart disease, 324. 

Pharyngeal diphtheria, 68. 

Pharyngitis, chronic, 400; aetiology of, 400; 
adenoid growths in pharynx, 401; anatom- 
ical changes in, 400; catarrh of the naso- 
pharynx. 400; hypertrophic catarrh in 
pharynx. 401: posterior nasal catarrh, 400; 
prognosis and treatment, 402; sicca. 401; 
symptoms and variations of, 400. 

Phenacetine, in neuritis, 892; in typhoid. 27. 

Phimosis in diabetes mellitus, 757. 

Phlegmon in small-pox, 58. 

Phloridzine-glycosuria, 749. 

Phosphorus, in osteomalacia, 707; in rachitis, 
704. 

Phosphorus poisoning, 1209; diagnosis from 

acute yellow atrophy of liver, 568. 
Physostigmine in paralysis agitans, 1160. 
Picro-nitrate of potassium in chyluria, 648. 
Pigment in the lungs, 271. 



IXDEX 



1235 



Pilocarpine hydrochlorate in acute nephritis, 
616. 

Pin-worms. See Intestinal Parasites. 

Piperine in leukaemia, 733. 

Plague, 107; adenitis in, 109: antitoxine of, 
111; bacillus pestis bubonicae, 107; convul- 
sions in, 109; course and symptoms, 108; 
diagnosis, prognosis, and treatment, 110; 
disinfection, 108; filth, relation to, 108; gan- 
grene, 109; haemorrhages, 109: headache 
in, 108; history in distribution, 107; im- 
munity, 111; incubation, 108; infection, 108; 
inguinal adenitis in, 108; inoculation. 108: 
in animals, 107; mortality. 110: in different 
races, 108; pestis minor, 110; pulse and tem- 
perature in, 108; therapeutic measures. Ill; 
urine, 109. 

Plasmodium rnalarise, 94, 95. 

Pleura, diseases of, 279: after emphysema, 
283; cicatricial contractions of, 282; new 
growths of, 300. 

Pleurisy, 279; absorption of effusion, 288; 
adhesions, 285; aetiology, 279; aspiration 
in, 293; auscultation, 285; complications, 
288; cough and expectoration, 283; course of 
the disease, 283; diagnosis, 290; diplococci 
in, 280; diuretics in, 292; dyspnoea in, 283, 
293; emphysema, 290; exploratory puncture, 
291; fever in, 284, 289; fibrine in, 281; fibri- 
nous, 285; haemorrhages in, 281; infection, 
281; inflammation. 280: orthopncea in, 286; 
pathological anatomy of, 2S1: percussion, 
285; pleuritic contraction, 288; pleuritic 
effusion, 285; pneumothorax, 290; primary 
rheumatic, 288; prognosis, 291; purulent, 281, 
284, 290; resonance, tympanitic, etc., 285; 
sicca, 285; symptoms. 283; temperature 
curve, 293; treatment, 291; tubercular, 280, 
289; urine in, 284; various forms of, 288; 
vocal fremitus in. 290. 

Pleurisy in influenza, 79; sanious, from pul- 
monary gangrene, 268; tubercular, 289. 

Pleuritis. See Pleurisy. 

Pleuro-pericarditis, 363. 

Pleuro-pneumonia. See Pneumonia, Croup- 
ous. 

Pneumatic treatment of pulmonary emphy- 
sema, 195. 

Pneumatosis pulmonum. See Pulmonary 

Emphysema. 
Pneumonia alba, 279; asthenic, 220; bilious. 

210. 

Pneumonia, catarrhal, 199 (see also 60); aeti- 
ology of, 199; bacteria in, 200; in childhood, 
202; expectoration, 201: fever, 201: in in- 
fluenza. 79; origin of, 199; pathological 
anatomy. 201; pulse in. 202; relation to lobu- 
lar, 200: respiration, 202; secondary catar- 
rhal, 202; symptoms of primary catarrhal, 
of adults, 201; treatment and prophylaxis, 
203; tuberculosis in, 203. 

Pneumonia, croupous, 204; aetiology of, 205; 
alcohol in, 225: asthmatic, 220; ausculta- 
tory signs, 211; baths in, 224; blood in. 
213; cardiac complications in, 214. 222, 
224; casts of bronchi in, 210: central, 219; 
cholesterine crystals in, 222: circulatory ap- 
paratus in, 213; course of the fever, 216; 



crisis in, 218; delayed resolution of, 220; 
delirium, 215; diagnosis, 222; digestive appa- 
ratus in, 214; diplococci of, 205, 208, 210, 215, 
219, 222; drunkard's, 218; dyspnoea in, 208, 
223; expectoration, 205, 209, 219, 221; exu- 
dation of, 207; fever in, 209, 216, 221; gen- 
eral course of, 208; haematoidine crystals 
in, 222; in animals, 205; in children and the 
aged, 218, 223; infection, 205, 220; jaundice 
in. 214; kidneys and urine in, 215: lung- 
symptoms, 209; meningitis in, 215, 216; 
nervous system in, 215; oxygen inhalation 
in, 225: pathological anatomy of, 207: pe- 
culiarities and anomalies, 218; peptonuria 
in. 215; physical examination, 210; pleural 
symptoms, 213; pleurisy in, 208; pre-exist- 
ing, 219; pneumo-typhoid, 220; predisposi- 
tion. 206; prodromata, 208; prognosis, 222; 
pulse, 213; rales in, 212, 219, 221; respiration 
in. 211: rudimentary and abortive forms, 
219; skin in, 216; sputum septicaemia, 205; 
stages of, 207; stitch in the side, 209: tem- 
perature curve of, 216; termination, 221; 
traumatic,. 206; treatment. 223: typhoid, 
217. 

Pneumonia, croupous, in influenza, 79; de- 
layed, 220; diplococci, 205: drunkard's, 218; 
fibrinous, see Pneumonia. Croupous: in the 
aged, 218; in children, 218; in erysipelas. 66; 
in foetid bronchitis, 168: in measles, 51: in 
plague, 110: in pre-existing chronic diseases, 
219; in scarlet fever, 43. 

Pneumonia, lobular, see Catarrhal Pneu- 
monia: after whooping-cough, 174; in bron- 
chial stenosis, 181: in diphtheria, 72: in 
influenza, 79; in septic and pyaemic diseases, 
120; in typhus, 33: rudimentary and abor- 
tive forms, 219. 

Pneumonia, stripe, in catarrhal pneumonia, 
203: typhoid, 220; wandering, 212. 

Pneumonic pulmonary tuberculosis, 245. 

Pneumonoconiosis. See Diseases from In- 
halation of Dust. 

Pneumothorax, 295; aetiology, 295; ausculta- 
tion, 297: composition of gas in, 298; diag- 
nosis, 298: effusion in, 296; forms of, 297; 
from phthisis, 295; hydro-pneumothorax, 
296; inflammation in, 296; metallic rales, 
297: pathological anatomy of, 296; per- 
cussion note in, 297 ; pleura in, 296; pulse in, 
296; pyo-pneumothorax, 296; sacculated, 
296; symptoms and course of, 296; treat- 
ment, 299. 

Pneumothorax, in pleurisy, 290: from pul- 
monary gangrene, 268. 
Pneumo-typhoid, 220. 
Podagra. See Gout. 

Poikilocytes. in anaemia and chlorosis, 724: in 

the blood. 448, 512, 518. 
Poisoning, symptoms and treatment, 1206. 
Poliomyelitis, acute and chronic, in children, 

1014; aetiology and pathological anatomy of. 

1014; clinical history, 1015; diagnosis, 1017; 

prognosis and treatment, 101S; reflexes in, 

1016. 

Poliomyelitis of adults, acute, 1019. 
Poliomyelitis, subacute and chronic, 1020. 
Polyarthritis, chronic, 6S8. 



1236 



INDEX 



Polymyositis, acute, 698; complications, 698; 
diagnosis and treatment, 699; polyneuritis 
in, 699; pulse in, 698; splenic tumor. 698. 

Polyneuritic psychoses, 894. 

Polyneuritis, 888 (see Multiple Neuritis). 

Polysarcia adiposa. See Obesity. 

Pomegranate root in tape-worm, 513. 

Portal vein, diseases of, 536; purulent inflam- 
mation of, 582. 

Portal vein, thrombosis of, 583; aetiology and 
pathology of, 583; clinical history, 584: col- 
lateral circulation, 584; diagnosis, 584; 
spleen in, 584. 

Posterior nasal catarrh, 400. 

Post-hemiplegic chorea, 1100. 

Potassic bromide in epilepsy, 1149. 

Potassic chlorate in stomatitis, 384. 

Potassic cyanide poisoning, 1210. 

Potassic nitrate poisoning, 1207. 

Potassium acetate in cirrhosis of the liver, 
562. 

Pott's disease, 934. 

Pressure paralyses of spinal cord, 934; aeti- 
ology, 934; clinical history of, 937; diagnosis, 
941; in cancer of the vertebrae, 935; patho- 
logical anatomy of, 935; reflexes in, 939; 
stasis of lymph in. 936: treatment, 942; 
tubercular spondylitis, 935; vertebral caries 
in, 934. 

Priapism, in leukaemia, 731; in traumatic 
lesions of spinal cord, 931. 

Professional neuroses, 882. 

Prosopalgia. See Neuralgia of Trigeminus. 

Pruritus in diabetes mellitus, 757. 

Psammoma, 1116. 

Pseudo-cirrhosis of the liver, 365. 

Pseudo-crises in croupous pneumonia, 217. 

Pseudo-hypertrophy of the muscles, 1000. 

Pseudo-leucocythaemia. See Pseudo-leuke- 
mia. 

Pseudo-leukaemia, 733; lymphatica, 734; patho- 
logical anatomy, 734; prognosis, 735; symp- 
toms, 734; treatment, 735; tumors in, 734. 

Pseudo-membranous bronchitis. See Croup- 
ous Bronchitis. 

Pseudo-sclerosis, 959. 

Pseudo-tabes (ataxia) of alcoholism, 893. 
Psoriasis, lingual, 388. 

Pulmonary anthrax. See Malignant Pus- 
tule. 

Pulmonary consumption. See Tuberculosis 
op Lungs. 

Pulse, arhythmic, 314, 328; bulbous, 322; curve 
in aortic insufficiency, 319: curve in mitral 
stenosis, 314; curve in stenosis of aortic 
orifice. 321; in acute peritonitis, 525: in 
anaemia and chlorosis. 713; in arterioscle- 
rosis, 372; in catarrhal pneumonia, 202: in 
cholera, 88; in croupous pneumonia. 213: in 
diphtheria. 69: in endocarditis, 306; in 
plague, 10.8; in pleurisy, 284; in pneumo- 
thorax, 296; in polymyositis, 698: in pul- 
monary tuberculosis, 250; in scarlet fever, 
47: in septic and pyaemic diseases, 120: in 
tabes dorsalis, 974; in tubercular meningitis, 
1062; in typhoid, 17: in valvular disease of 
the heart, 313, 319. 

Pulse rate in catarrhal jaundice, 538. 



Pulsus bigeminus, 328. 

Pulsus paradoxus, 363; in tracheal stenosis, 
ISO. 

Purpura, 744: cutaneous ecchymosis in. 744. 

745; rheumatica, 745; treatment, 745. 
Pyaemia. See Septic and Pyemic Diseases. 
Pyelitis, 654. 

Pyelitis calculosa. See Nephrolithiasis. 
Pylephlebitis, chronic adhesive, 583; from 

typhlitis and perityphlitis, 485. 
Pylephlebitis, suppurative, 582; aetiology and 

clinical Mstory, 582; in the new-born, 582; 

pathology, 582: pyaemic symptoms, 5S3; 

splenic enlargement in, 582. 
Pylethrombosis. See Thrombosis of Portal 

Vein, 583. 

Pyloric stenosis, in cancer of the stomach, 
447; from gastric ulcer, 434, 438, 443: vomit- 
ing in, 439. 

Pyo-pneumothorax. See Pneumothorax. 

Quincke's capillary pulse, 319. 

Quinine, injection. 101; in amyloid kidney. 
639; in malarial diseases, 96, 100; in 
Meniere's disease, 1140; in neuralgia, 809; in 
relapsing fever, 38; in small-pox, 62. 

Quinsy, 396. 

Quotidian fever, 97. 

Rabies canina. See Hydrophobia. 

Rachitis, 699; aetiology, 699; clinical history, 
701; diagnosis and treatment. 703: head and 
thorax in. 702; pathology, 700; symptoms, 
702. 

Radial paralysis, 866. 

Ragpickers' disease. See Anthrax. 

Railway spine. See Traumatic Neuroses. 

Rales, bronchial, 159; in bronchiectasis. 177; 
in chronic bronchitis, 163; in croupous pneu- 
monia, 212, 219, 221; in pleurisy, 287; in pul- 
monary oedema, 198; in tuberculosis, 242; 
metallic, in pneumothorax, 297. 

Rash, initial, of small-pox, 55; in plague, 109; 
in scarlet fever, 39. 

Raynaud's disease, 900. 

Reaction of degeneration, 848. 

Rectum, syphilis of, 490. 

Recurrent endocarditis, 307. 

Reflex asthma, 182. 

Reflex epilepsy, 1142. 

Reflex neuralgia, 805. 

Reflex paralysis, 803. 

Reflexes, abdominal, 839: in amyotrophic 
lateral sclerosis, 989,; in cerebral haemor- 
rhage, 1097; in cerebro-spinal meningitis, 
114: in chorea. 1154; cremaster, 839; cuta- 
neous, 839; in. hysteria. 1175; in multiple 
sclerosis. 956: in myelitis, 94S: in neu- 
ralgia, 804; in neuritis, 890; in paralysis, 
834, 1022. 1057: in primary degeneration 
of motor tract. 955: in polyneuritis, 891: 
in progressive bulbar paralysis, 1041: in 
sciatica, 818; in segmental diagnosis, 927: in 
spinal infantile paralysis. 1015; in spinal 
progressive muscular atrophy. 995: in tabes, 
965, 971: tendon. 834: in tetanus, 1167: in 
traumatic lesions, 931; in trigeminal anaes- 
thesia. 931: in vertebral caries, 939. 



IXDEX 



1237 



Regeneration of nerves, S50. 
Relapses, in scarlet fever, 46; in typhoid, 
20. 

Relapsing fever, 33: blood in, 33: clinical j 
history, 34; complications and varieties. 37; 
contagiousness, 34: course of, 35: epidemics 
of. in Germany. 34; in America. 34: epistaxis 
in. 37; inoculation of, 34: number of attacks, 
36: peritonitis in, 37; perturbatio critica, 35; 
prognosis and treatment, 37: stage of incu- 
bation and prodromal symptoms, 34: tem- 
perature, 34, 35. 

Relapsing typhus. See Relapsing Fever. 

Remittent malarial fever. See Malarial Dis- 
eases. 

Ren mobilis, 648. 

Resorcine, in acute gastric catarrh. 425; in 
thrush, 3S7. 

Respiration, in acute peritonitis, 526; in 
ascites, 533; in bronchial asthma. 1S4: in 
capillary bronchitis. 160: in retropharyn- 
geal abscess, 403. 

Respiratory muscles, spasms of. 881. 

Retina, in nephritis, 622. 

Retinitis, albuminuric, 622, 632; leukaemia, 
730. 

Retropharyngeal abscess. 403: deglutition in. 
403: dyspnoea of, 403; treatment, 404. 

Rheumatic peritonitis. 521. 

Rheumatism, acute articular, 675; aetiology of, 
675; cardiac symptoms, 679; course, 682; j 
diagnosis, 683; duration. 682; fever in. 677; 
general symptoms, 682: hyperpyrexia in, 681, t 
687; infection, 675; joints in, 678: nervous 
symptoms in. 683: peculiarities of. 678; pro- 
dromata, 677; prophylaxis. 688; prognosis. 
682: purulent arthritis in. 676; serous and j 
mucous membranes in. 6S0: skin. 680; ! 
staphylococci, 676; symptomatology of, 677: 
symptoms referable to different organs, 678; 
temperature in, 683: treatment, 684; viscera, 1 
682. 

Rheumatism, acute and chronic muscular, 694; j 
baths in, 697; clinical history of. 695; defi- 
nition and aetiology of. 694; omalgia, 695; \ 
treatment, 697. 

Rheumatism, cerebral, 681. 

Rheumatism, chronic articular, 688: aetiology 
of, 688; baths in, 693; course, 692; pathology 
of, 689; prognosis, 693: spondylitis defor- 
mans, 691; symptomatology, 690: treatment, 
693. 

Rheumatoid influenza. 78. 

Rhinitis, chronic. 137; ozaena simplex, 137: 
relation to syphilis, 138: treatment, 137, 
138; turbinated bones in. 137. See also 
Coryza. 

Rhonci in acute catarrh of trachea and \ 

bronchi, 159. 
Rickets. See Rachitis. 

Rigor, in erysipelas, 64; in septic and pyaemic 
diseases. 122; in small-pox, 55: in typhus. I 
33. 

Rontgen rays, in aneurism, 376: in nephro- ! 

lithiasis, 660: in tumor of the brain. 1121. 
Roseola, in cerebro-spinal meningitis. 114: in 

influenza, 80: in miliary tuberculosis, 262: 

in typhoid. 18: vaccine. 61. 



Rotheln. 53: period of incubation, 53: prog- 
nosis, 54: relation to measles, 53. 
Round-worms. See Intestinal Parasites. 

Saccular bronchiectasis, 177. 

Salicylic acid, in articular rheumatism, 684; 

in neuritis, 892; in relapsing fever, 38; in 

tetanus, 1168. 
Salivation in progressive bulbar paralysis, 

1041. 

Santonica in ascarides, 516. 

Sapo viridis in scrofula, 788. 

Sarcinae in cancer of the stomach, 446. 

Sarcoma, in brain, 1116: of the kidneys, con- 
genital, 644; in lungs, 277; mediastinal, 301; 
melanotic, 574; of the nerves, 897. 

Sausages, poisoning from. 1212. 

Scarlatina. See Scarlet Fever. 

Scarlatinal angina, 42: diphtheria, 39; erup- 
tions, 39; nephritis, 39; synovitis, 44: tongue, 
42. 

Scarlet fever, 38: aetiology of, 38; anasarca in, 
43; baths in, 47: clinical history, 39; con- 
tagiousness, 38: diagnosis, 46; diet in. 46; 
diphtheritic rhinitis in, 42: fever in. 40; geo- 
graphical distribution of. 39: hygienic treat- 
ment of, 28, 48; intestinal symptoms, 45; 
joints in, 44; kidneys in. 43: miliary, 42: 
otitis media, 40, 42, 47; papular, 42: predis- 
position to, 38; prodromata. 39: prognosis, 
46; rash in, 39; relapses, 46; rudimentary 
forms, 45; severe forms of, 45; spleen in, 39; 
streptococci in, 41: temperature in, 39, 43; 
tenacity of contagium. 3S: throat in. 40: 
treatment. 46; variations in course of, 45. 

Sciatic nerve, paralyses in region of, S72; 
paralysis of trunk of, 873. 

Sciatica, 817; aetiology, 817; diagnosis and 
treatment, 819; myokymia in, S18: nerve- 
stretching in. 820; sciatic scoliosis, 818; 
symptoms, 817; treatment, S19. 

Scleroderma, 902. 

Sclerosis, amyotrophic lateral, 986; arterio-, 
370; diffuse cerebral, 1110; lateral primary, 
1006: multiple, 954; of the coronary arteries, 
see Interstitial Myocarditis; posterior 
spinal, see Tabes Dorsalis: pseudo-, 959. 

Scoliosis in tuberculosis, 244. 

Scorbutus. See Scurvy. 

Scrofula. 787; complications, 7S7: definition 
and symptoms, 787; lymph glands in, 787; 
treatment, 788; tubercle bacilli in. 78S. 

Scrofula, relation to tuberculosis, 226. 236. 

Scurvy, 738: aetiology of. 739: clinical history. 
740; complications, 742; contagiousness, 740: 
course of. 742: diagnosis. 742: gums and 
mucous membranes in. 741: haemorrhages 
in, 739. 742: prognosis. 742: treatment, 743; 
ulceration. 741: varieties of, 742. 

Seat-worms. See Intestinal Parasites. 

Secretion, disturbances of. 904. 

Sensory conduction tracts, 796; localization 
of. 1075. 

Septic and pyaemic diseases, 116; abdominal 
symptoms. 121: affections of the joints in. 
120; cerebral symptoms, 120; circulatory 
disturbances. 120: clinical history". 119: 
course of the disease. 121: course of fever in, 



123S 



INDEX 



119; cutaneous symptoms, 119: diagnosis, 
121; empyema, 120; . haemorrhages, 120; in- 
fection, 118; ocular disturbances, 121; osteo- 
myelitis, 117; pathological anatomy, 118; 
prognosis, 121; pulmonary symptoms, 120; 
pyaemic fever, 119; renal changes, 120; 
spleen in, 121; streptococci and staphy- 
lococci, 117 ; treatment, 122. 

Septic ulcerative endocarditis. 307. 

Serum reaction (Widal's) in typhoid, 22. 

Sexual neurasthenia, 1197. 

Sexual organs, relation to hysteria. 1174. 

Shaking palsy. See Paralysis Agitans. 

Ship fever. See Typhus. 

Sick headache. See Migraine. 

Silver nitrate in cystitis, 672. 

Singultus, 882. 

Sinuses, cerebral, thrombosis of, 1064; symp- 
toms, 1065. 

Skin, in erysipelas, 64; in malarial diseases, 
98; in pulmonary tuberculosis, 247; in ty- 
phoid, 18. 

Small-pox, 54; anomalies in, 58; articular 
swelling, 58; bacteria in, 54; circulatory 
system. in, 58; complications, 58; contagious- 
ness, 54; course of, 55; course of fever, 57; 
diagnosis and prognosis, 59; digestive system 
in, 58; eyes in, 62; haemorrhagic, 55, 59, 62; 
in animals, 55, 60; incubation stage, 55; 
initial stage, 55; inoculation of, 55; mor- 
tality of, 60; nervous system in, 58: organs 
of special sense, 58; predisposition to, 54; 
prodromal symptoms, 55: prophylaxis, 60; 
respiratory organs in, 58; skin in, 57; spinal 
disease after, 58; suppurative fever in, 57; 
temperature curve, 57; tenacity of poison 
of, 54; treatment, 60; variola vera. 55: vario- 
loid, 56. 

Smegma bacilli vs. tubercle bacilli. 663. 
Smell, anomalies in sense of, 826. 
Snuffles. See Coryza. 

Sodium salicylate, in articular rheumatism, 

685; in migraine, 907. 
Softening of the brain, from embolism or 

thrombosis, 1103; idiopathic, 1110. 
Soor. See Thrush. 

Sopor, in acute yellow atrophy of liver, 566; 
in cholera, 90; in diphtheria, 71. 

Sore throat, 394; aetiology of, 394; bacteria in, 
394; catarrhal. 395; clinical history, 394; 
diagnosis, prognosis, and treatment, 398; 
fever in, 395; infection, 394: parenchym- 
atous, 396; phlegmonous. 397: predispo- 
sition, 394; quinsy. 396; various forms of. 
395. 

Sore throat in erysipelas, 64. 
Soul-blindness, 1076. 
Soul-deafness, 1076. 

Spasm, of accessory nerve, 878; of diaphragm, 
882; in epilepsy, 1144; facial, 876; of leg 
muscles, 880; lingual, 877; localized. 875: in 
neck muscles, 875; in paralysis. 835: in pro- 
fessional neuroses, 882; of respiratory mus- 
cles, 881; saltatory reflex, 881: of shoulder 
and arm muscles, 880: in writer's cramp, 
882. 

Spastic* infantile hemiplegia. 1111. 
Spastic paraplegia, congenital. 1012. 



Spastic spinal paralysis, 1007; diagnosis, 1012; 

prognosis, 1012; treatment, 1012. 
Spastic spinal paralysis, syphilitic, 1028. 
Speech, centers of, and disturbances of, 1077. 

See also Aphasia. 
Spina bifida, 1032. 
Spinal apoplexy, 929. 

Spinal cord, diseases from variation of atmos- 
pheric pressure, 932; disturbances of circu- 
lation in, 928; in haemorrhage into, 929; in 
multiple sclerosis of, 954; in new growths of, 
1024; in pressure paralyses of, 934. 

Spinal cord, secondary degeneration in, 1033; 
after amputations, 1036; after cerebral 
lesions. 1033; in affections of spinal cord, 
1034. 

Spinal cord, segmentation of, 927. 
Spinal cord, syphilitic affections of, 1026. 
Spinal cord, traumatic lesions of, 930; reflexes 
in, 931. 

Spinal cord, tumors of, 1024. 
Spinal cord, unilateral lesions of, 1036. 
Spinal localization, 920 et seq. ; reflexes in, 
927. 

Spinal meninges, acute inflammation of, 915; 
aetiology and pathology of, 915; leptomenin- 
gitis, 915; symptoms, diagnosis, prognosis, 
and treatment, 916. 

Spinal meninges, haemorrhage into, 919. 

Spinal meningitis, acute, 915; chronic, 917. 

Spinal neurasthenia, 933. 

Spinal paralysis, Brown-S§quard's, 1036; acute 

ascending, 1021; of children, 1014. 
Spinal progressive muscular atrophy, 990. 
Spirilli in blood, 33-36. 

Spleen, in acute yellow atrophy of liver, 566, 
567; in cholera. 90; in cirrhosis of liver, 558; 
in leukaemia. 727; in malarial diseases, 
95; in plague, 109: in relapsing fever, 34; 
in septic and pyaemic diseases, 121; in small- 
pox, 55; in suppurative pylephlebitis, 582; 
in thrombosis of portal vein, 584: in ty- 
phoid. 12: amyloid, 250. 

Splenic fever. See Malignant Pustule. 

Spondylitis. 934; deformans, 691; tubercular, 
935. 

Spotted fever. 30. See also Cerebro-spixal 

Meningitis. 
Sputum crudum and sputum coctum, 15S. 
Sputum of bronchiectasis, 178; of bronchitis, 

164; foetid, 168; of central pneumonia, 219. 
Staphylococci, in articular rheumatism, 676- 

679: in endocarditis, 304; in septic and 

pyaemic diseases, 117; in sore throat, 394; 

in typhoid, 19. 
Staphylococci and streptococci in septic and 

pyaemic diseases, 117, 120. 
Stenocardia, 355. 

Stenosis, from cicatrices, etc.. 507; mitral, 
312; of aortic orifice, 320; pulse curve in. 
321. 

Stenosis of the intestines, 499. 

Stenosis of the oesophagus, 409: aetiology and 
pathology of. 409; auscultation in. 410: 
causes of. 409: dysphagia in, 409: nutrient 
enemata in. 412: prognosis and treatment. 
411: regurgitation of food in. 410: symp- 
toms, 410. 



INDEX 



1239 



Stenosis of pylorus in gastric ulcer, 434. 438, 
443. 

Stenosis of the rectum in syphilis, 490. 

Stenosis, of trachea and bronchi, 180; aeti- 
ology and symptoms of, 180; bronchial, 
181; pneumonia from, 181; prognosis and 
treatment, 181; pulsus paradoxus, ISO. 

Stenosis, valvular, 314, 320, 322. 

Stercoraceous vomiting, 503. 

Stitch in the side, in croupous pneumonia, 209; 
in pleurisy, 283. 

Stomacace. See Stomatitis, Ulcerative. 

Stomach, abnormal position of, 462; abscess, 
432; anacidity of, 452; atony of. 460; can- 
cer of, 444; chronic catarrh of, 425: cicatri- 
cial contraction of, 434. 

Stomach, diseases of, 415; estimation of size 
and position, 420 (see also 460); motor dis- ' 
turbances of, 460: purulent inflammation of, 
see Phlegmonous Gastritis; tests of ab- 
sorptive power of, 421. 

Stomach, motor activity of, 419: in gastric 
ulcer, 437. 

Stomatitis, aphthous, 385. 

Stomatitis, catarrhal, 382; aetiology, 382; bac- 
teria in, 382; clinical history, 3S2; from 
chemical irritation, 382; infection, 382: in 
drunkards, 383; gingivitis, 382; in scarlet 
fever. 41: superficial ulcers in. 3S3; treat- 
ment, 383: in typhoid. 12. 

Stomatitis. disseminated fibrinous. See 
Stomatitis, Aphthous. 

Stomatitis, mercurial, 384. 

Stomatitis, ulcerative, 383; aetiology of, 383; 
fever in, 384; gingivitis in, 384; infection, 
383; swollen lymph glands in, 384; symp- 
toms, prophylaxis, and treatment, 384: ul- 
ceration in, 384. 

Strabismus in ocular paralysis, 855. 

Streptococci, in diphtheria, 70; in influenza. 
79; in septic and pyaemic diseases. 117: in 
sore throat, 394; in tuberculosis, 234. 

Streptococcus pyogenes, in endocarditis, 304: 
in erysipelas, 63: in pleurisy, 290. 

Stripe-pneumonia in catarrhal pneumonia, 203. 

Strongylus, 647. 

Strophanthus, in arterio-sclerosis, 374; in 

heart disease, 338. 
Strychnine, in alcoholic neuritis, 895; in al- 

cohol poisoning, 1210; in muscular atrophy, 

996; in myelitis, 953; poisoning, 1211. 
St. Anthony's fire. See Erysipelas. 
St. Vitus's dance. See Chorea. 
Subnitrate of bismuth, in gastric ulcer, 441, 

442; in intestinal catarrh, 481. 
Suggestion in hysteria, 1184. 
Sulphonal. in chorea, 1156: in neurasthenia, 

1201. 

Sulphur, in cirrhosis, 719: in haemorrhoids, 
495. 

Sulphur baths in lead paralysis, 874. 
Sulphuretted-hydrogen poisoning. 1210. 
Sulphuric-acid poisoning. 1206. 
Sulphurous-acid poisoning. 1206. 
Sunstroke. See Insolation. 
Suppuration in plague. 109. 
Suppurative encephalitis. 1108: hepatitis. 553; 
pylephlebitis, 582. 



Supra-renal capsules, diseases of, 650; tuber- 
culosis of, 651. 

Swamp fever. See Malarial Diseases. 

Sydenham's chorea. See Chorea. 

Syncope. See Cerebral An.emia. 

Synovitis in articular rheumatism, 678. 

Syphilis as cause of aneurism, 374. 

Syphilis, by vaccinia, 61; cerebral, 1125; in 
myelitis, 943, 102S. 

Syphilis of the liver, 571; aetiology, pathology, 
and clinical history, 571; diagnosis and treat- 
ment, 572. 

Syphilis of the rectum, 490 (see also 499); 

stenosis in, 490; tenesmus in, 490; treatment, 

491; ulceration of. 490. 
Syphilis, pulmonary, 276. 

Syphilis, relation to general paralysis, 1130; 

relation to tabes dorsalis. 960. 
Syphilitic affections of spinal cord, 1026. 
Syphilitic endarteritis, 341: myelitis, 1028: 

spinal paralysis, 102S. 
Syphiloma, cerebral, 1127. 

Syringomyelia, 803, 1029: central gliosis, 1030; 
clinical symptoms, 1030; pathological 
anatomy and pathogenesis, 1029. 

Tabes dorsalis, 960; aetiology of. 960: anaes- 
thesia in, 969; arthropathy in, 974; ataxic 
gait in, 966; cerebral symptoms, 976: clini- 
cal history, 964; diagnosis, 977: degenera- 
tion in, 962; disturbances of bladder, rec- 
tum and sexual organs, 973; disturbances of 
motility in. 966: disturbances of special 
sense organs, 972; gastric crisis in. 973: 
laryngeal crisis in, 974; ocular disturbances 
in, 972; patellar reflex in, 965; other reflexes. 
971: pathological anatomy, 962; pulse in, 
974; relation to syphilis, 960; symptoms in 
internal organs, 973; treatment, 97S: trophic 
disturbances, 974. 

Tabes mesenterica, 532; motor, 1006. 

Tachycardia, 327, 357: from scarlet fever, 45. 

Tactile sensibility. 790. 

Taenia cucumerina, 511: echinococcus. 575: 
mediocanellata, 510: nana. 511: solium. 508. 
Taenicides, 513. 
Talalgia, 821. 

Tannin, in intestinal catarrh, 4S1: in tuber- 
culosis of the intestines, 490. 
Tape-worms, 508. 
Tapping in ascites, 535. 
Tarsalgia, 821. 

Taste, anomalies of sense of. S27. 

Temperature, sense of, 792: variations, in 
traumatic lesions of the spinal cord, 931: in 
syringomyelia, 1031. 

Tendon reflexes, 834, S40, 995, 1022: in amyo- 
trophic lateral sclerosis, 9S9; tests of, 840. 

Tenesmus, in children, 478; in dysentery, 82; 
in intestinal catarrh, 472; in syphilis of the 
rectum, 490. 

Tertian intermittent fever. 97. 

Test breakfast, etc.. use of. 417, 437, 439, 455. 

Tetanilla. See Tetany. 

Tetanus. 1165: bacilli of. 1165; clinical history 
of, 1166: diagnosis, 1168; hydrophobic, 1167; 
opisthotonos in. 1166: pulse and temperature 
in. 1167; symptoms of. 1166: treatment, 1168. 



1240 



INDEX 



Tetanus neonatorum, 1166. 

Tetany, 1162; aetiology, 1162: clinical history, 
1163; diagnosis, 1164; exciting causes, 1163; 
prodromata, 1163; symptoms, 1164; tempera- 
ture in, 1164; treatment, 1165. 

Thermic fever. See Insolation. 

Thermo-cautery, in noma, 390; in spondylitis, 
943. 

Thomsen's disease. See Congenital Myo- 
tonia. 

Thorax, in emphysema, 187, 219, 414; in osteo- 
malacia, 706; in rachitis, 702. 

Thrombosis, in typhoid, 18; of basilar artery, 
1050. 

Thrombosis of the cerebral sinuses. 1064; aeti- 
ology and pathology of, 1064; symptoms, 
1065. 

Thrombosis of the portal vein, 583. 

Thrush, 386; aetiology of, 386: fungus of, 386; 
symptoms and treatment, 3S7. 

Thymic asthma. See Spasm of the Glottis. 

Thyroid extract, in rnyxeedeina and cretin- 
ism, 901; in scleroderma, 902. 

Tibial nerve, paralysis of. 873. 

Tic convulsif. See Spasm, Clonic Facial. 

Tic douloureux. See Neuealgia of Trigemi- 
nus. 

Tinnitus aurium, 113: in cerebral anaemia, 
1067; from salicylic acid, 685. 

Tobacco-poisoning. See Nicotine. 

Tonsillar and peritonsillar abscess, 396. 

Tonsillitis, follicular, 396; necrotic, 397. 

Tonsils, chronic hypertrophy of, 399. 

Topical diagnosis of cerebral lesions, 1068; 
of spinal lesions. 920. 

Toxic paralyses, 832. 873. 

Trachea, diseases of. 156. 

Tracheal stenosis, 180. 

Tracheitis. See Bronchitis, Acute. 

Tracheotomy in diphtheria, 69, 74, 76. 

Tract, chief centripetal, 1089; motor, 10S9; 
optic and acoustic, 10S9. 

Transfusion of blood in pernicious anaemia, 726. 

Traumatic lesions of spinal cord, 930. 

Traumatic neuroses (so-called), 1201: prog- 
nosis and treatment, 1205; psychical factors 
in. 1202; relation to hysteria. 1204. 

Tremor, in amyotrophic lateral sclerosis, 9S8: 
in epilepsy, 1147; in exophthalmic goitre, 
911: intention, in multiple sclerosis, 955; 
osteomalacia. 706; in typhoid, 15. 

Tremor, hysterical. 1172: mercurial, 836, 1208. 

Trichina spiralis, 131. 

Trichinosis. 131: aetiology and clinical history. 
132: blood in, 133; diagnosis, 133: fever in. 
133: infection, 132; in animals. 132; muscles 
in. 133; myositis in, 132; oedema in. 133: 
treatment, 134. 

Trichocephalus dispar. See Intestinal Para- 
sites. 

Trigeminus, anaesthesia of. 802. See also Dis- 
eases of the Nervous System. 

Trigeminus, neuralgia of, 810. 

Trional in neurasthenia, 1201. 

Triple phosphate crystals, 669. 

Trommer's test for sugar, 752. 

Trophic disturbances, in arsenical paralysis. 
875; in bones and joints, 975: in cerebral 



haemorrhage, 1096: in facial hemiatrophy. 
909; in myelitis, 949; in nails and skin, 869, 
974; in neuralgia, 807: in paralysis, 833; in 
progressive muscular atrophy, 993; in tabes, 
974. 

Trophic influence of nerves, 834, 849, 899; in 

facial hemiatrophy. 909. 
Tubercle bacilli. 227, 231, 240 ; 489; in scrofula, 

788. 

Tubercula dolorosa, 897. 

Tubercular meningitis, 1059: pericarditis. 365: 
peritonitis, 249, 530; pleurisy, 289: spondy- 
litis, 935. 

Tuberculine. 252. 

Tuberculosis, acute miliary. 261; aetiology of, 
261; caseation in. 261; circulatory apparatus 
in, 264; clinical history, 262; diagnosis, 265; 
digestive apparatus in, 264; dyspncea in. 262. 
263; eyes in, 265; fever in. 263; lumbar 
puncture in, 265; miliary tubercles. 261; 
nervous system in. 265: pathological 
anatomy of, 262: prognosis and treatment, 
266; protracted intermitting form, 263: re- 
spiratory apparatus in, 264; single symp- 
toms, 263; typhoidal form, 262; with pre- 
dominant cerebral or pulmonary symptoms. 
263. 

Tuberculosis, after catarrhal pneumonia, 203: 
after measles, 52: disseminated pulmonary. 
245; distinguished from bronchiectasis, 178. 

Tuberculosis of the genito-urinary apparatus, 
662: aetiology and pathological anatomy of, 
662; bacilli in. 663; clinical symptoms, 663; 
diagnosis. 664: infection. 662; treatment. 
664; ulceration in. 663. 

Tuberculosis of the intestines, 488; diarrhoea 
in, 4S9: infection, 4S8; miliary tubercles in. 
489; tubercle bacilli, 4S9; treatment, 489; 
ulceration in. 489. 

Tuberculosis of the larynx, 147; clinical symp- 
toms, 148; diagnosis, 148; pathological 
anatomy, 147: resemblance to syphilis, 148; 
treatment, 149; tubercle bacilli, 148: tuber- 
culine injection in. 149: ulcers in. 14S. 

Tuberculosis of lungs, 226: aetiology of. in 
man, 228: anaemia in, 247: bacilli of, 227, 
231, 234; caseation. 226, 232, 250; cicatricial 
formations. 233: circulatory organs, 250: 
clinical history, 234: contraction of lungs, 
243; cough in, 237: diagnosis. 251; physical. 
242: of cavities, 243: diarrhoea in, 249: diet. 
257; disseminated pulmonary tuberculosis. 
245; dyspnoea in, 241: elastic fibers. 240: 
emaciation in. 235: expectoration, 227, 23S. 
245: fever in. 246: fibroid phthisis, 243; gen- 
eral pathology and aetiology of. 226: general 
symptoms. 246; genito-urinary tuberculosis, 
229, 250; haemorrhage, pulmonary. 238. 253: 
haemorrhage, influence on temperature. 239; 
health resorts, 257: hectic fever, 246, 260: 
hemoptysis in, 236, 259: hereditary influence. 
229: hydrotherapy in. 259: in animals, 226; 
individual predisposition. 229: in drunkards. 
230: infection. 226: influence of age. 231: 
inoculation. 226: intestinal infection. 229: 
kidneys. 250: larynx, pharynx, and trachea 
in. 248: liver and spleen. 249: lobular atelec- 
tasis, 233; lung symptoms. 237: lupxis. 229: 



INDEX 



1241 



miliary tubercles, 232, 248; night-sweats. 
235: nervous disturbances, 247: pathological 
anatomy, 231; percussion note, 241; peri- 
toneum in, 249; physical symptoms. 241: 
pleural complications. 248; pneumonic pul- 
monary tuberculosis. 245; prognosis. 253: 
pulse in, 250: rales in, 242; respiration in, 
241; scoliosis in, 244: skin in, 247; special 
symptoms and complications, 237: stomach 
and intestinal canal, 249; swelling of lymph 
glands in, 230, 236, 250; temperature curve, 
246: treatment and prophylaxis, 254; tuber- 
culine. 252: ulcers. 232. 248; urinary pas- 
sages and sexual organs, 250: after whoop- 
ing-cough. 174. 

Tuberculosis, peritoneal, 249. 

Tufnell's method in aneurism, 379. 

Tumors and cicatricial strictures of the intes- 
tines. 499. 

Tumors, of the brain, 1115; of the cerebellum. 
1121; of the kidneys, 644; of the larynx. 155. 

Tumors, of the lungs, 276; expectoration of, 
277; sequelae, 278: of the lymph glands. 734; 
mediastinal, 301: of the spinal cord, 1024. 

Turbinated bones in chronic rhinitis, 137. 

Turpentine, oil of, in chronic bronchitis, 166; 
in cystitis, 671; in genito-urinary tubercu- 
losis, 664: in pulmonary gangrene. 270. 

Tussis convulsiva. See Whoopixg-cough. 

Tympanites in jaundice, 539. 

Tympanitic resonance, in catarrhal pneu- 
monia, 203; pleurisy, 286, 287. 

Typhlitis and perityphlitis, 482; aetiology and 
pathological anatomy of. 482; colon bacilli, 
483: diagnosis, 486; faecal calculi, 483; fever 
in, 484, 485, 487; perforation in, 485: prog- 
nosis, 486; symptoms and clinical course, 
483; treatment, 486: typhlitis stercoralis, 
482: ulceration in, 483. 

Typho-malarial fever. See Malabial Dis- 
eases. 

Typhoid fever, 1: abortion in, S: affections of 
respiratory organs in. 13. 28: albtiminuria 
and cystitis in. 19: antipyrine in. 26: arti- 
ficial infection. 2: bacilli. 1; bacilli in the 
lungs. 14. 22: bacilli, culture of. 1: baths in, 
24; bed-sores, 23: blood changes and oedenia 
in, 18; bones and joints in, 19; bronchitis and 
pleurisy in, 13: care of mouth. 12. 23: 
changes in mouth and throat. 12: circu- 
latory system in. 17, 28: clinical symptoms, 
10; cold-pack in. 26: contagiousness, 2: 
course of fever. 6: diagnosis of. 21; diag- 
nosis of, in the aged, 20: diarrhoea in. 10. 2S: 
diet. 23: disinfection. 28: entrance of 
bacilli into human body. 4: epidemic from 
polluted water supply. 4: Ehrlich's reaction, 
19; fastigium in, 6. 25: febrile sequelae. 9: 
fumigation. 30; general course. 5: genito- 
urinary apparatus, 19: hepatic symptoms. 
12: hyperesthesia in. 17: influence of amount 
of water in the soil on development of 
bacilli, 3: intestinal haemorrhage and epi- 
staxis. 8. 11. 27: immunity. 4: manner of in- 
fection, 2. 23: miliaria in. 18: mortality in. 
22: muscle changes in. 19; nephritis in 
nephro-typhoid. 19. 26: nervous symptoms 
in. 16-28: neuralgia in. 17: opium in, 27, 28; 



orchitis in, 20: orchitis, prognosis in, 22; 
outcry of children in, 20; paralysis in, 17; 
pathognomonic changes, 9; peculiarities in 
the course of. 20; period of incubation, 5; 
perforation, 11, 12; peritonitis, 12,27; Peyer's 
patches in, 9; phenomena and complications, 
8; predisposing influences, 5; prodromal 
symptoms, 5: prophylaxis, 28; relapses, 20; 
roseola in, 18; sewer gas not a cause of, 4; 
skin in. 18, 27; stomach changes in, 12; swell- 
ing of lymph glands and spleen, 12; tempera- 
ture, 6, 25; thrombosis in, 18; treatment, 22; 
tympanites. 10: typhus levissimus, 20; urine 

- in. 19: Widal's serum reaction in, 22. 

Typhoid measles, 51. 

Typhoid pneumonia, 217. 

Typhoidal form of miliary tuberculosis, 262. 

Typhus fever, 30; aetiology of, 31; complica- 
tions and varieties in, 32; contagiousness, 
31: course and symptoms of, 31; diagnosis, 
•33: distinguished from typhoid. 30: epi- 
demics of. 31: geographical distribution of, 
31: nervous symptoms of, 32; perturbatio 
critica. 32: prognosis, 33; rigor in, 33; tem- 
perature in, 32; treatment, 33; urine in, 32. 

rffelmann's test for lactic acid, 419. 

Ulcer, atheromatous, 371: cancerous, 445; 
catarrhal, 468: dysenteric, 83; gastric, 432; 
in glanders, 125; in intestinal tubercu- 
losis. 489; in perityphlitis and typhlitis, 
483; in septic and pyaemic diseases, 119; 
in syphilis of the rectum, 490 (see also 499); 
in tuberculosis of the larynx, 148; of the 
duodenum, 488; of the oesophagus, 404; 
of the stomach, 432: on the tongue in whoop- 
ing-cough, 173: peptic. 433; scorbutic, 741; 
superficial, in stomatitis, 383: tuberculous, 
232, 248. 

Ulcerative stomatitis, 383. 

Ulnar paralysis, 868. 

Unilateral lesions of spinal cord, 1036. 

Uraemia, 596; in acute nephritis, 617; amau- 
rosis, 599; clinical symptoms. 599: convul- 
sions, 599; diarrhoea in, 600; dyspnoea, 601; 
eclampsia, 599: pulse in, 600; sequelae, 599; 
vomiting, 600. 

Urea elimination, in acute yellow atrophy of 
liver. 567: in cirrhosis of liver, 599; in ty- 
phoid. 19. 

Uric acid, in contracted kidney. 627: in gout, 
772. 

Urinary sediments, 594. 

Urine, in acute gastric catarrh, 424: in acute 
yellow atrophy of liver. 566: in amyloid kid- 
ney, 637: in anaemia. 714: in cancer of the 
stomach, 449: in cerebro-spinal meningitis, 
114: in cholera. 87: in chronic gastritis, 
428; in chyluria, 647: in cirrhosis of the liver, 
559: in contracted kidney, 628. 631: in 
croupous pneumonia. 215; in cystitis, 669; in 
diabetes insipidus, 768; in diabetes mellitus, 
752: in diphtheria, 74; in epilepsy. 1144; 
in erysipelas. 66: in gastric ulcer. 436; 
in haemoglobinuria. 737: in heart disease, 
331: in hydronephrosis. 666: in hydro- 
thorax, 299: in interstitial obstruction. 
504: in jaundice, 539: in nephritis. 608. 



1242 



INDEX 



621; in neurasthenia, 1196; in phosphorous- 
poisoning, 1209; in plague, 109; in pleurisy, 
284; in pulmonary emphysema, 193; in scar- 
let fever, 43; in septic and pyaemic diseases, 
120; in small-pox, 55; in typhoid, 19; in ty- 
phus, 32; in yellow fever, 105. 

Urotropine, in cystitis, 671; in genito-urinary 
tuberculosis, 664. 

Urticaria, in articular rheumatism, 680; in 
goitre, 912; in neuralgia, 807. 

Vaccination, 60. 
Vaccinia, 60. 

Valerian, in diabetes insipidus, 770: in epi- 
lepsy, 1150; in hysteria, 1191. 

Valvular disease of the heart, 308. 

Valvular pneumothorax, 297. 

Varicella, 62: diagnosis, 62; eruption of, 62; 
fever of, 62; prognosis, 63; stage of incu- 
bation, 62. 

Variola. See Small-pox. 

Varioloid. See Small-pox. 

Vascular stasis, in cirrhosis of the liver, 557; 
in mediastinal tumors, etc., 301. 

Vaso-motor spasm, 899. 

Vaso-motor and trophic neuroses, 898; paraly- 
sis, 898; spasm, 899. 
Venesection in apoplectic shock, 1102. 
Verdigris poisoning, 1208. 

Vertigo, in anaemia, 712; in cerebellar disease, 
984, 1086; in cerebral abscess, 1110: in cere- 
bral haemorrhage, 1092; in cerebral tumor. 
1118: in chlorosis, 712: in epilepsy. 1145: 
in insolation. 1114; labyrinthine, see 
Meniere's Disease; in leukaemia, 731: in 
multiple sclerosis, 957: in oculo-motor 
paralysis. 856: in cerebro-spinal meningitis. 
113. 

Vesical catarrh. See Ctstitis. 
Vesicatory treatment of neuralgia, 808. 
Vicarious menstruation, 139. 
Vitiligo in goitre, 912. 

Vocal fremitus, in pleurisy, 290; in pneumo- 
thorax, 297. 
Volvulus, 500. 
Vomit, black, 105. 1206. 

Vomiting, in acute yellow atrophy of liver, 
568; cerebral, 1118; in cholera, 88; in chronic 
gastritis, 426-428; in croupous pneumonia, 
214: in diphtheria, 70; in dysentery, 82; in 
erysipelas, 64; in gastric ulcer, 435, 442: in 
influenza, 78; in intestinal anthrax. 129: in 
migraine, 906; in nephritis. 611: in ocular 
paralysis, 857; in peritonitis. 525: in pyloric 



stenosis, 439; in scarlet fever, 39; in typhoid, 
12; in uraemia, 600; in whooping-cough. 173. 
Vomiting, stercoraceous, 503. 

Warmth, sensation of. in paralysis agitans, 
1159. 

Water cancer. See Noma. 
Water-cures for chronic laryngitis, 144. 
Waxy liver, 580. 

Weights and measures, table of, 1214. 

Weil's disease. See Acute Febrile Jaundice. 

Wernicke's hemiopic pupillary reaction (see 
footnote), 1076. 

Whip-worm. See Intestinal Parasites. 

Whooping-cough, 172; aetiology, symptoms, 
and course of. 172; catarrhal stage. 173: 
complications and sequelae, 174; contagious- 
ness, .172; diagnosis. 174; fever in. 172: 
haemorrhages in, 173; hemiplegia in, 173; 
prodromal symptoms, 173; prognosis, 175; 
pulmonary emphysema in, 174. 189; treat- 
ment, 175; ulcer in, 173. 

Widal's seruin reaction, 22; in acute miliary 
tuberculosis, 265; in septic and pyaemic dis- 
eases, 121. 

Wintergreen, oil of, in articular rheumatism, 
685. 

Word-blindness, 1083. 
Word-deafness, 1080. 

Worms, seat. See Intestinal Parasites. 
Writer's cramp, 882. 

Xanthelasma in jaundice, 538. 
Xanthine, 766; calculi, 658. 

Yawning, spasmodic, 712. 

Yellow fever, 104; aetiology of, 104; bacillus 
icteroides, 104; baths in, 106; black vomit, 
105: boxwood liver, 105; capillary con- 
gestion, 105; contagiousness. 104; course 
and symptoms, 105; diagnosis, prognosis, 
and treatment, 106; disinfection, 106; haem- 
orrhage, 105; headache in, 105; immunity, 
104; influence of temperature, 104: jaundice 
in, 105; negro susceptibility to, 104: patho- 
logical anatomy, 105; prognosis, 106: tem- 
perature in. 105; urine, 105. 

Zinc oxide, in epilepsy, 1150; in localized 

spasm, 877. 
Zinc oxide and valerianate in chorea. 1156. 
Zinc poisoning, 1208. 
Zones, hysterogenous. 1149, 11S6. 
Zoster, 805. 815: in tabes dorsalis. 974. 



THE END 



